pituitrin has been researched along with Hypotension--Orthostatic* in 40 studies
8 review(s) available for pituitrin and Hypotension--Orthostatic
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[Orthostatic hypotension in the elderly].
Orthostatic hypotension (OH) is defined as a decrease in systolic blood pressure of 20 mmHg, or a decrease in diastolic blood pressure of 10 mmHg within three minutes of standing. It results from an inadequate response to postural changes in blood pressure. Common symptoms include dizziness, light-headedness, blurred vision, weakness, fatigue, nausea, palpitations, sweating, head and neck ache, slow cognitive performance and transient loss of conscientiousness. OH is a common problem among elderly patients and its aetiology is diverse, including autonomic nervous system dysfunction, cardiac problems, medication side effects, ageing changes or transitory deregulation of blood volume. The instrumental diagnosis can be easily accomplished by the tilt-table test, with continuous monitoring of blood pressure and cardiac parameters. It is a non-invasive technique and needs minimal collaboration from the patient. In our experience, when reviewing 327 patients, aged over 40 years and examined because of clinical suspicion of OH, the prevalence thereof was 51% whereas if focused in subjects older than 70, OH was proven in 90% of the cases. The older the patients, the more frequently they presented general deterioration, neurological or cardiac problems as well as pharmacological side effects. Ruling out neurological or cardiac malfunction can drastically improve the prognosis with possible reversibility of symptoms. Some nonpharmacological and pharmacological approaches to improve management of OH and life quality are described for guidance. Topics: Adult; Age of Onset; Aged; Aged, 80 and over; Autonomic Nervous System Diseases; Cardiovascular Diseases; Central Nervous System Stimulants; Dehydration; Diagnostic Techniques, Neurological; Fludrocortisone; Fluid Therapy; Humans; Hypotension, Orthostatic; Metabolic Diseases; Middle Aged; Stockings, Compression; Sympathomimetics; Vasopressins | 2013 |
Orthostatic hypertension-a new haemodynamic cardiovascular risk factor.
Orthostatic hypertension-a condition characterized by a hyperactive pressor response to orthostatic stress-is an emerging risk factor for cardiovascular disease and is associated with hypertensive target-organ damage (resulting in silent cerebrovascular disease, left ventricular hypertrophy, carotid atherosclerosis and/or chronic kidney disease) and cardiovascular events (such as coronary artery disease and lacunar stroke). The condition is also considered to be a form of prehypertension as it precedes hypertension in young, normotensive adults. Orthostatic blood pressure changes can be assessed using orthostatic stress tests, including clinic active standing tests, home blood pressure monitoring and the head-up tilting test. Devices for home and for ambulatory blood pressure monitoring that are equipped with position sensors and do not induce a white-coat effect have increased the sensitivity and specificity of diagnosis of out-of-clinic orthostatic hypertension. Potential major mechanisms of orthostatic hypertension are sympathetic hyperactivity (as a result of hypersensitivity of the cardiopulmonary and arterial baroreceptor reflex) and α-adrenergic hyperactivation. Orthostatic hypertension is also associated with morning blood pressure surge and extreme nocturnal blood pressure dipping, both of which increase the pulsatile haemodynamic stress of central arterial pressure and blood flow in patients with systemic haemodynamic atherothrombotic syndrome. Topics: Age Factors; Arteriosclerosis; Blood Pressure Monitoring, Ambulatory; Blood Volume; Brain Infarction; Cardiovascular Diseases; Diabetes Mellitus; Hemodynamics; Humans; Hypertriglyceridemia; Hypotension, Orthostatic; Posture; Prehypertension; Receptors, Adrenergic, alpha; Renal Insufficiency, Chronic; Risk Factors; Sympathetic Nervous System; Thrombosis; Tilt-Table Test; Vasopressins; Ventricular Remodeling | 2013 |
Current pharmacologic treatment for orthostatic hypotension.
Orthostatic hypotension is treated effectively with the combined use of non-pharmacological and pharmacological interventions. Patients should be counseled as to the nature of the underlying disorder and reversible causes of orthostatic hypotension should be removed. Should symptoms persist, pharmacological treatment is implemented. First line pharmacotherapeutic interventions include volume repletion in combination with alpha-adrenoreceptor agonists. If unsuccessful there are several supplementary agents with different mechanisms of action that may provide an additive effect. Topics: Anti-Inflammatory Agents; Blood Pressure; Dopamine Uptake Inhibitors; Enzyme Inhibitors; Fludrocortisone; Humans; Hypotension, Orthostatic; Sympathomimetics; Vasoconstrictor Agents; Vasopressins | 2008 |
Blood pressure disturbance in diabetes mellitus.
Arterial hypertension and, less often, postural hypotension are frequently associated with diabetes mellitus, and with diabetic complications and death.. To review data on the relationship between hypertension and nephropathy in diabetes mellitus.. We reviewed data on both retinopathy and nephropathy in hypertensive diabetic patients. Data suggesting that vasopressin levels might affect blood pressure in upright patients with postural hypotension due to cardiocirculatory diabetic neuropathy were also examined. Antihypertensive treatment during different phases of diabetic nephropathy in insulin-dependent diabetes was reviewed.. The data showed that hydrochlorothiazide and nitrendipine reduce urinary protein excretion in parallel with a reduction in blood pressure. However, the decreases in urinary protein excretion induced by captopril are not correlated with a reduction in blood pressure and may be related to decreases in intraglomerular pressure found in patients with mild renal failure taking furosemide. Domperidone, a peripherally acting dopaminergic antagonist is an additional therapeutic option for the treatment of diabetic postural hypotension. Topics: Antihypertensive Agents; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Diabetic Neuropathies; Diabetic Retinopathy; Female; Humans; Hypertension; Hypertension, Renal; Hypotension, Orthostatic; Male; Vasopressins | 1992 |
[Idiopathic orthostatic hypotension--humoral disorders].
Topics: Angiotensin II; Blood Pressure; Catecholamines; Humans; Hypotension, Orthostatic; Prostaglandins F; Receptors, Adrenergic; Renin-Angiotensin System; Vasopressins | 1984 |
Renal consequences of nonsteroidal antiinflammatory drugs.
