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)

After 30 min rest in the lying position, 12 healthy male volunteers (average age 22 years) received, in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg iv followed by a continuous infusion of 10 mg/hr). Thereafter they rested for a further 30 min in the recumbent position and for 15 min sitting on a bicycle ergometer; they then exercised to exhaustion. At rest plasma levels of adrenocorticotropin (ACTH), cortisol, and aldosterone increased during infusion of naloxone, while body temperature decreased. During exercise the difference in plasma ACTH between naloxone and saline periods was abolished, while the differences in plasma cortisol and aldosterone lost statistical significance. Intra-arterial pressure, heart rate, ventilation, O2 uptake, and CO2 output were continuously monitored throughout the experiment and were not affected by naloxone. This was also the case for several hormonal and biochemical measurements, including those of plasma renin, angiotensin II, norepinephrine, 13,14-dihydro-15-keto-prostaglandin F2 alpha, glucose and lactate, and serum insulin and growth hormone. Exercise performance was not changed by naloxone. In conclusion (1) during exhaustive graded exercise of short duration opioidergic inhibition of the pituitary-adrenocortical axis is probably not sustained, (2) apart from the latter mechanism, the present study does not support the hypothesis that endogenous opioids are involved in various hemodynamic, respiratory, and hormonal responses to this type of exercise.
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PMID:The nature of opioid involvement in the hemodynamic respiratory and humoral responses to exercise. 404 6

Blood pressure, heart rate and evoked cardiovascular reflexes were examined in cats following chronic treatment with haloperidol, at a dose of 1 mg kg-1 per day, orally for 23 days. Five days after the final dose the animals were anaesthetized and tested for their reaction to various cardiovascular stimuli and to a number of agonist and antagonist drugs, given both intravenously and into the vertebral artery. It was found that treatment with haloperidol caused hypertension in the cats, as well as a potentiation of the pressor response to bilateral carotid occlusion. The response to 30 degrees head-up tilting was also altered so that in treated cats, the blood pressure returned to normal more rapidly during the tilt. There was no difference in the heart rate of the two groups of cats, nor in the pressor response to intravenous noradrenaline or angiotensin II or to afferent brachial nerve stimulation, nor was the depressor action of bradykinin altered. Hexamethonium reduced the blood pressure in both control and treated cats to approximately the same level. Blood O2, CO2, pH and bicarbonate levels were also unaltered by the treatment, as was plasma renin activity. Of the drugs given into the vertebral artery, only noradrenaline, prazosin, ketanserin and haloperidol caused a significantly greater fall in blood pressure in treated than in control cats, while clonidine and St91 were equally effective in both groups. These results suggest that haloperidol treatment has caused a greater modulation of central alpha 1- than of alpha 2-adrenoceptors.
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PMID:The effect of chronic haloperidol treatment on some cardiovascular parameters in cats. 406 87

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3 to 6.8 mM), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mM), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/hr), high plasma aldosterone (32 to 100 ng/dl), normal GFR (131 +/- 2.5 ml/min/1.73 m2). During hyperkalemic period, urine was highly acidic (pH 4.6 to 5.0), urinary NH4 excretion (13 mumoles/min) and urinary net acid excretion (24 mumoles/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, maximal tubular HCO3 reabsorption (Tm HCO3) was markedly diminished (19 mmoles/liter GF), fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized, was 20%. Urine-minus-blood PCO2 increased normally (31 mmHg) during NaHCO3 infusion, and urinary pH remained maximally low (less than 5.3) when buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while urinary pH remained maximally low (4.9 to 5.2), Tm HCO3 returned to normal value (24.8 mmoles/liter GF), and FE HCO3 became nil. The renal handling of K was improved with acute NaHCO3 loading and normalized after DDAVP nasal insufflation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Type II pseudohypoaldosteronism: proximal tubular acidosis and distal tubular hyperkalemia corrected by DDAVP]. 408 72

