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)

The physiology of atrial natriuretic peptide (ANP) secretion was studied in normotensive subjects and hypertensive patients both young and old. Basal plasma ANP concentration was least in young normotensives, intermediate in old normotensives and young hypertensives, and highest in old hypertensives. Nifedipine, a known stimulator of ANP secretion, acutely increased plasma ANP in young and old normotensive subjects but not in young hypertensive patients and half of the old hypertensive patients. Increase in serum ANP level in response to nifedipine did not augment its hypotensive effect. However, the increase of aldosterone in response to nifedipine-induced rise in plasma renin activity (PRA) seemed to be suppressed by elevated ANP.
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PMID:Differential effects of nifedipine on plasma atrial natriuretic peptide in normal subjects and hypertensive patients. 153 85

The purpose of this study was to compare the early postoperative effects of heart and heart-lung transplantation on the secretion of atrial natriuretic peptide (alpha-ANP), renin, aldosterone, and vasopressin. This was carried out from the first to the eighth postoperative day in ten heart and five heart-lung recipients. The changes in the release of these hormones were similar in both groups. Vasopressin release remained stable while that of the renin-angiotensin-aldosterone system progressively returned to more normal levels. Grafted heart tissue was capable of high alpha-ANP release early on in both heart and in heart-lung recipients. This sustained alpha-ANP release was not a function of the resulting overall atrial tissue mass. Our findings suggest that it might be the consequence of an intrinsic hypersecretion of alpha-ANP resulting from the loss of normal heart innervation occurring in both heart and heart-lung transplantation.
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PMID:Changes in endocrine control of electrolyte homeostasis and blood pressure following heart and heart-lung transplantation. A comparative study. 153 48

The hormonal regulation of sodium and volume homeostasis was investigated in three patients (two related) with the syndrome of familial hyperkalemic acidosis and hypertension with normal glomerular filtration rate. Recumbent plasma renin activity was low during normal sodium intake (135 mmol daily), and the response to upright posture or to low sodium diet (10 mmol daily) was blunted. Recumbent plasma aldosterone levels were normal in two patients and high in one, and the standing values were elevated in one; responses to upright posture were brisk on low sodium diet. Angiotensin II infusion induced a marked increase in plasma aldosterone. Plasma atrial natriuretic peptide was at the upper limit of normal during normal sodium intake, decreased during diuretic therapy, and increased during sodium chloride infusion in one patient. Basal urinary prostaglandin E2, prostaglandin F2 alpha, and 6-ketoprostaglandin F1 alpha excretion rates were decreased, and thromboxane B2 was increased. Total blood and plasma volumes were subnormal, whereas extracellular fluid volume and exchangeable sodium values were close to or above (in one patient) the mean normal values. Chronic treatment with hydrochlorothiazide in two patients corrected the hyperkalemic acidosis and hypertension, but on its discontinuation (in one patient) all biochemical abnormalities promptly reappeared.
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PMID:Endocrine sodium and volume regulation in familial hyperkalemia with hypertension. 153 66

Sixteen middle-aged men with primary hypertension were treated with the calcium antagonist isradipine over a 9-week period in a randomized, placebo-controlled, double-blind cross-over manner. At the end of the intervention period the urinary albumin excretion rate, systemic and renal haemodynamics, haemorheological properties of blood and plasma concentrations of atrial natriuretic peptide, noradrenaline and peripheral renin activity were determined. Treatment with isradipine resulted in a substantial reduction in blood pressure due to a reduction in peripheral resistance. The mean albumin excretion rate was not influenced by the isradipine treatment. In a multivariate analysis, changes in the urinary albumin excretion rate were only related to changes in blood pressure.
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PMID:Calcium antagonism in essential hypertension: effect on renal haemodynamics and microalbuminuria. 153 13