Nonsteroidal antiinflammatory drugs can adversely affect the kidney. They may induce sodium retention and antagonize the action of diuretics, impair free-water clearance and cause hyponatremia, and prevent aldosterone production and cause hyperkalemic hyperchloremic acidosis. If patients taking these drugs are exposed to a renal insult, acute renal failure becomes more likely. Similarly, patients with chronic renal disease who are taking them appear to be at greater risk of chronic renal failure. However, not all renal effects of nonsteroidal antiinflammatory drugs are adverse. Beneficial effects have been reported in patients with Bartter's syndrome and in those with severe orthostatic hypotension. Topics: Acidosis; Acute Kidney Injury; Aged; Anti-Inflammatory Agents; Bartter Syndrome; Female; Humans; Hyponatremia; Hypotension, Orthostatic; Ibuprofen; Indomethacin; Kidney; Kidney Failure, Chronic; Lupus Erythematosus, Systemic; Nephrotic Syndrome; Prostaglandin Antagonists; Sodium; Vasopressins | 1982 |
Vincristine neurotoxicity.
Topics: Abdomen; Autonomic Nervous System; Axons; Constipation; Cranial Nerves; Depression; Diabetic Neuropathies; Drug Interactions; Hallucinations; Humans; Hyponatremia; Hypotension, Orthostatic; Intestinal Obstruction; Muscular Atrophy; Nervous System Diseases; Neural Conduction; Norepinephrine; Pain; Paresthesia; Parkinson Disease; Peripheral Nervous System Diseases; Seizures; Vasopressins; Vincristine | 1974 |
[ON SO-CALLED "POSTURAL HYPOTENSION." HYPOTENSION DEPENDENT ON POSTURE IN IDIOPATHIC DISORDERS OF THE AUTONOMIC REGULATION OF CIRCULATION].
Topics: Aldosterone; Angiotensins; Autonomic Nervous System; Autonomic Nervous System Diseases; Desoxycorticosterone; Ephedrine; Fludrocortisone; Humans; Hypotension, Orthostatic; Posture; Sweating; Tachycardia; Vasopressins | 1964 |
5 trial(s) available for pituitrin and Hypotension--Orthostatic
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Does resistance exercise prevent body fluid changes after a 90-day bed rest?
Although various exercise regimens are commonly used as countermeasures to reduce the cardiovascular deconditioning induced by microgravity, the underlying mechanisms are not well understood. In this study we aimed to test whether lower limb resistance exercise with flywheel technology can prevent the fluid homeostasis alterations induced by 90-day head-down tilt bed-rest (HDT), and thus improve orthostatic tolerance. Total body water (TBW, measured by isotope dilution) and plasma volume (PV, calculated from the haemoglobin and the haematocrit) were measured in a control group (Co, n=9) and a countermeasure group (CM, n=9). Simultaneously, plasma atrial natriuretic peptide (ANP), renin (AR), and aldosterone (Aldo), as well as urinary anti-diuretic hormone (ADH), were measured. Orthostatic tolerance was evaluated with a 10 min +80 degrees tilt-test the first day of recovery. After HDT, both groups showed a comparable decrease in orthostatic tolerance [8.2 (0.9) min, Co; 8.0 (0.7) min, CM], PV [-4.7 (1.8)%, Co; -6.2 (2.5)%, CM, P<0.05] and TBW [-6.3 (5.4)%, Co; -3.7 (2.1)%, CM, P<0.05]. AR [97.4 (22.0)%, Co; 117.3 (26.4)%, CM] and Aldo [111.3 (58.4)%, Co; 100.6 (52.0)%, CM] increased significantly in both groups but the countermeasures produced no noticeable effects [data are expressed as mean (SE)]. The drop in ANP was also similar in both groups [-42.0 (15.2)%, Co; -51.1 (27.7)% for the CM]. Surprisingly, urinary ADH declined similarly in both groups during the basal data control period [-25.3 (5.2)%, Co; -26.1 (9.6)%, CM) and was sustained at this level during the 90-day HDT. These results show that, under the conditions described, the flywheel exercise device failed to improve characteristic manifestations of cardiovascular deconditioning and suggest that more frequent and powerful exercise, associated with another device (e.g. LBNP) might be a better countermeasure. Topics: Adult; Aldosterone; Bed Rest; Blood Cell Count; Blood Pressure; Blood Volume; Body Fluids; Body Mass Index; Body Water; Body Weight; Erythrocyte Count; Heart Rate; Hemoglobins; Humans; Hypotension, Orthostatic; Male; Physical Fitness; Plasma Volume; Renin; Rest; Urodynamics; Vasopressins; Water-Electrolyte Balance; Weightlessness Countermeasures | 2004 |
Hypovolemic intolerance to lower body negative pressure in female runners.
An attenuated baroreflex response and orthostatic intolerance have been reported in endurance-trained male athletes; however, it is still unknown whether this occurs also in females. The purpose of the present study was to examine whether endurance exercise-trained women had a predisposition to orthostatic compromise, and if so, what causative factor(s) may induce orthostatic intolerance.. We studied cardiovascular and hormonal responses to graded lower body negative pressure (LBNP) (0 to -60 mm Hg) in 26 middle-distance female runners (18.6 +/- 0.1 yr) as the exercise-trained (ET) subjects and 23 age-matched untrained (UT) control subjects. On the basis of the occurrence of syncope episodes during LBNP, ET and UT subjects were further allocated to two groups; ET with presyncope (ET+syncope) and without presyncope (ET-syncope) and UT with presyncope (UT+syncope) and without presyncope (UT-syncope).. Occurrence of presyncope episodes during LBNP was higher in ET (65.4%, P < 0.05) than that for UT (34.8%). Leg compliance was higher (P < 0.05) in ET than in UT. LBNP reduced stroke volume (SV) more (P < 0.05), increased heart rate (HR) higher (P < 0.05), and increased forearm vascular resistance (FVR) more in ET+syncope as compared with the other groups. Response of vasoactive hormones to LBNP was higher in ET+syncope (P < 0.05) than that of the other groups except for norepinephrine (NE); high in both ET+syncope and UT+syncope. The relationship between SV and NE, an index of sympathetic neuronal response, had no training-related changes during LBNP.. We conclude that exercise-trained females have a high incidence of orthostatic intolerance during LBNP, with a greater reduction of SV independent of changes in baroreflex and neurohumoral function. A lower incidence of LBNP intolerance in UT may be accounted for by a lower reduction of SV during LBNP. An increase in leg compliance in the exercise-trained females may play an important role in inducing pronounced reduction of SV and hence the intolerance to LBNP. Topics: Adolescent; Adult; Baroreflex; Female; Humans; Hypotension, Orthostatic; Hypovolemia; Lower Body Negative Pressure; Norepinephrine; Physical Endurance; Renin; Running; Sex Factors; Stroke Volume; Syncope; Vasopressins | 2001 |
A potent pressor response elicited by drinking water.