We studied the effect of chronic carotid body denervation on renin (plasma renin activity, PRA), adrenocorticotropin (ACTH), blood pressure, and hematocrit responses to acute normocapnic (arterial CO2 partial pressure, PaCO2, 35 Torr) and hypercapnic (PaCO2, 65 Torr) hypoxia (arterial O2 partial pressure, PaO2, 31 Torr) in five anesthetized, artificially ventilated dogs. Animals were studied at least 3 days before and again at least 10 days after carotid body denervation (bilateral carotid sinus nerve resection). Increases in PRA during hypercapnic normoxia [21.8 +/- 6.4 ng angiotensin I (ANG I) X ml-1 X 3 h-1] and normocapnic hypoxia (13.3 +/- 4.2 ng ANG I X ml-1 X 3 h-1) were not attenuated by carotid body denervation. Increases in ACTH during normocapnic hypoxia (117 +/- 34 pg/ml) were attenuated but not eliminated by carotid body denervation; the increase in ACTH during hypercapnic hypoxia (295 +/- 93 pg/ml) was not attenuated by carotid body denervation. Both the blood pressure and hematocrit responses to normocapnic and hypercapnic hypoxia were attenuated by carotid body denervation. We concluded that 1) the renin response to hypercapnia and hypoxia is not a carotid chemoreflex, 2) the ACTH response to hypoxia is partially a carotid chemoreflex, and 3) blood pressure and hematocrit responses to hypoxia are primarily carotid chemoreflexes.
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PMID:Renin and ACTH responses to hypercapnia and hypoxia after chronic carotid chemodenervation. 608 93

Patients with pulmonary dysfunction and CO2 retention have renal hemodynamic abnormalities accompanied by increased plasma renin activity. To determine if hypercapnia impairs renal function, particularly through the renin-angiotensin system, the effects of acute hypercapnic acidosis (HC), using 8.5% CO2, were measured in five unanesthetized dogs during (a) the intact state; (b) renin-angiotensin antagonism using either 1-sarcosine, 8-glycine angiotensin II ( [Sar1, Gly8] AII) or SQ 14,225; and (c) exogenous angiotensin II infusion. As partial arterial carbon dioxide pressure (PaCO2) increased (p less than 0.05) from control (C) of 35 +/- 1 (SEM) to 48 +/- 1 mm Hg during HC, arterial pH fell (p less than 0.05) from 7.36 +/- 0.01 to 7.24 +/- 0.005. Renal function was uncompromised with HC, and glomerular filtration rate (GFR) and urinary sodium excretion increased (p less than 0.05) despite a fourfold rise in plasma renin activity from C of 0.6 +/- 0.3 to 2.2 +/- 0.8 ng AI ml-1 h-1 during HC. Administration of [Sar1, Gly8] AII during HC did not consistently alter systemic or renal hemodynamic responses, and effects of SQ 14,225 during HC were also observed during normocapnia. Although systemic vascular responses to exogenous AII infusion were similar, the renal vasoconstrictor response was antagonized during HC with unchanged GFR and renal blood flow. These findings indicate that despite activation of the renin-angiotensin system, acute hypercapnic acidosis is unassociated with impairment of renal function in unanesthetized dogs. This may be related to diminished renal vascular AII responsiveness during hypercapnia.
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PMID:Renal and cardiovascular responses to acute hypercapnic acidosis in conscious dogs: role of renin--angiotensin. 618 44

The response of the systemic circulation to acute inhibition of the converting enzyme with 25 mg of oral Captopril (Squibb) was studied in six normal sodium-replete male volunteers at rest and during exercise, together with its effects on exercise capacity for graded uninterrupted exercise. In recumbent subjects at rest Captopril did not affect arterial pressure or heart rate, and plasma renin activity rose 2.5-fold (P less than 0.05). In subjects in the sitting position, at rest and during exercise until exhaustion, Captopril reduced mean brachial intra-arterial pressure by an average of 7 Torr in comparison to placebo (P less than 0.001). Captopril's hypotensive effect was caused by a reduction of systemic vascular resistance (P less than 0.01), without changes of cardiac output (measured by CO2 rebreathing), heart rate, or stroke volume. Plasma renin activity was significantly higher during Captopril (P less than 0.001). Peak oxygen uptake and exercise duration were the same after administration of Captopril or placebo. The data demonstrate that the renin-angiotensin system is not involved in the homeostasis of blood pressure in supine sodium-replete humans, but has a modest role in blood pressure regulation when posture is changed from supine to upright. The orthostatic effect of Captopril is maintained during upright exercise. Furthermore the reduction of systemic vascular resistance by Captopril does not affect peak oxygen uptake.
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PMID:Hemodynamic response to converting enzyme inhibition at rest and exercise in humans. 629 Apr 35

