atrial-natriuretic-factor and Hypovolemia

This study aimed to evaluate available volume status assessment tools in nephrotic syndrome (NS). Sixty children with INS were subdivided into hypovolemic and nonhypovolemic groups based on fractional excretion of sodium (FeNa%); all were studied for inferior vena cava collapsibility index (IVCCI), plasma atrial natriuretic peptide (ANP), and body composition monitor (BCM). Forty-four patients had nonhypovolemic and 16 had hypovolemic states. ANP did not differ between both groups. IVCCI was higher in hypovolemic group (p < 0.001) with sensitivity 87.5% and specificity 81.8% for hypovolemia detection, while BCM overhydration (BCM-OH) values were higher in nonhypovolemic group (p = 0.04) with sensitivity = 68.2% and specificity = 75% for detection of hypervolemia. FeNa% showed negative correlation with IVCCI (r =  -0.578, p < 0.001) and positive correlation with BCM-OH (r = 0.33, p = 0.018), while FeNa% showed nonsignificant correlation to ANP concentration. IVCCI is a reliable tool for evaluating volume status in NS and is superior to BCM.

Topics: Atrial Natriuretic Factor; Child; Edema; Humans; Hypovolemia; Nephrotic Syndrome; Sodium; Ultrasonography; Vena Cava, Inferior

Cardiovascular mortality remains the commonest cause of death for peritoneal dialysis patients. As such, preventing persistent hypervolemia is important. On the other hand, hypovolemia may potentially risk episodes of acute kidney injury and loss of residual renal function, a major determinant of peritoneal dialysis technique survival. Bioimpedance has developed from a single-frequency research tool to a multi-frequency bioelectrical impedance analysis readily available in the clinic and capable of measuring extracellular, intracellular, and total body water. Similarly, natriuretic peptides released from the heart because of myocardial stretch and increased intracardiac volume have also been variously reported to be helpful in assessing volume status in peritoneal dialysis patients. The question then arises whether these newer technologies and biomarkers have supplanted the time-honored clinical assessment of hydration status or whether they are merely adjuncts that aid the experienced clinician.

Topics: Atrial Natriuretic Factor; Biomarkers; Body Fluids; Electric Impedance; Humans; Hypovolemia; Natriuretic Peptides; Nomograms; Peritoneal Dialysis; Protein Precursors

Sepsis causes changes in vascular resistance and hypovolemia. Previous studies have demonstrated that the spleen regulates blood volume via atrial natiuretic peptide (ANP). We hypothesized that LPS alters extrasplenic responses to ANP via endothelial-dependent mechanisms and studied the role of NO and endothelin 1 (ET-1). Isolated extrasplenic arteries and veins (vessels in mesentery adjoining spleen) were obtained from male Wistar rats weighing 200 to 280 g (n = 102) and mounted on a pressure myograph to determine intraluminal diameter for 4 h. Isolated vessels constricted in response to the half-maximum response of ANP (veins, 30% +/- 1.7%; arteries, 34.5 +/- 1.7%; P < 0.05), and this was abolished by the NO donor S-nitroso-N-acetylpenicillamine (SNAP 75 microM). Arteries and veins incubated with LPS (50 microg mL(-1) for 4 h) were unresponsive to ANP, and constriction was not restored by the NOS inhibitor N omega-nitro-L-arginine methyl ester (L-NAME 100 microM). However, venular constriction returned in the presence of the ET-1 antagonist Bosentan, increasing from -1.5 +/- 1.2 (10 min) to -10 +/- 2.5% (4 h) with LPS + Bosentan (3 x 10(-6) M) compared with -2.3 +/- 1.2 and 0% with LPS alone. In conclusion, LPS abolished endothelial-dependent extrasplenic venular constriction to ANP partially due to increased ET-1, whereas NO seemed to modulate vascular responses to ANP.

Topics: Animals; Antihypertensive Agents; Arteries; Atrial Natriuretic Factor; Blood Volume; Bosentan; Endothelin-1; Enzyme Inhibitors; Hypovolemia; Lipopolysaccharides; Male; Mesentery; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Donors; Penicillamine; Rats; Rats, Wistar; Sepsis; Spleen; Sulfonamides; Vascular Resistance; Vasoconstriction; Veins