Topics: Aged; Blood Pressure; Drinking; Humans; Hypotension, Orthostatic; Middle Aged; Norepinephrine; Pressoreceptors; Renin; Vasopressins | 1999 |
Pathogenesis and management of delayed orthostatic hypotension in patients with chronic fatigue syndrome.
The relationship between orthostatic hypotension and chronic fatigue syndrome (CFS) has been reported previously. To study the pathogenesis and management of delayed orthostatic hypotension in patients with CFS, a case comparison study with follow-up of 8 weeks has been designed. A group of 78 patients with CFS (mean age 40 years; 49% men and 51% women), who fulfilled the Centre for Disease Control and Prevention criteria were studied. There were 38 healthy controls (mean age 43 years; 47% men and 53% women). At entry to the study each subject underwent an upright tilt-table test, and clinical and laboratory evaluation. Patients with orthostatic hypotension were offered therapy with sodium chloride (1200 mg) in a sustained-release formulation for 3 weeks, prior to resubmission to the tilt-table testing, and clinical and laboratory evaluation. An abnormal response to upright tilt was observed in 22 of 78 patients with CFS. After sodium chloride therapy for 8 weeks, tilt-table testing was repeated on the 22 patients with an abnormal response at baseline. Of these 22 patients, 10 redeveloped orthostatic hypotension, while 11 did not show an abnormal response to the test and reported an improvement of CFS symptoms. However, those CFS patients who again developed an abnormal response to tilt-test had a significantly reduced plasma renin activity (0.79 pmol/ml per h) compared both with healthy controls (1.29 pmol/ml per h) and with those 11 chronic fatigue patients (1.0 pmol/ml per h) who improved after sodium chloride therapy (p = 0.04). In conclusion, in our study CFS patients who did not respond to sodium chloride therapy were found to have low plasma renin activity. In these patients an abnormal renin-angiotensin-aldosterone system could explain the pathogenesis of orthostatic hypotension and the abnormal response to treatment. Topics: Adult; Catecholamines; Delayed-Action Preparations; Fatigue Syndrome, Chronic; Female; Follow-Up Studies; Humans; Hypotension, Orthostatic; Male; Posture; Renin-Angiotensin System; Sodium Chloride; Vasopressins | 1997 |
Cardiovascular adaptation during simulated microgravity: lower body negative pressure to counter orthostatic hypotension.
The cardiovascular function is one of the main functions disturbed by microgravity. It is particularly affected by the astronaut's return to Earth, where one of the symptoms of the cardiovascular adaptation syndrome is orthostatic hypotension; the clinical consequence can be presyncopal state or a syncope. Lower body negative pressure (LBNP) is intended to stimulate the venous system of the lower limbs. Studies performed in the U.S. have shown that LBNP constitutes an efficient countermeasure, but this approach is impractical because 4 to 6 h/d of application are required. Five volunteers took part in two recent antiorthostatic bed rest experiments for 30 days. In the first experiment, three subjects were submitted to several sessions of LBNP per day and two others were controls; in the second, the LBNP group of the first experiment became control and vice versa. Two orthostatic investigations were performed: 5 d before bed rest; and at the end of the 30-d bed rest period. The results showed that: 1) when the subjects were controls, a high orthostatic hypotension post bed rest with three syncopes and one presyncopal state during the first minutes of the tilt test appeared; 2) when the subjects were submitted to LBNP sessions, no orthostatic hypotension was noted. These two experiments proved the beneficial effects of the LBNP as a countermeasure against orthostatic hypotension. Topics: Adaptation, Physiological; Adult; Bed Rest; Blood Pressure; Cardiovascular Physiological Phenomena; Catecholamines; Gravitation; Heart Rate; Humans; Hypotension, Orthostatic; Lower Body Negative Pressure; Plasma Volume; Renin; Space Flight; Vasopressins | 1991 |
27 other study(ies) available for pituitrin and Hypotension--Orthostatic
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Distinct neurohumoral biomarker profiles in children with hemodynamically defined orthostatic intolerance may predict treatment options.
Studies of adults with orthostatic intolerance (OI) have revealed altered neurohumoral responses to orthostasis, which provide mechanistic insights into the dysregulation of blood pressure control. Similar studies in children with OI providing a thorough neurohumoral profile are lacking. The objective of the present study was to determine the cardiovascular and neurohumoral profile in adolescent subjects presenting with OI. Subjects at 10-18 yr of age were prospectively recruited if they exhibited two or more traditional OI symptoms and were referred for head-up tilt (HUT) testing. Circulating catecholamines, vasopressin, aldosterone, renin, and angiotensins were measured in the supine position and after 15 min of 70° tilt. Heart rate and blood pressure were continuously measured. Of the 48 patients, 30 patients had an abnormal tilt. Subjects with an abnormal tilt had lower systolic, diastolic, and mean arterial blood pressures during tilt, significantly higher levels of vasopressin during HUT, and relatively higher catecholamines and ANG II during HUT than subjects with a normal tilt. Distinct neurohumoral profiles were observed when OI subjects were placed into the following groups defined by the hemodynamic response: postural orthostatic tachycardia syndrome (POTS), orthostatic hypotension (OH), syncope, and POTS/syncope. Key characteristics included higher HUT-induced norepinephrine in POTS subjects, higher vasopressin in OH and syncope subjects, and higher supine and HUT aldosterone in OH subjects. In conclusion, children with OI and an abnormal response to tilt exhibit distinct neurohumoral profiles associated with the type of the hemodynamic response during orthostatic challenge. Elevated arginine vasopressin levels in syncope and OH groups are likely an exaggerated response to decreased blood flow not compensated by higher norepinephrine levels, as observed in POTS subjects. These different compensatory mechanisms support the role of measuring neurohumoral profiles toward the goal of selecting more focused and mechanistic-based treatment options for pediatric patients with OI. Topics: Adolescent; Aldosterone; Angiotensin I; Angiotensin II; Angiotensins; Arterial Pressure; Blood Pressure; Catecholamines; Child; Diastole; Dopamine; Epinephrine; Female; Heart Rate; Humans; Hypotension, Orthostatic; Male; Norepinephrine; Orthostatic Intolerance; Postural Orthostatic Tachycardia Syndrome; Prospective Studies; Renin; Syncope; Systole; Tilt-Table Test; Vasopressins | 2016 |
Vasopressin release induced by hypothension is blunted in patients with diabetic autonomic neuropathy.