Systolic time measurements, echocardiography, and bicycle exercise testing with cardiac output determinations (CO2 rebreathing) were used to evaluate cardiac performance in 16 male hypertensives at the end of a 4-wk placebo period and after 12 wk of treatment with increasing doses (maximum = 40 mg/day) of enalapril maleate (N = 11) and of placebo (N = 5). The effect of exercise on plasma renin activity (PRA) and plasma norepinephrine (NE) concentration was also measured. Mean arterial pressure was reduced by 10 mm Hg or more in all but one subject who received enalapril. In both the enalapril- and placebo-treated subjects, the preejection period/left ventricular ejection time ratio and fractional shortening of the left ventricle at rest and cardiac output and stroke volume during moderate exercise did not change during the study. Enalapril induced a compensatory rise in PRA (N = 10). Compared to plasma NE concentration, 1124 +/- 380 pg/ml (mean +/- SD), during exercise at the end of the initial placebo period, there was attenuation of the rise of plasma NE concentration, 851 +/- 290, at the same load of exercise during enalapril therapy. Unchanged cardiac performance despite effective long-term lowering of blood pressure with enalapril may relate to inhibition of angiotensin II-mediated facilitation of NE release from peripheral nerve endings.
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PMID:Cardiac and hormonal effects of enalapril in hypertension. 631 74

Intracarotid prostaglandin E2 (PGE2) infusions (10 ng X kg-1 X min-1) increased arterial pressure in conscious dogs, sheep, and calves. Total and regional peripheral resistances (renal, superior mesenteric, and iliac) increased in conscious calves. Arterial pH and CO2 tension did not change, implying no activation of the chemoreflex. The arterial baro-reflex was reset upward during intracarotid PGE2 infusion; arterial pressure increased with little heart rate change, but baroreflex sensitivity was unchanged. In contrast, equipotent intracarotid angiotensin II infusions (10 ng X kg-1 X min-1) both reset the baroreflex upward and decreased baroreflex sensitivity. Pretreatment with alpha-, but not beta-, adrenoceptor blocking agents attenuated the intracarotid PGE2 pressor effect. Increasing PGE2 infusions (10-200 ng X kg-1 X min-1) caused dose-related arterial pressure increases; plasma renin activity was increased only at the largest infusion rate. Pretreatment with captopril, an inhibitor of the angiotensin-converting enzyme, attenuated the PGE2 pressor effect. During barbiturate-halothane and chlorolose-urethan anesthesia, no pressor effect was observed during intracarotid PGE2. We conclude that intracarotid PGE2 acts centrally to augment sympathetic vasomotor outflow. The central action of PGE2 is not affected by activation of the arterial chemoreflex or alteration of baroreflex sensitivity and has a small renin-angiotensin component.
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PMID:Mechanisms of central prostaglandin E2 hypertension in conscious dogs, sheep, and calves. 638 Mar 12

Severe hyperkalemia developed in an 85-year-old man after he had been receiving piroxicam treatment for several months. At admission his serum potassium level was 9.3 mEq/L; total CO2 level, 11 mmole/L; chloride level, 122 mEq/L; serum urea nitrogen level, 54 mg/dL; and creatinine level, 2.5 mg/dL. Hyperkalemia resolved after withdrawal of the drug and polystyrene sodium sulfonate therapy and the nonanion gap acidosis subsided concomitantly. His serum urea nitrogen and creatinine levels remained unchanged. He had abnormally low plasma renin activity, which gradually returned to normal, and aldosterone concentration, which remained low. The nonsteroidal drug may have impaired renin secretion, adrenal responsiveness to angiotensin, or the action of aldosterone on the renal tubule.
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PMID:Severe hyperkalemia during piroxicam therapy. 650 49

It has been feared that lowering the blood pressure (BP) of elderly patients with systolic hypertension (SH) may compromise cerebral perfusion. To test this hypothesis, BP, cerebral blood flow (CBF), plasma renin activity (PRA), blood counts, urinary and serum electrolytes and other blood chemistries were measured in fifteen elderly patients (ages 61-76 years) with SH (systolic BP greater than 170 and diastolic BP less than 100 mmHg). Gray matter flow (Fg) was calculated from clearance curves of inhaled 133-Xenon. All subjects were studied while untreated, as well as during long-term treatment (average 15 weeks) with hydrochlorothiazide. BP fell during treatment from 186/90 to 160/86 while average Fg and cerebrovascular resistance (CVR) were not significantly changed. There was some suggestion, however, that in patients who became normotensive the CVR decreased (p less than 0.05) while in those who did not Fg fell (p less than 0.05). Cerebrovascular response to 5% CO2 inhalation was impaired during both the treated and untreated states. Individual changes in Fg and CVR did not correlate with changes in BP or with changes in PRA, electrolytes or other chemistries. In general, cautious, gradual reduction of BP with a thiazide diuretic in SH of the elderly seems not to impair cerebral perfusion, but individual differences exist and further studies are needed to characterize them.
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PMID:Cerebral blood flow changes with diuretic therapy in elderly subjects with systolic hypertension. 674 44


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