To study the mechanisms of alcohol-induced diuresis, the plasma concentration of immunoreactive atrial natriuretic peptide and arginine vasopressin, serum sodium and osmolality, plasma renin activity and aldosterone, urinary sodium and volume, free water clearance, blood pressure and heart rate were measured in seven healthy men after oral intake of ethanol (1.5 g kg-1 in 6 h). Serum ethanol levels increased to 27 +/- 4 mmol l-1 (mean +/- SD) in 30 min and remained detectable for 14 h. Serum osmolality rose from 280 +/- 10 to 340 +/- 4 mosm kg-1 in 2 hours (P less than 0.01) and was 300 +/- 4 at 14 h (P less than 0.01). Formation of hypotonic urine began after the alcohol intake and resulted in a net loss of 0.9 +/- 0.1 kg water in 2 h. Free water clearance increased from -3.4 +/- 1.4 to 2.8 +/- 1.5 ml min-1 in 2 h (P less than 0.01). Plasma immunoreactive arginine vasopressin decreased from 5.7 +/- 2.1 to 3.3 +/- 1.3 ng l-1 (P = 0.05) in 30 min and increased to 17 +/- 25 and 12 +/- 10 ng l-1 at 6 and 12 h, respectively (P less than 0.05 for both). Plasma immunoreactive atrial natriuretic peptide levels decreased from 17 +/- 9 to the minimum of 11 +/- 3 ng l-1 in 2 h (P less than 0.01) and returned to the initial levels in 6 h. Serum sodium, plasma renin activity and plasma aldosterone increased maximally by 4 +/- 2, 165 +/- 153 and 143 +/- 101% (P less than 0.01 each) during 1-6 h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma immunoreactive atrial natriuretic peptide and vasopressin after ethanol intake in man. 153 84

In this pilot study we investigated the effects of a 4-h infusion of atrial natriuretic peptide (8-33 Met ANP) on hemodynamic, renal, and hormonal parameters in 12 patients with hypertension. Either 8-33 ANP in 5% mannitol (0.7 microgram/min [eight patients] and 1.05 micrograms/min [four patients]) or placebo (5% mannitol) was infused for 4 h on 2 consecutive days in a randomized double-blind crossover design. The plasma levels of ANP were not significantly different between the two doses of ANP and therefore the results from the two doses were combined. Plasma ANP increased from 61 +/- 24 pg/mL to 291 +/- 55 pg/mL after 2 h and to 288 +/- 40 pg/mL after 4 h. ANP caused a significant lowering of systolic blood pressure after 2 h of infusion from 148 +/- 5 mm Hg to 142 +/- 5 mm Hg (P less than .05) and to 128 +/- 6 after 4 h (P less than .01). Two hours after discontinuation of the infusion, systolic blood pressure was 126 +/- 6 and 135 +/- 7 mm Hg 4 h after the end of the infusion. Diastolic blood pressure did not change. Heart rate increased from 69 +/- 3 beats/min to 74 +/- 3 beats/min after 4 h and to 78 +/- 4 beats/min 2 h after termination of the infusion. Cardiac output did not change significantly. Urinary sodium and chloride increased significantly but creatinine clearance did not change. Plasma aldosterone decreased after 2 h of ANP infusion from 9.8 +/- 1.7 ng/dL to 6.7 +/- 0.9 ng/dL (P less than .01) and to 6.5 +/- 1.2 ng/dL after 4 h (P less than .05). Plasma renin activity decreased from 0.81 +/- 0.1 ng angiotensin I/mL/h to 0.57 +/- 0.1 after 2 h of infusion (P less than .05). There were no significant changes in plasma catecholamines or arginine vasopressin. Two patients developed severe hypotension and bradycardia and one of them had a sinus pause of 7.4 sec associated with loss of consciousness. Neither of these two patients had a significant increase in plasma catecholamines in response to the severe hypotension, suggesting that ANP may have inhibited their sympathetic response and increased their sensitivity to vagal cardioinhibitory reflexes. In conclusion, infusion of ANP in hypertensive patients causes prolonged lowering of systolic blood pressure with no change in diastolic pressure and cardiac output.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of atrial natriuretic peptide (8-33-Met ANP) in patients with hypertension. 153 72