The response of arginin-vasopressin (AVP) to baroreceptor activation (tilt testing) was investigated in patients with diabetic autonomic neuropathy (DAN). The present data show that hypothension induced by upright position showed a slight increase of AVP in patients with DAN in comparison with normal subjects and diabetic patients without DAN. These findings suggest that the blunted AVP response to hypothension may be due to lesions of afferent autonomic pathways present in DAN and plays a role in the pathogenesis of postural hypothension. Topics: Afferent Pathways; Aged; Autonomic Pathways; Case-Control Studies; Diabetes Mellitus, Type 1; Diabetic Neuropathies; Female; Hemodynamics; Humans; Hypotension, Orthostatic; Male; Middle Aged; Saline Solution, Hypertonic; Tilt-Table Test; Vasopressins | 2011 |
Plasma volume restoration with salt tablets and water after bed rest prevents orthostatic hypotension and changes in supine hemodynamic and endocrine variables.
Head-down bed rest changes the values of many cardiovascular and endocrine variables and also elicits significant hypovolemia. Because previous studies had not controlled for hypovolemia, it is unknown whether the reported changes were primary effects of bed rest or secondary effects of bed rest-induced hypovolemia. We hypothesized that restoring plasma volume with salt tablets and water after 12 days of head-down bed rest would result in an absence of hemodynamic and endocrine changes and a reduced incidence of orthostatic hypotension. In 10 men, we measured changes from pre-bed-rest to post-bed-rest in venous and arterial pressures; heart rate; stroke volume; cardiac output; vascular resistance; plasma norepinephrine, epinephrine, vasopressin, renin activity (PRA), and aldosterone responses to different tilt levels (0 degrees, -10 degrees, 20 degrees, 30 degrees, and 70 degrees); and plasma volume and platelet alpha2- and lymphocyte beta2-adrenoreceptor densities and affinities (0 degrees tilt only). Fluid loading at the end of bed rest restored plasma volume and resulted in the absence of post-bed-rest orthostatic hypotension and changes in supine hemodynamic and endocrine variables. Fluid loading did not prevent post-bed-rest increases in beta2-adrenoreceptor density or decreases in the aldosterone-to-PRA ratio (P = 0.05 for each). Heart rate, epinephrine, and PRA responses to upright tilt after bed rest were increased (P < 0.05), despite the fluid load. These results suggest that incidents of orthostatic hypotension and many of the changes in supine hemodynamic and endocrine variables in volume-depleted bed-rested subjects occur secondarily to the hypovolemia. Despite normovolemia after bed rest, beta2-adrenoreceptors were upregulated, and heart rate, epinephrine, and PRA responses to tilt were augmented, indicating that these changes are independent of volume depletion. Topics: Adult; Aldosterone; Baroreflex; Bed Rest; Blood Pressure; Drinking; Endocrine System; Epinephrine; Heart Rate; Humans; Hypotension, Orthostatic; Male; Norepinephrine; Plasma Volume; Receptors, Adrenergic; Renin; Sodium Chloride; Space Flight; Stroke Volume; Supine Position; Vascular Resistance; Vasopressins; Weightlessness Simulation | 2005 |
Gender influence on vasoactive hormones at rest and during a 70 degrees head-up tilt in healthy humans.
To evaluate the influence of age and gender on the neuroendocrine control of blood pressure in normal subjects, a 13-min 70 degrees head-up tilt (HUT) was applied after 3 h of recumbency to 109 healthy men and women aged 23-50 yr (age group I) and 51-77 yr (age group II). We found that age and gender had a significant influence on plasma norepinephrine (PNE) concentration at baseline and in the upright position. PNE was significantly higher in older men compared with the younger men and women of both age groups, suggesting a divergent age-related activation of the sympathetic nervous system between genders at baseline as well as during a sustained orthostatic challenge. There was no significant influence of age or gender on plasma epinephrine at baseline or during HUT. Plasma renin activity was significantly higher at baseline as well as in the upright position during HUT in elderly men than in women. Age or gender had no influence on plasma vasopressin (PAVP), and, regardless of age, nonhypotensive HUT induced an extremely modest increase in PAVP. The syncopal subjects displayed a hormonal pattern associating increased PNE and a surge in plasma epinephrine and PAVP minutes before syncope during HUT. The orthostatic intolerance appears not to be a feature of healthy aging per se. In healthy subjects, both age and gender modulate markedly the cardiovascular and neuroendocrine responses to an orthostatic challenge and must be taken into consideration, particularly when catecholamine responses are studied. Topics: Adult; Age Factors; Aged; Blood Pressure; Epinephrine; Female; Heart Rate; Humans; Hypotension, Orthostatic; Male; Middle Aged; Neurosecretory Systems; Norepinephrine; Posture; Renin; Rest; Sex Factors; Vasopressins | 2002 |
Mechanisms of inhibition of vasopressin release during moderate antiorthostatic posture change in humans.
The hypothesis was tested that the carotid baroreceptor stimulation caused by a posture change from upright seated with legs horizontal (Seat) to supine (Sup) participates in the suppression of arginine vasopressin (AVP) release. Ten healthy males underwent this posture change for 30 min without or with simultaneous application of lower body negative pressure (LBNP) adjusted to maintain left atrial diameter (LAD) at the Seat level. Throughout Sup, mean arterial pressure and heart rate decreased from 98 +/- 2 to 91 +/- 2 mmHg and from 63 +/- 2 to 55 +/- 2 beats/min (P < 0.05), respectively, whereas the corresponding decreases during Sup + LBNP were attenuated and of shorter duration (98 +/- 2 to 93 +/- 2 mmHg and 62 +/- 2 to 58 +/- 3 beats/min, P < 0.05). During Sup, LAD increased from 30 +/- 1 to 33 +/- 1 mm, and arterial pulse pressure (PP) increased from 40 +/- 2 to 47 +/- 2 mmHg, whereas plasma AVP decreased from 0.9 +/- 0.2 to 0.5 +/- 0.1 pg/ml (P < 0.05), and plasma norepinephrine (NE) decreased from 176 +/- 20 to 125 +/- 16 pg/ml (P < 0.05). During Sup + LBNP, there were no changes in LAD, PP, plasma AVP, or NE. In conclusion, vasopressin secretion is suppressed during an antiorthostatic posture change, which increases carotid sinus pressure, PP, and LAD. The suppression is absent when PP and LAD are prevented from increasing and is thus critically dependent on at least one of these stimuli. Topics: Adult; Blood Pressure; Humans; Hypotension, Orthostatic; Lower Body Negative Pressure; Male; Posture; Vasopressins | 1999 |
The role of potassium in postural hypotension: electrolytes and neurohumoral factors in elderly hypertensive patients using diuretics.