Neonatal foals succumb rapidly to hypovolaemic shock in comparison to mature horses; they do not consistently increase their heart rate in response to hypotension and respond differently to fluid administration. The hormonal responses to hypovolaemia in the horse and foal require investigation.. The hormonal responses to hypovolaemia and fluid administration differ between mature and neonatal horses.. Five mature horses and 5 neonatal foals fulfilling predetermined criteria for hypovolaemia, were included in the study. A blood sample was taken at admission and after normalisation of fluid balance. These were analysed for plasma aldosterone, vasopressin (AVP) and atrial natriuretic peptide (ANP). Normally distributed variables were compared using the Student's t test and nonparametric data using the Mann-Whitney U test.. ANP, AVP and aldosterone were higher before fluid resuscitation than after fluid resuscitation in mature horses. Aldosterone was higher before than after fluid resuscitation in foals, and was higher in foals both before and after fluid resuscitation than in mature horses. ANP was lower in mature horses after fluid resuscitation than in foals. No other comparisons were significantly different.. The hormonal responses of the mature and neonatal horses are different during hypovolaemia and following fluid resuscitation.. The differences in the hormonal responses to hypovolaemia and fluid resuscitation may be important when considering fluid resuscitation of hypovolaemic horses and foals, and warrants further investigation.

Topics: Aging; Aldosterone; Animals; Animals, Newborn; Atrial Natriuretic Factor; Body Fluids; Female; Fluid Therapy; Horse Diseases; Horses; Hypovolemia; Male; Statistics, Nonparametric; Treatment Outcome; Vasopressins

Symptoms of hyponatremia and diuresis due to cerebral salt wasting syndrome (CSWS) are often observed after aneurysmal subarachnoid hemorrhage (SAH). Inadequately treated CSWS is known to work as a trigger of symptomatic vasospasm in SAH patients. Therefore, it is indispensable to detect and treat CSWS as early as possible in ICU. A 36-year-old man with SAH was admitted to our ICU. His urine volume increased excessively 3 days after ICU admission, and it reached a peak (39,250 ml x day(-1)) on the 6th day in ICU. Since infusion volume was controlled with regard to daily urinary output, hyponatremia was not noticeable and excessive urine volume stood out conspicuously. Though vasopressin and desmopressin were administered, the symptoms of natriuresis and hyponatremia were aggravated, associated with hyper secretion of natriuretic peptides (ANP 160 pg x dl(-1), BNP 172 pg x dl(-1)). Recent studies revealed that hyponatremia and hypovolemia following SAH might be caused by exaggerated secretion of natriuretic peptides. Experimental studies showed that the administration of vasopressin and desmopressin cause excessive secretion of natriuretic peptides under the circumstance of volume expansion in rats. We infer that the administration of vasopressin and desmopressin to our patient deterionated natriuresis in CSWS as in the previous experimental findings.

Topics: Adult; Animals; Atrial Natriuretic Factor; Brain Diseases; Contraindications; Humans; Hyponatremia; Hypovolemia; Male; Natriuresis; Rats; Subarachnoid Hemorrhage; Syndrome; Urination Disorders; Vasopressins

Atrial natriuretic peptide (ANP), via its vasodilating and diuretic effects, has an important physiological role in the maintenance of arterial blood pressure and volume. Its guanylyl cyclase-A (GC-A) receptor is highly expressed in vascular endothelium, but the functional relevance of this is controversial. To dissect the endothelium-mediated actions of ANP in vivo, we inactivated the GC-A gene selectively in endothelial cells by homologous loxP/Tie2-Cre-mediated recombination. Notably, despite full preservation of the direct vasodilating effects of ANP, mice with endothelium-restricted deletion of the GC-A gene (EC GC-A KO) exhibited significant arterial hypertension and cardiac hypertrophy. Echocardiographic and Doppler flow evaluations together with the Evan's blue dilution technique showed that the total plasma volume of EC GC-A KO mice was increased by 11-13%, even under conditions of normal dietary salt intake. Infusion of ANP caused immediate increases in hematocrit in control but not in EC GC-A KO mice, which indicated that ablation of endothelial GC-A completely prevented the acute contraction of intravascular volume produced by ANP. Furthermore, intravenous ANP acutely enhanced the rate of clearance of radio-iodinated albumin from the circulatory system in control but not in EC GC-A KO mice. We conclude that GC-A-mediated increases in endothelial permeability are critically involved in the hypovolemic, hypotensive actions of ANP.

