Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the relationship of aerobic fitness to the response of volume-regulating hormones to acute simulated microgravity. Six untrained (UT) and six endurance-trained (ET) healthy young males were studied in the head-down tilt (HDT) position of -6 degrees for 4 h. Peak oxygen uptake (VO2peak) and plasma volume (PV) were significantly greater in the ET (VO2peak = 61.7 +/- 1.6 ml.min-1.kg-1 and PV = 53.1 +/- 2.8 ml.kg-1) than in the UT (VO2peak = 38.4 +/- 1.7 ml.min-1.kg-1 and PV = 38.8 +/- 1.0 ml.kg-1). Plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP), norepinephrine (NE), renin activity (PRA), and aldosterone (PA) were measured prior to HDT and at minutes 2, 5, 15, 30, 60, 120, 180, and 240 during HDT. PRA and PA significantly decreased during the time of HDT in both groups. The changes in ANP and NE concentrations were not significantly different between the groups nor across time. However, in the ET subjects, the changes in PRA and NE were significantly correlated with the changes in ANP (r = 0.49, P less than 0.01; and r = 0.86, P less than 0.001, respectively); in the UT subjects, the changes in AVP, PRA, and PA were significantly associated with changes in NE (r = 0.34, P less than 0.03; and r = 0.59; and r = 0.53, P less than 0.01, respectively). PV significantly decreased during HDT, and was primarily related to the decrease in PA in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aerobic fitness: I. Response of volume regulating hormones to head-down tilt. 140

We investigated the effects of acute hypoxia (10% O2) on plasma level of atrial natriuretic peptide (ANP) and pulmonary hemodynamics in five subjects with a history of high-altitude pulmonary edema (HAPE). Plasma renin activity and plasma levels of aldosterone, epinephrine and norepinephrine were also measured. The plasma ANP levels in HAPE-susceptible subjects rose significantly in response to 10% O2 (from 34.8 +/- 5.4 to 51.4 +/- 7.3 pg.ml-1; P less than 0.05), not associated with any increase in either atrial pressure. Compared with six control subjects, the rise of ANP level was greater in HAPE-susceptible subjects (16.6 +/- 4.4 vs 3.9 +/- 1.2 pg.ml-1; P less than 0.05). There was a significant positive correlation between the rise of ANP level and the increase of pulmonary arterial pressure. No significant difference was observed in any of other hormonal responses to acute hypoxia between the two groups. We interpret these results as indicating that the ANP secretory response to acute hypoxia in HAPE-susceptible subjects, which is not mediated by an increase in atrial pressure, may be greater than that in nonsusceptible subjects in association with a greater pressor response of pulmonary circulation.
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PMID:Hypoxia-induced ANP secretion in subjects susceptible to high-altitude pulmonary edema. 141 Aug 44

Urinary excretion of albumin and beta 2-microglobulin were measured in 13 patients with congestive heart failure, NYHA class II-IV, before and after captopril treatment for 4 weeks, and in 13 healthy control subjects. The urinary excretion of albumin was enhanced in heart failure patients compared to control subjects (12.0 micrograms min-1 vs 2.8 micrograms min-1; medians, p less than 0.01), whereas beta 2-microglobulin excretion was normal. No significant change in urinary excretion of albumin was observed after captopril. Using Spearmann's test the urinary excretion of albumin was correlated to the NYHA class (Px = 0.681, p less than 0.05, plasma renin (Px = 0.886, p less than 0.01) and plasma angiotensin II (Px = 0.5840, p less than 0.05). Correlations with atrial natriuretic peptide (rho = 0.412, p = 0.153) and aldosterone (Px = 0.487, p = 0.106) did not reach significance. By multiple linear regression analysis only plasma renin activity was correlated to albumin excretion. In conclusion, patients with congestive heart failure had an increased urinary excretion of albumin. It is suggested that the enhanced transglomerular passage of albumin in congestive heart failure is partly due to an increased intra-renal angiotensin II generation, but elevated plasma level of atrial natriuretic peptide and increased renal venous pressure may also be important pathogenetic factors.
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PMID:Enhanced urinary excretion of albumin in congestive heart failure: effect of ACE-inhibition. 141 Dec 51