To study the association between postural hypotension and (i) electrolyte levels and (ii) neurohumoral factors in elderly hypertensive patients using diuretics.. Cross-sectional study of patients and controls.. The subjects were gathered from senior citizen clubs or they were referred to the study by general practitioners. The subjects were examined on a geriatric ward in Turku City Hospital.. Seven subjects with postural hypotension and 13 controls.. Plasma electrolyte levels and neurohumoral response to head-up tilt.. There were significantly more hypokalaemic subjects in the postural hypotension group (5/7) than in the control group (1/13) (P < 0.01). The plasma potassium level was negatively correlated to plasma aldosterone (r = -0.57; P < 0.01) and renin activity (r = -0.69; P < 0.001). Subjects with postural hypotension had higher levels of noradrenaline, both supine (P < 0.05) and during tilt (P < 0.05). There were no significant differences in supine or tilt levels of plasma adrenaline, vasopressin, atrial natriuretic peptide, aldosterone and renin activity between the groups.. The results suggest that potassium depletion is associated with postural hypotension in elderly hypertensive patients using diuretics. However, it is unclear whether there is a causative link between potassium depletion and postural hypotension or whether they are both caused by some other factor, e.g. volume contraction. Topics: Aged; Aged, 80 and over; Aldosterone; Atrial Natriuretic Factor; Case-Control Studies; Cross-Sectional Studies; Diuretics; Electrolytes; Epinephrine; Female; Humans; Hypertension; Hypotension, Orthostatic; Male; Neurotransmitter Agents; Potassium; Renin; Tilt-Table Test; Vasopressins | 1995 |
Changes in plasma vasopressin levels and cardiovascular function due to postural changes in diabetic neuropathy.
Decreases in blood pressure are well known to increase the release of vasopressin. Studies were carried out to investigate whether vasopressin responses to postural changes in blood pressure are maintained in diabetic patients with orthostatic hypotension [DM-OH(+)] as well as non-diabetic patients with orthostatic hypotension [nonDM-OH(+)] and these responses were compared with those observed in normal subjects and diabetic patients without orthostatic hypotension [DM-OH(-)]. After 30 min in the supine position, the upright posture for 40 min was maintained and then the supine for 10 min. Blood pressure and heart rate (HR) were measured every 5 min and plasma vasopressin levels (plasma AVP) were determined every 10 min. In normal subjects and DM-OH(-), mean arterial blood pressure (MABP) did not change, but HR increased significantly by the upright position. Plasma AVP did not change in these groups. On the other hand, in DM-OH(+) MABP fell abruptly and remained to decrease during the upright posture. The HR responses in this group, however, were similar to those in normal control and DM-OH(-). Plasma AVP in DM-OH(+) significantly increased only at 30 min during upright. These increases were significantly greater than those in normal and DM-OH(-). There were significant correlation in changes in MABP (delta MAP) and plasma AVP (delta AVP) in DM-OH(+) (delta AVP = -0.13 MABP + 1.5, r = -0.32, p < 0.01). Relationship between delta MABP and delta AVP in nonDM-OH(+) was similar to that in DM-OH(+). It is concluded that AVP responses to orthostatic hypotension in diabetic and non-diabetic neuropathies were attenuated, but heart rate responses in these patients ware well reserved. Topics: Adult; Aged; Baroreflex; Diabetic Neuropathies; Female; Heart Rate; Hemodynamics; Humans; Hypotension, Orthostatic; Male; Middle Aged; Osmolar Concentration; Posture; Vasopressins | 1995 |
Loss of osmotic thirst in multiple system atrophy: association with sinoaortic baroreceptor deafferentation.
We evaluated plasma osmolality (pOsm), thirst, and vasopressin response to hypertonic saline infusion in 14 patients with multiple system atrophy (MSA). This disease is characterized by the degeneration of noradrenergic neurons in the central nervous system and severe orthostatic hypotension. Seven patients were also characterized by the lack of vasopressin response to hypotension (group B) and seven by a preserved response (group A). In group A pOsm rose from 290 +/- 2 to 312 +/- 6 mosmol/kgH2O, vasopressin from 0.9 +/- 0.3 to 5.7 +/- 0.5 pmol/l, and thirst from 1.1 +/- 0.1 to 8.7 +/- 1.1 cm on the visual analog scale. After saline, patients drank 1,215 +/- 150 ml of water (no different from healthy controls). In group B patients' pOsm rose from 296 +/- 3 to 325 +/- 6 mosmol/kgH2O and vasopressin from 1.2 +/- 0.1 to 19.6 +/- 0.4 pmol/l (P < 0.01 vs. group A and controls). Group B patients had no thirst during saline and drank little after the challenge (175 +/- 50 ml; P < 0.01 vs. group A and control). Forced drinking decreased vasopressin in patients before changes in pOsm, showing that inhibitory afferents from oropharyngeal mucosa were intact. In MSA patients with altered afferent control of vasopressin there is a dissociation between the osmotic control of thirst and the osmotic control of vasopressin. Topics: Afferent Pathways; Atrophy; Denervation; Drinking; Female; Hemodynamics; Humans; Hypotension, Orthostatic; Male; Middle Aged; Nervous System Diseases; Norepinephrine; Osmosis; Pressoreceptors; Saline Solution, Hypertonic; Sinus of Valsalva; Thirst; Vasopressins | 1994 |
Opioid peptides, adrenocorticotrophic hormone, and idiopathic (orthostatic) edema.
