pituitrin and Diabetic-Neuropathies

The renin angiotensin system (RAS) is a peptide hormone system that plays an important role in the pathophysiology of various diseases, including congestive heart failure, hypertension, myocardial infarction, and diabetic nephropathy. This has led researchers to focus extensively on this system, leading to the discovery of various peptides, peptidases, receptors and signal transduction mechanisms intrinsic to the RAS. Angiotensinogen (AGT), angiotensin (Ang) II, Ang III, Ang IV, and Ang-(1-7) are the main biologically active peptides of RAS. However, most of the available studies have focused on Ang II as the likely key peptide from the RAS that directly and indirectly regulates physiological functions leading to pathological conditions. However, data from recent studies suggest that Ang III may produce physiologically relevant effects that are similar to those produced by Ang II. Hence, this review focuses on Ang III and the myriad of physiological effects that it produces in the body.

Topics: Angiotensin III; Animals; Atrial Natriuretic Factor; Blood Pressure; Blood Volume; Cardiovascular Diseases; Diabetic Neuropathies; Humans; Rats; Renin-Angiotensin System; Signal Transduction; Sodium; Thirst; Vasopressins

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

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

To evaluate the role of vasopressin (AVP) on blood pressure (BP) in diabetic patients with autonomic neuropathy (AN), 10 patients were studied on a fixed sodium and potassium diet. On days 4 and 7, a 24-h BP monitoring, as well as blood and urine samples for sodium, potassium, creatinine, and osmolality determinations were obtained for every 4-h period; either placebo or an AVP-V1-antagonist (d(CH2)5Tyr(me)AVP; 0.5 mg; AVPi) were given iv at 1 PM. On placebo, systolic BP (SBP) showed a progressive elevation during the day, declining after 12 PM (8 AM to 12 AM 122+/-9; 12 AM to 4 PM 125+/-11; 4 PM to 8 PM 134+/-14; 8 PM to 12 PM 136+/-14; 12 PM to 8 AM 131+/-17 mm Hg). On AVPi this rise in SBP was blunted: 8 AM to 12 AM 125+/-122; 12 AM to 4 PM 121+/-21; 4 PM to 8 PM 126+/-16; 8 PM to 12 PM 129+/-14; 12 PM to 8 AM 124+/-12 mm Hg. Creatinine clearance and diureses were greater during the night, both with placebo and AVPi. Plasma osmolality did not change on either day, although serum sodium decreased after AVPi, reaching the lowest values at 4 PM to 8 PM period (137+/-4.7 v 131+/-3.8 mEq/L; P < .05). With placebo, fractional excretion of sodium (FENa) increased from 0.43%+/-0.32% during 12 h of orthostasis to 0.92%+/-1.05% during 12 h of recumbency (P < .02). With AVPi, the FENa on orthostasis did not differ from that with placebo, although BP values were lower and did not increase with recumbency (0.58+/-0.57 v 0.73%+/-0.49%; NS). In conclusion, our results show that in diabetic patients with AN, vasopressin participates in BP control by stimulating vascular and renal V1 receptors, which results in vasoconstriction and sodium reabsorption.

Topics: Adult; Aldosterone; Arginine Vasopressin; Autonomic Nervous System Diseases; Blood Pressure; Circadian Rhythm; Diabetic Neuropathies; Female; Hormone Antagonists; Humans; Male; Middle Aged; Osmolar Concentration; Renin; Sodium; Vasopressins; Water-Electrolyte Balance

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

Topics: Amitriptyline; Carbamazepine; Comorbidity; Demeclocycline; Diabetic Neuropathies; Diuretics; Furosemide; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Saline Solution, Hypertonic; Spain; Urea; Vasopressins

Gastrointestinal (GI) dysmotility and autonomic neuropathy are common problems among diabetics with largely unknown aetiology. Many peptides are involved in the autonomic nervous system regulating the GI tract. The aim of this study was to examine if concentrations of oxytocin, cholecystokinin (CCK), gastrin and vasopressin in plasma differ between diabetics with normal function and dysfunction in GI motility.. Nineteen patients with symptoms from the GI tract who had been examined with gastric emptying scintigraphy, oesophageal manometry, and deep-breathing test were included. They further received a fat-rich meal, after which blood samples were collected and plasma frozen until analysed for hormonal concentrations.. There was an increase in postprandial oxytocin plasma concentration in the group with normal gastric emptying (p = 0.015) whereas subjects with delayed gastric emptying had no increased oxytocin secretion (p = 0.114). Both CCK and gastrin levels increased after the meal, with no differences between subjects with normal respective delayed gastric emptying. The concentration of vasopressin did not increase after the meal. In patients with oesophageal dysmotility the basal level of CCK tended to be higher (p = 0.051) and those with autonomic neuropathy had a higher area under the curve (AUC) of gastrin compared to normal subjects (p = 0.007).. Reduced postprandial secretion of oxytocin was found in patients with delayed gastric emptying, CCK secretion was increased in patients with oesophageal dysmotility, and gastrin secretion was increased in patients with autonomic neuropathy. The findings suggest that disturbed peptide secretion may be part of the pathophysiology of digestive complications in diabetics.

Topics: Autonomic Nervous System Diseases; Case-Control Studies; Cholecystokinin; Diabetic Neuropathies; Esophageal Motility Disorders; Female; Gastric Emptying; Gastrins; Gastroparesis; Humans; Male; Oxytocin; Vasopressins

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

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

Thirty-three insulin-dependent diabetic patients were separated into two groups from the results of three different tests for cardiac vagal neuropathy: heart rate response to deep breathing, Valsalva manoeuvre and heart rate response to postural change. Seventeen patients were considered as without ('intact' patients) and 16 as with ('denervated' patients) cardiac autonomic dysfunction. One patient with a transplanted heart was also studied. Plasma antidiuretic hormone (ADH), plasma aldosterone and plasma renin activity (PRA) were measured immediately before and 60 min after intravenous administration of frusemide and passage from lying to standing. The kinetics of hormonal responses were analysed more precisely (five blood collections) in six patients of each group who were studied again. Heart rate and blood pressure were recorded before each blood collection. Volume depletion estimated from the rise in plasma protein (+ 11.9 and + 12.2% in 'denervated' and 'intact' patients respectively) and heart rate response (+ 1.06 and + 14.7%) were similar in both groups. Mean blood pressure was unchanged in the 'intact' patients whereas it fell in the 'denervated' patients (-13.5%). PRA (+ 161.5 and + 231.2% in 'denervated' and 'intact' patients respectively) and plasma aldosterone (+ 318.2 and 279%) increased in both groups whereas plasma ADH was stimulated only in 'intact' patients (+ 55.3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aldosterone; Autonomic Nervous System Diseases; Blood Pressure; Blood Volume; Diabetic Neuropathies; Female; Furosemide; Heart Diseases; Heart Rate; Heart Transplantation; Humans; Male; Middle Aged; Renin; Vasopressins