Topics: Animals; Arteries; Atrial Natriuretic Factor; Capillary Permeability; Cardiomegaly; Endothelium, Vascular; Guanylate Cyclase; Hematocrit; Humans; Hypotension; Hypovolemia; Integrases; Mice; Mice, Knockout; Myocytes, Cardiac; Receptors, Atrial Natriuretic Factor; Vasodilation; Viral Proteins

Hypovolemia is thought to have an important role in the pathogenesis of dialysis-related hypotension.. We studied the effect of hypovolemia simulated by lower body negative pressure (LBNP) in 11 hypotension-prone (HP) and 11 hypotension-resistant (HR) hemodialysis patients. LBNP was applied stepwise from 0 to -20 to -40 mm Hg. Systolic arterial pressure, heart rate, and central venous pressure (CVP) were recorded continuously after cannulation of the right jugular vein. Stroke volume index was measured at each step echocardiographically. At the end of each level of LBNP, blood samples were obtained to measure norepinephrine (NE), epinephrine (E), and atrial natriuretic peptide (ANP) levels.. At baseline, CVP (12 +/- 5 and 16 +/- 7 mm Hg), heart rate (72 +/- 9 and 70 +/- 13 beats/min), cardiac index (2.3 +/- 0.6 and 2.5 +/- 0.9 L/min), NE (median, 341 pg/mL [range,198 to 789 pg/mL] and 365 pg/mL [range, 177 to 675 pg/mL] or 2.02 nmol/L [range, 1.17 to 4.66 nmol/L] and 2.16 nmol/L [range, 1.05 to 4.00 nmol/L]), E (median, 46 pg/mL [range, 18 to 339 pg/mL] and 58 pg/mL [range, 21 to 122 pg/mL] or 251 pmol/L [range, 98 to 1,951 pmol/L] and 317 pmol/L [range, 115 to 666 pmol/L]) were similar, whereas systolic arterial pressure (141 +/- 26 versus 164 +/- 22 mm Hg) and ANP (median, 441 pg/mL [range, 152 to 1,330 pg/mL] versus 804 pg/mL [range, 517 to 3,560 pg/mL] ng/L) were lower (P < 0.05) in HP patients. In response to LBNP (-40 mm Hg), CVP decreased by 6.5 +/- 4.0 mm Hg in the HP group and 4.9 +/- 4.9 mm Hg in the HR group. In HP patients, this decrease was associated with a greater decrease in SI (37% +/- 16% versus 27% +/- 16%) and systolic arterial pressure (19% +/- 21% versus 4% +/- 14%) than in HR patients. Plasma ANP levels did not change, whereas increases in NE and E levels were similar in HP and HR patients.. Patients who frequently experience episodes of hypotension during dialysis also are prone to develop hypotension during LBNP, which results from reduced myocardial contractile reserve and/or inadequate sympathetic tone.

Topics: Aged; Atrial Natriuretic Factor; Cardiac Output, Low; Catecholamines; Disease Susceptibility; Female; Hemodynamics; Humans; Hypotension; Hypovolemia; Lower Body Negative Pressure; Male; Middle Aged; Myocardial Contraction; Renal Dialysis; Stroke Volume; Sympathetic Nervous System

This study was performed to integratively investigate the vasoregulatory response during standardized splanchnic hypoperfusion in pigs. Splanchnic perfusion was reduced to 50% of baseline by: haemorrhage by 20 and 40% of the estimated total blood volume; femoral venous infusion of live E. coli to establish sepsis of systemic origin; portal venous infusion of live E. coli to establish sepsis of splanchnic origin. Invasive haemodynamic monitoring and radioimmunoassay analyses of arterial plasma concentrations of angiotensin II, endothelin-1 and atrial natriuretic peptide were carried out. Acute hypovolaemia reduced systemic and splanchnic vascular resistances following transient increases and increased angiotensin II levels (+587%), whereas endothelin-1 and atrial natriuretic peptide levels did not change significantly. Systemic sepsis following femoral venous infusion of E. coli resulted in increased splanchnic vascular resistance and increased levels of angiotensin II (+274%), endothelin-1 (+134%) and atrial natriuretic peptide (+185%). Infusion of E. coli via the portal venous route induced an increase in splanchnic vascular resistance associated with particularly elevated levels of angiotensin II (+1770%) as well as increased endothelin-1 (+201%) and atrial natriuretic peptide (+229%) concentrations. Hypovolaemia and sepsis, although standardized with a predefined level of splanchnic hypoperfusion, elicited differentiated cardiovascular and vasopeptidergic responses. Sepsis, particularly of portal origin, notably increased splanchnic vascular resistance related to increased production of the vasoconstrictors angiotensin II and endothelin-1. The role of atrial natriuretic peptide as a vasodilator seems to be of subordinate importance in hypovolaemia and sepsis.

Topics: Acute Disease; Anesthesia; Angiotensin II; Animals; Atrial Natriuretic Factor; Endothelin-1; Escherichia coli Infections; Female; Femoral Vein; Hemorrhage; Hypovolemia; Male; Neuropeptides; Portal Vein; Sepsis; Splanchnic Circulation; Swine; Vasoconstrictor Agents