The effect of dextroamphetamine sulfate (Dexedrine) on plasma opioid peptides, hormones, and other metabolites was studied in eight female subjects with idiopathic (orthostatic) edema and five healthy females. All subjects were given 20 mg of dextroamphetamine sulfate, a drug widely used in the treatment of this disorder, and blood samples were collected before and 30, 60, and 90 minutes after treatment. Patients with idiopathic (orthostatic) edema had significantly lower plasma sodium levels but higher blood urea nitrogen, aldosterone, and renin levels. D-amphetamine decreased aldosterone and renin levels in both groups. Plasma adrenocorticotropin levels were lower whereas met-enkephalin levels were higher in idiopathic (orthostatic) edema subjects compared to control subjects. D-amphetamine had no significant effect on plasma beta-endorphin, adrenocorticotrophic hormone, or enkephalins. Our data indicate that opioid peptides, especially enkephalins, and adrenocorticotrophic hormone may be involved in the pathogenesis of idiopathic (orthostatic) edema syndrome, but they seem uninvolved in the aldosterone- and renin-lowering action of amphetamine. It is possible that amphetamine is acting further down the chain, either directly on the adrenal and kidney or the microvasculature, rather than at hypothalamus-pituitary axis. Topics: Adrenocorticotropic Hormone; Adult; Aldosterone; beta-Endorphin; Blood Urea Nitrogen; Body Weight; Dextroamphetamine; Dopamine; Edema; Endorphins; Enkephalin, Leucine; Enkephalin, Methionine; Female; Humans; Hypotension, Orthostatic; Middle Aged; Renin; Sodium; Spironolactone; Syndrome; Vasopressins | 1994 |
Possible involvement of hypersecretion of ADH in hyponatremia in a diabetic patient complicated with severe neuropathy.
The present case was a 44-year-old man who had been diagnosed as having noninsulin-dependent diabetes mellitus 2 years before admission. He gradually showed severe neuropathy and emaciation because of poor control of his blood glucose levels. He was admitted to our hospital because of disturbance of consciousness with hyponatremia. The endocrinological findings including thyroid and adrenal functions revealed no abnormalities. Insufficiency of water diuresis was noted in the water loading test. Severe orthostatic hypotension was noted during the standing up test, and an excessive response in the plasma ADH level was also noted. These findings demonstrated that excessive ADH secretion occurred to compensate for the fall in blood pressure because of the breakdown of homeostatic regulation in blood pressure due to diabetic neuropathy. It is suggested that hyponatremia seemed to be subsequently induced by hypersecretion of ADH. Topics: Adult; Blood Pressure; Diabetes Mellitus, Type 2; Diabetic Neuropathies; Diuresis; Emaciation; Humans; Hyponatremia; Hypotension, Orthostatic; Male; Osmotic Pressure; Saline Solution, Hypertonic; Vasopressins | 1993 |
Cardiovascular deconditioning during weightlessness simulation and the use of lower body negative pressure as a countermeasure to orthostatic intolerance.
The cardiovascular function is one of the main disturbed by weightlessness: it is particularly affected by the astronaut's return to Earth, where symptoms linked to the cardiovascular deconditioning syndrom appear in the following forms: (1) orthostatic intolerance with its risk of syncope: (2) higher submaximal oxygen consumption for an equivalent work load. Lower Body Negative Pressure (LBNP) is intended to stimulate the venous system of the lower limbs; however, the specific effects of periodical LBNP sessions on the orthostatic intolerance have never been studied. With this objective in mind, 5 volunteers took part in two recent antiorthostatic bedrest experiments for 30 days. In the first experiment 3 subjects were submitted to several sessions of LBNP experiment per day and 2 others were controls; in the second experiment the LBNP group of the 1st one became controls and vice-versa. Two orthostatic investigations were performed: (1) 5 days before the bedrest; (2) at the end of the 30 day bedrest period. The results showed: (1) when the subjects were control, a high orthostatic intolerance post bedrest with 3 syncopes and one presyncopal state during the first minutes of the tilt test; (2) when the subjects were submitted to LBNP sessions, no orthostatic intolerance. Topics: Adult; Aerospace Medicine; Arginine Vasopressin; Bed Rest; Blood Pressure; Cardiovascular Deconditioning; Catecholamines; Evaluation Studies as Topic; Fluid Shifts; Heart Rate; Humans; Hypotension, Orthostatic; Lower Body Negative Pressure; Plasma Volume; Renin; Renin-Angiotensin System; Tilt-Table Test; Vasopressins; Weightlessness Countermeasures; Weightlessness Simulation | 1990 |
Haemodynamic and neurohumoral responses in elderly patients with postural hypotension.
Haemodynamic and neurohumoral responses to head-up tilt were measured in 28 elderly patients with postural hypotension (EPPH) and 12 healthy elderly subjects (HE). There were no differences in catecholamines between the groups and only noradrenaline increased on tilt (P less than 0.001). Plasma renin activity and aldosterone were similar in HE and EPPH in the supine and tilt positions. In both groups vasopressin increases (P = 0.032), and plasma volume decreases were the same (P = 0.673). Supine EPPH had higher heart rates (P = 0.019) but similar cardiac indices (P = 0.621). Both had similar changes on tilting (P = 0.975 and P = 0.341). Stroke volume decrease was higher in HE (35%) than EPPH (23%; P less than 0.001). HE showed an increase in peripheral resistance on tilting with no change in EPPH (P = 0.005). EPPH had larger coefficients of variation for all variables. The differences in haemodynamic responses and the similarity of neurohumoral responses during tilting suggest end-organ failure in EPPH with individual variations. Postural hypotension in old age is not a single entity. Topics: Aged; Aging; Blood Pressure; Catecholamines; Hemodynamics; Humans; Hypotension, Orthostatic; Neurotransmitter Agents; Renin-Angiotensin System; Vascular Resistance; Vasopressins | 1990 |
Is orthostatic hypotension in the elderly due to autonomic failure?