Recent studies in our laboratory indicated that a blunted (40-50%) renal excretory response to isotonic intravenous saline loads occurred in conscious, renal-denervated dogs after 70% of the atrial mass was removed. The blunted responses could not be explained by differences in the responses of arterial pressure, renal nerve activity, or by measured changes of plasma immunoreactive atrial natriuretic peptide (iANP), arginine vasopressin (AVP), plasma renin activity (PRA), or aldosterone (Aldo). The present study was designed to determine whether the central nervous system (CNS) was the source of an unidentified substance, which could account for the blunting of the urine excretory response seen in the atrial-resected dogs. Renal denervation was performed in all dogs to eliminate alterations in efferent renal sympathetic nerve activity derived from reflexes activated during volume expansion. Cardiac denervation (CDX) was used to eliminate sensory cardiac afferent nerve activity to the CNS. A group of five renal-denervated dogs was given an isotonic volume load (400 ml/30 min) before and after complete CDX. Plasma AVP was fixed at normal plasma levels of 3 pg/ml by continuous intravenous infusion. Na and H2O excretion were not different in renal-denervated dogs compared with combined renal and cardiac denervation during the 5 h after the saline load. Plasma AVP and Aldo were unchanged with the volume loads, although PRA rose gradually over the 5 h after the saline loads. Plasma iANP increased transiently in the combined renal and cardiac-denervated state rising from a control of 65-120 pg/ml at the end of the load period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Saline diuresis and natriuresis in unanesthetized dogs: a missing atrial factor? 141 4

The influence of physiological increments in circulating atrial natriuretic peptide (ANP) on renin release was determined in conscious dogs. Renin stimulus-response curves (RSRCs) were obtained by controlled reductions of renal perfusion pressure (RPP) under control conditions and during intrarenal or intravenous ANP infusions. Under all experimental conditions, the RSRCs were characterized by a plateau, a threshold pressure (Pth), and a steep slope below Pth. Intrarenal ANP infusion (0.9 ng.kg-1.min-1), which induced a calculated threefold elevation of renal arterial ANP concentration (but did not change systemic arterial ANP levels), increased the slope of the RSRC by 81% (P less than 0.05) with no effect on Pth. A quantitatively similar effect on the slope of the RSRC (+90%; P less than 0.05) was observed when systemic ANP levels were raised (from 37 +/- 2 to 71 +/- 9 pg/ml; P less than 0.05) by intravenous infusions (3.6 ng.kg-1.min-1). In addition, however, intravenously infused ANP reduced Pth from 91 to 85 mmHg (P less than 0.05), which caused a complete suppression of the renin response to a reduction of RPP down to 85 mmHg. These findings indicate that ANP can inhibit renin release at physiological plasma concentrations by shifting the RSRC to a lower pressure level; this shift is mediated by a modulation of extrarenal renin control mechanisms. The direct effect of ANP on renin release is one of stimulation.
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PMID:Physiological concentrations of ANP exert a dual regulatory influence on renin release in conscious dogs. 141 38

To evaluate the role of atrial natriuretic peptide (ANP) in exercise-related cardiovascular and hormonal adjustments in hypobaric conditions, 14 young athletes performed a maximal ergometer test in a hypobaric chamber adjusted to simulate the altitudes of sea level and 3,000 m. Plasma immunoreactive ANP levels rose from 5.89 to 35.1 pmol/l at sea level and rose significantly less (P less than 0.05), from 5.36 to 22.3 pmol/l, at simulated 3,000 m. Plasma immunoreactive amino-terminal peptide of proANP (NT-proANP) levels increased to the same extent at sea level and at simulated 3,000 m (from 240 to 481 pmol/l and from 257 to 539 pmol/l, respectively). Plasma immunoreactive aldosterone increased significantly less at simulated 3,000 m (P less than 0.05), but the changes in plasma renin were similar in both conditions. Plasma immunoreactive endothelin-1 and serum erythropoietin levels remained unchanged. In conclusion, we found a blunted ANP response to maximal exercise of ANP in acute hypobaric exposure compared with that in normobaric conditions, but no significant difference in the NT-proANP responses between the two conditions. The divergence may be due to stimulation of the elimination mechanism of ANP.
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PMID:Effect of physical exercise in hypobaric conditions on atrial natriuretic peptide secretion. 141 53