Eighteen beagles were chronically instrumented with an anterior third ventricular (A3V) infusion device to analyze, in conscious dogs, the involvement of central atrial natriuretic peptide (ANP) in body fluid and blood pressure control. The dogs' osmotic and body fluid homeostasis was challenged by 24 h water deprivation or blood withdrawal (12 ml/kg body wt) to elucidate possible modifying influences on the release of arginine vasopressin (AVP), angiotensin II (ANG II), and drinking. Three series of experiments were performed: 1) infusion of ANP (500 ng/min) dissolved in artificial cerebrospinal fluid (aCSF) and given for 10 min, 2) infusion of aCSF alone for the same length of time, and 3) time control experiments without infusion. Plasma AVP and ANG II were analyzed by radioimmunoassay, and in several experiments on dehydrated dogs, plasma norepinephrine and epinephrine were additionally determined by high-performance liquid chromatography. Various blood parameters and rectal and ear skin temperatures were measured. Arterial pressure and heart rate were recorded in three animals additionally equipped with carotid loops. Changes in plasma AVP and ANG II induced by dehydration and bleeding were not significantly modified by A3V infusions of ANP and aCSF in comparison to time controls. Blood pressure changes were similar in experiments with A3V ANP infusion and time controls during bleeding and reinfusion. It is concluded that central ANP is not important in the control of vasopressin and renin-angiotensin systems during osmotic and volume challenges in conscious dogs.
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PMID:Central ANP administration in conscious dogs responding to dehydration and hypovolemia. 153 4

To examine the influence of an increase in central blood volume with head-out water immersion (WI) on fluid-regulating hormones during exercise, 10 healthy men underwent upright leg cycle exercise on land and with WI. Venous plasma renin activity and plasma venous concentrations of atrial natriuretic peptide, plasma aldosterone, and arginine vasopressin were determined at exercise intensities corresponding to approximately 40, 60, 80, and 100% peak oxygen consumption (VO2) and at minutes 1 and 5 of seated rest recovery within each environment. Peak VO2 did not differ on land and with WI. Atrial natriuretic peptide concentration was higher (P less than 0.05) and plasma renin activity was lower (P less than 0.05) in water than on land at 40% peak VO2 through minute 5 of recovery. Plasma aldosterone and arginine vasopressin concentrations were lower (P less than 0.05) in water at peak exercise and at minutes 1 and 5 of recovery. Osmolality and plasma sodium and potassium concentrations during exercise were similar in water and on land. The results indicate that WI alters the circulating levels of several hormones involved in fluid and electrolyte regulation during exercise. These hormonal alterations can best be explained by stimulation of low-pressure baroreceptors and atrial stretch due to increased central blood volume with head-out WI.
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PMID:Fluid-regulating hormones during exercise when central blood volume is increased by water immersion. 153 5

Human atria through release of atrial natriuretic peptide play an important role in extracellular fluid homeostasis. This study investigates the perioperative role of atrial natriuretic peptide, renin, angiotensin, aldosterone, and vasopressin in patient response to cardiopulmonary bypass after coronary artery bypass operations. Serum levels of these hormones were measured, along with hemodynamic profiles, urine output, and urine electrolytes, before induction of anesthesia, after discontinuation of cardiopulmonary bypass, 1 hour postoperatively, and 3 hours postoperatively. Serum levels of atrial natriuretic peptide were found to be significantly elevated immediately after discontinuation of cardiopulmonary bypass. These elevations did not correspond temporally to elevated central venous pressure or tachycardia. Significant natriuresis and diuresis were observed during the first postoperative hour. This diuresis failed to correspond temporally with alterations noted in serum levels of atrial natriuretic peptide, renin, angiotensin, aldosterone, and vasopressin. The mechanism responsible for the increases in serum atrial natriuretic peptide and the postoperative natriuresis and diuresis after cardiopulmonary bypass remain unknown.
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PMID:Atrial natriuretic peptide may not play a role in diuresis and natriuresis after cardiac operations. 153 91

In congestive heart failure (CHF), excessive vasoconstriction is present, which is due to overactive vasoconstrictor mechanisms although vasodilator mechanisms may be impaired. In the present study, we examined vasodilation in CHF by measuring forearm blood flow with a strain gauge plethysmograph. Patients with CHF had higher forearm vascular resistance than normal control subjects. Patients with CHF had decreased forearm vasodilation in response to intra-arterial infusions of atrial natriuretic peptide (ANP) and acetylcholine, but not in response to sodium nitroprusside or nitroglycerin. Oral captopril did not alter the degree of forearm vasodilation during handgrip exercise. These results suggest that endothelium-dependent and ANP-induced forearm vasodilation is impaired in patients with CHF but the decreased vasodilation is not due to impaired vascular smooth muscle responsiveness to a vasodilator. The renin-angiotensin system does not seem to play a major role in the maintenance of vascular resistance during exercise in CHF.
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PMID:Decreased skeletal muscle vasodilation in patients with congestive heart failure. 153 58


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