In order to investigate whether orthostatic hypotension in elderly people is due to autonomic nervous system dysfunction or blood vessel abnormalities, we have measured platelet and lymphocyte adrenoceptor numbers and agonist binding in addition to venous plasma catecholamine concentrations. Eight elderly subjects with orthostatic hypotension and six control elderly subjects were studied. None of the subjects had other symptoms of autonomic failure. There was no significant difference between the heart rate or plasma catecholamine responses to standing of the two groups. The orthostatic hypotension subjects had a significant rise of their plasma vasopressin levels whereas the control group had no significant change. The number of alpha 2-adrenoceptor sites in platelets was lower in the orthostatic hypotensive group compared to the controls and the binding affinity was greater than in the controls. There were no significant differences in beta-adrenoceptor binding sites or affinities in isolated lymphocytes between the two groups. The similar changes in heart rate and catecholamines together with the vasopressin changes suggest that, in these elderly patients with an abnormal drop of blood pressure on standing, there is no dysfunction of autonomic pathways concerned with cardiovascular function. The lower numbers of alpha 2-adrenoceptor sites on isolated platelets in subjects with orthostatic hypotension could indicate reduced alpha 2-adrenoceptor numbers on their blood vessels which could contribute to their inability to maintain blood pressure while standing. Topics: Aged; Aged, 80 and over; Autonomic Nervous System; Blood Platelets; Blood Pressure; Female; Heart Rate; Humans; Hypotension, Orthostatic; Lymphocytes; Male; Norepinephrine; Receptors, Adrenergic; Vasopressins | 1990 |
The effect of moderate hypotension on vasopressin levels in normal humans.
Isosmotic decreases in central venous pressure do not stimulate arginine vasopressin (AVP) secretion in normal humans, while symptomatic vasovagal hypotension produces large rises in plasma AVP levels. The effects of an asymptomatic fall in arterial pressure on plasma AVP in humans are poorly documented. Heart rate, mean arterial pressure, plasma osmolality, and plasma AVP were measured in seven healthy volunteers during infusion of sodium nitroprusside on two occasions, with and without central venous pressure measurements. On both study days, heart rate increases (5 +/- 3 and 8 +/- 4 beats/min) and mean arterial pressure reductions (12 +/- 3 and 13 +/- 2.0 mm Hg) were comparable. Plasma AVP (3.2 +/- 1.4 and 4.0 +/- 1.7 pg/ml at control) did not change on either study day after nitroprusside titration (30-40 minutes) or after an additional 90 minute observation on the first day. When measured on the second day, central venous pressure declined from 5.6 +/- 1.9 to 2.9 +/- 1.5 mm Hg, p less than .001. Osmolality was constant on both days at all times. Unloading of sinoaortic baroreceptors produced by asymptomatic hypotension, coupled with a moderate reduction in central venous pressure, does not, therefore, stimulate plasma AVP secretion in normal humans. This observation has relevance to understanding the mechanisms involved in the reported increases in plasma AVP during orthostatic stress and in various diseases. Topics: Analysis of Variance; Blood Pressure; Evaluation Studies as Topic; Female; Heart Rate; Humans; Hypotension, Orthostatic; Male; Nitroprusside; Norepinephrine; Osmolar Concentration; Pressoreceptors; Time Factors; Vasopressins | 1989 |
Effect of longitudinal physical training and water immersion on orthostatic tolerance in men.
To test the hypothesis that moderately intense physical training has no effect on orthostasis, orthostatic and fluid-electrolyte-endocrine responses to 60 degrees head-up tilt were compared before and after 6 h of water immersion (34.5 +/- 0.1 degrees C) up to the neck following 6 months of exercise training. During the tilt test the five male subjects (27-42 years) each wore a lower-body positive-pressure suit (MAST-111A antishock trousers). The tilt procedure consisted of a 40-min supine control period (suit deflated), followed by a maximum 90-min tilt period (suit inflated to 50 +/- 5 mm Hg for 30 min, then deflated for 60 min or until presyncope). The mean +/- S.E. pretraining cycle ergometer peak VO2 was 3.20 +/- 0.14 L.min-1 (39 +/- 2 ml.min-1.kg-1), 3.36 +/- 0.27 L.min-1 (42 +/- 4 ml.min-1.kg-1) after 3 months (N.S.), and increased by 18% to 3.78 +/- 0.36 L.min-1 (48 +/- 5 ml.min-1.kg-1, +22%, p less than 0.05) posttraining. During pretraining, water immersion tilt tolerance decreased from 74 +/- 16 min before to 34 +/- 9 min (delta = 40 min, p less than 0.05) after immersion. During posttraining, water immersion tilt tolerance decreased similarly from 74 +/- 16 min preimmersion to 44 +/- 13 min (delta = 30 min, p less than 0.05) postimmersion (74 vs. 74 min, N.S.; 34 vs. 44 min, N.S.).(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Adult; Blood Pressure; Gravity Suits; Heart Rate; Hematocrit; Hemoglobins; Humans; Hypotension, Orthostatic; Immersion; Male; Oxygen Consumption; Physical Education and Training; Potassium; Pressure; Renin; Sodium; Vasopressins | 1988 |
[Interpretation of laboratory tests in idiopathic orthostatic hypotension].
Topics: Autonomic Nervous System Diseases; Diagnosis, Differential; Humans; Hypotension, Orthostatic; Shy-Drager Syndrome; Vasopressins | 1984 |
Vasopressin response to orthostatic hypotension. Etiologic and clinical implications.
Plasma vasopressin was measured before and after tilt testing in 18 patients with orthostatic hypotension of various causes. In six patients, all of whom had normal osmotic regulation of vasopressin, normal stimulation of vasopressin did not occur on tilt testing; all six had clinical evidence of defects in the afferent or central connections of the baroregulatory reflex arc. In the remaining 12 patients, plasma vasopressin increased to levels appropriate for the degree of hypotension; none of these patients had clinical evidence of defects in afferent or central portions of the baroregulatory arc. Those with subnormal vasopressin response had significantly more severe orthostatic hypotension than the patients with normal vasopressin response, but none had plasma hypotonicity, an abnormality present in one-quarter of those with normal response. It is concluded that the vasopressin response to orthostatic hypotension may serve as a test of the integrity of the afferent and central components of the baroregulatory reflex arc. Furthermore, this study suggests that the normal vasopressin response to orthostatic hypotension may moderate the fall in blood pressure but may adversely affect water balance. Topics: Adult; Aged; Female; Hemodynamics; Humans; Hypotension, Orthostatic; Male; Middle Aged; Norepinephrine; Pressoreceptors; Sympathetic Nervous System; Vasopressins; Water-Electrolyte Imbalance | 1983 |
Hyponatremia in Rocky Mountain spotted fever: role of antidiuretic hormone.
Topics: Humans; Hyponatremia; Hypotension, Orthostatic; Inappropriate ADH Syndrome; Infusions, Parenteral; Osmolar Concentration; Rocky Mountain Spotted Fever; Sodium Chloride; Vasopressins | 1983 |
Deficient catecholamine release as the basis of orthostatic hypotension in pernicious anaemia.