Controlled mechanical ventilation (CMV) with positive end-expiratory airway pressure decreases urine output and renal sodium excretion. This study investigates--independent of surgical stress, general anesthesia, and sedation--the influences of antidiuretic hormone, atrial natriuretic peptide, plasma renin activity, and aldosterone on decreased urine output and renal sodium excretion during CMV with positive end-expiratory airway pressure. Hemodynamic, renal, and hormonal parameters were measured over a 4-h period in six trained, nonanesthetized, chronically tracheotomized dogs under two conditions: 1) control: hours 1-4, spontaneous breathing at continuous positive airway pressure of 4 cmH2O; and 2) CMV 20: hour 1, continuous positive airway pressure of 4 cmH2O; hours 2 and 3, CMV with a mean airway pressure of 20 cmH2O; and hour 4, continuous positive airway pressure of 4 cmH2O. Throughout the experiments, 0.5 ml.kg body weight-1.min-1 balanced electrolyte solution was administered intravenously. During the 2nd and 3rd h of CMV 20, urine volume decreased by 43% and sodium excretion decreased by 44% when compared with control values (P less than 0.05). The glomerular filtration rate decreased from 4.4 +/- 0.1 to 3.9 +/- 0.1 ml.kg-1.min-1 (P less than 0.05) during the 2nd h and from 4.4 +/- 0.1 to 4.1 +/- 0.1 ml.kg-1.min-1 (P less than 0.05) during the 3rd h of CMV 20. Fractional sodium excretion decreased from 4.7 +/- 0.3% to 2.9 +/- 0.2% (P less than 0.05) during the 2nd h and from 7.5 +/- 0.3% to 4.6 +/- 0.2% (P less than 0.05) during the 3rd h of CMV 20, compared with values during the control period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Positive end-expiratory pressure reduces renal excretion without hormonal activation after volume expansion in dogs. 141 67

The pathophysiological mechanisms in hypertension may differ in men and women. Plasma renin activity was measured in 27 premenopausal, never-treated hypertensive women (blood pressure 141 +/- 2/93 +/- 1 mm Hg) and in 18 age-matched normotensive women (blood pressure 113 +/- 2/71 +/- 2 mm Hg). All subjects were unaware of their blood pressure status. The hypertensive women had on average lower plasma renin activity (0.21 +/- 0.03 nmol/L/h) than their normotensive controls (0.42 +/- 0.07 nmol/L/h, P less than .01). Serum estradiol was also lower in the hypertensive women (0.57 +/- 0.06 v 0.81 +/- 0.09 nmol/L, P less than .05). No difference in epinephrine, norepinephrine, atrial natriuretic peptide, or vasopressin was found between the groups. Plasma renin activity was positively correlated to plasma norepinephrine in the hypertensive women only (r = 0.41, P less than .05). Since low renin hypertension is associated with less cardiovascular complications, this may offer an explanation for the better prognosis of hypertension in women.
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PMID:Mild essential hypertension in nonobese premenopausal women is characterized by low renin. 141 46

Pulmonary artery pressure (PAP) increased significantly in rats after hypobaric hypoxic exposure for 15 days (CH15) (P less than 0.001) and was maintained at the same level after prolonged hypoxic exposure for 40 days (CH40). There were no significant changes in carotid systolic and diastolic blood pressure in CH15 and CH40 rats. The contractility of the right and left ventricles of CH15 and CH40 rats showed no difference as compared with the control group. Plasma atrial natriuretic peptide (ANP) content in CH40 rats was obviously increased (P less than 0.001), while angiotensin II (AII) dropped markedly (P less than 0.05). Plasma renin activity was increased in both hypoxic groups (P less than 0.05 respectively). These results indicate that during chronic hypoxia, plasma ANP and the renin-angiotensin system (RAS) play an important role in the modulation of pulmonary as well as systemic hemodynamics. They may work cooperatively to limit the development of pulmonary hypertension and to maintain systemic blood pressure within the normal range.
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PMID:The relationship between the changes in plasma atrial natriuretic peptide and renin angiotensin contents and hemodynamics in pulmonary hypertensive rats. 142 60

1. This study investigated the effect of atrial natriuretic peptide on renin release from the kidney. The in vitro direct effect was examined in the animal experiment using renal cortical slices of rat, and the in vivo effect was observed in the human infusion study. 2. In the in vitro experiments, alpha-human atrial natriuretic peptide (alpha-hANP) ranging 10(-9) to 10(-6) mol/L did not change the basal renin release rate from the renal cortical slices (-9% at 10(-6) mol/L, NS). Isoproterenol (10(-6) mol/L) increased renin release by 40% (P < 0.001), whereas angiotensin II (10(-6) mol/L) suppressed it by 48% (P < 0.001). However, alpha-hANP did not affect the stimulative effect of isoproterenol or the inhibitory effect of angiotensin II. 3. Also in the human study, infusion of 25 ng/kg per min alpha-hANP failed to change the plasma renin activity in normotensive subjects (-4%) or patients with essential hypertension (+5%), or even in patients with raised renin levels such as renovascular hypertension (+10%) or congestive heart failure (-13%). 4. These results put forth negative views on the direct involvement of atrial natriuretic peptide in renin release from the juxtaglomerular apparatus.
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PMID:In vivo and in vitro effects of atrial natriuretic peptide on renin release. 142


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