A patient with peripheral neuropathy and orthostatic hypotension was found to have pernicious anaemia. Symptoms improved after vitamin B12 replacement therapy. Insulin tolerance testing showed that the patient lacked catecholamine, heart rate, and sweating responses to hypoglycaemia. This indicates that pernicious anaemia may cause orthostatic hypotension owing to failure of noradrenaline release. Topics: Aged; Anemia, Pernicious; Catecholamines; Epinephrine; Humans; Hypesthesia; Hypotension, Orthostatic; Male; Norepinephrine; Vasopressins; Vitamin B 12 Deficiency | 1982 |
Application of vasopressin radioimmunoassay to clinical study: role of vasopressin in hypo- and hypernatremia and some other disorders of water metabolism.
Plasma and urinary arginine vasopressin (AVP) in normal subjects and in patients with various water metabolism disorders was measured using a sensitive, specific radioimmunoassay. The AVP plasma levels in normal subjects were 3.1 +/- 1.2 pg/ml. The parallel changes in plasma osmolality, plasma AVP concentration, and urinary osmolality were observed after water load. In patients with various kinds of hyponatremia and impaired water excretion, plasma AVP concentrations were within or over normal levels, suggesting that persistent secretion of AVP may play an important role in the pathogenesis of hyponatremia. Variable levels of plasma AVP were observed in patients with essential hypernatremia, which in turn suggested that osmoreceptors may be selectively damaged in some patients, and that ADH-secreting neurons are also involved in others. Our radioimmunoassay facility made it possible for us to measure plasma and urinary DDAVP in the treatment of diabetes insipidus. Topics: Adrenal Insufficiency; Adult; Animals; Arginine Vasopressin; Ascites; Diabetes Insipidus; Dogs; Edema; Humans; Hypernatremia; Hyponatremia; Hypotension, Orthostatic; Infant; Neoplasms; Osmolar Concentration; Radioimmunoassay; Vasopressins; Water | 1978 |
Case reports and studies of paraneoplastic hypotension: abnormal low pressure baroreceptor responses.
Intrathoracic stretch receptors regulate adjustments of the vasculature to gravitational changes and influence urinary water and solute excretion. Few reports of pathologic states involving interruption of these regulatory mechanisms have appeared. Two patients with orthostatic hypotenstion related to advanced intrathoracic carcinoma were studied, utilizing tilt-table examinations and immersion of the entire body in water to test the function of their intrathoracic baroreceptor reflex arcs. Both patients showed abnormalities of antidiuretic hormone level and sodium excretion as compared with normal controls. This suggests that total immersion is a safe and convenient test of the low-pressure baroreceptor system in patients with suspected dysfunction. Three patients are also reported whose charts were reviewed posthumously. Although they were not tested in the laboratory, their clinical data suggest that they too had been suffering from an interference with the transmission of impulses from the intrathoracic receptors. Topics: Adult; Aged; Female; Humans; Hypotension, Orthostatic; Male; Middle Aged; Osmolar Concentration; Sodium; Thoracic Neoplasms; Vasopressins | 1977 |
Basis of nocturnal polyuria in patients with autonomic failure.
Five dysautonomic patients with the Shy-Drager syndrome were studied to determine the basis of their nocturnal polyuria. The results indicated excessive postural modification of renal function in dysautonomic patients. This may, in fact, relate to excessive release of ADH while these patients are up and about, and excessive inhibition while they are recumbent. Treatment with vasopressin produced an inconsistent response. Topics: Aged; Circadian Rhythm; Dysautonomia, Familial; Evaluation Studies as Topic; Fecal Incontinence; Female; Humans; Hydrocortisone; Hypotension, Orthostatic; Kidney; Male; Middle Aged; Nervous System Diseases; Osmolar Concentration; Parkinson Disease; Posture; Potassium; Sodium; Syndrome; Urinary Incontinence; Vasopressins; Water Deprivation | 1974 |
Complications of diuretic therapy: severe alkalosis and syndrome resembling inappropriate secretion of antidiuretic hormone.
Topics: Alkalosis; Bicarbonates; Blood Pressure; Blood Urea Nitrogen; Diet, Sodium-Restricted; Diuresis; Edema; Ethacrynic Acid; Female; Furosemide; Humans; Hyponatremia; Hypotension, Orthostatic; Kidney Concentrating Ability; Middle Aged; Potassium Deficiency; Sodium; Vasopressins; Water-Electrolyte Balance | 1970 |
An assessment of various methods of treatment of idiopathic orthostatic hypotension.
Topics: Aged; Angiotensin II; Blood Volume; Ephedrine; Fludrocortisone; Forearm; Hand; Humans; Hypotension, Orthostatic; Iodine Isotopes; Male; Middle Aged; Norepinephrine; Phenylephrine; Plasma Volume; Vascular Resistance; Vasopressins | 1969 |
Relative effectiveness of selected space flight deconditioning countermeasures.
Topics: Adult; Body Temperature; Cold Temperature; Diuresis; Epinephrine; Heart Rate; Humans; Hypotension, Orthostatic; Immersion; Male; Norepinephrine; Plasma Volume; Posture; Space Flight; Tourniquets; Vasopressins; Veins; Weightlessness | 1968 |
[IDIOPATHIC ORTHOSTATIC HYPOTENSION. SEMIOLOGICAL DATA, HEMODYNAMIC INVESTIGATIONS AND THERAPEUTIC RESULTS].
Topics: Angiotensins; Blood Pressure; Cardiac Catheterization; Diagnosis; Drug Therapy; Fludrocortisone; Hemodynamics; Humans; Hypotension, Orthostatic; Norepinephrine; Pharmacology; Pulmonary Circulation; Pure Autonomic Failure; Valsalva Maneuver; Vasomotor System; Vasopressins | 1964 |
IDIOPATHIC ORTHOSTATIC HYPOTENSION. DIAGNOSIS AND TREATMENT.
Topics: Cortisone; Desoxycorticosterone; Diagnosis; Ephedrine; Extrapyramidal Tracts; Fludrocortisone; Humans; Hypotension; Hypotension, Orthostatic; Neurologic Manifestations; Phenylephrine; Physical Therapy Modalities; Posture; Pure Autonomic Failure; Vasopressins | 1963 |