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)

It is well known that the alternations on humoral homeostasis such as a decrease of pH, an elevation of PaCO2 and changes of electrolytes have been detected during respiratory acidosis. The author is of the opinion that the renin-angiotensin-aldosterone system might be related to these changes during respiratory acidosis. Recently, Fujii and Morita have reported that an increase in plasma renin activity appeared during acute respiratory acidosis. These reports prompted me to question whether the renin-angiotensin-aldosterone system was related to the pathophysiological evidence concerning the respiratory acidosis. It is generally accepted that plasma aldosterone concentration is controlled by (1) the renin-angiotensin system, (2) ACTH and (3) serum potassium. Therefore, the purpose of this experiment was to investigate the roles of the renin-angiotensin system and electrolyte metabolism on plasma aldosterone concentration during acute respiratory acidosis. I initiated acute respiratory acidosis with 10% CO2 inhalation in healthy mongrel dogs, and then plasma aldosterone concentration, plasma renin activity, electrolytes and cardiorenal hemodynamics were measured. The results were as follows: 1. The increase of plasma aldosterone concentration was delayed and blurred, in contrast with a significant increase of plasma renin activity, during the acute respiratory acidosis, due to delayed time course of angiotensin II stimulation and also the expected changes in the concentration of angiotensin II receptors on the zona glomerulosa in the adrenal cortex. 2. There was a possibility that the increase in the reabsorption of sodium and water in the proximal tubules, and the increase of ADH secretion during the acute respiratory acidosis, could be related to a decrease in excreted sodium and potassium as well as urine volume. These results suggest that the changes of plasma aldosterone concentration may be affected partially by renin-angiotensin system but not by serum potassium, and plasma aldosterone should be a minimal determinant on the electrolyte metabolism during respiratory acidosis with 10% CO2 inhalation.
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PMID:[The changes on plasma aldosterone concentration during acute respiratory acidosis in dogs. The relationship to renin-angiotensin system and electrolyte metabolism (author's transl)]. 706 60

Prazosin improves hemodynamics promptly in patients with congestive heart failure (CHF), but tolerance to repeated doses may develop rapidly. To determine if the kidneys play a role in this attenuation of effect, we studied renal responses in nine CHF patients treated with prazosin (5 mg three times a day for 3 days) preceded and followed by 3 days of placebo. Prazosin decreased mean arterial blood pressure from 87.0 +/- 2.2 (mean +/- SEM) to 84.0 +/- 2.0 mm Hg (p < 0.05) with no change in heart rate (73.1 +/- 3.3 bpm on placebo and 73.6 +/- 3.5 bpm on prazosin). The change in creatinine clearance from 81.6 +/- 8.7 to 96.3 +/- 10.4 ml/min with prazosin was not statistically significant, but the slight increase in urine volume from 2.33 +/- 0.22 to 2.51 +/- 0.23 1/24 hr was (p < 0.01). There were no significant changes in serum sodium, potassium, chloride, CO2, blood urea nitrogen, osmolality or glucose, urinary excretion of sodium or potassium, or sodium balance. The data were analyzed for changes within each period but there were no significant changes from day to day. Plasma renin activity rose from 3.93 +/- 0.69 to 4.96 +/- 0.84 ng/ml/hr during prazosin (p < 0.02). Significant alterations in renal function are not likely when patients with CHF are treated with prazosin, and any attenuation of effect of prazosin after repeated doses is not likely due to mechanisms involving alterations in renal function.
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PMID:Effect of prazosin on renal function in congestive heart failure. 740 92

We reported that intravenous infusion of angiotensin II (ANG II) stimulated ventilation (VE) in conscious dogs. Other studies in our laboratory have demonstrated that increases in respiration occurred in association with activation of the renin-angiotensin system during acute hypotension and during hypercapnia. Therefore, in conscious dogs (n = 5), we examined the effects of ANG II receptor blockade with intravenous saralasin (0.5 micrograms.kg-1.min-1) on respiratory responses during progressive nitroprusside-induced hypotension and during the ventilatory response to increased inspired fraction of CO2 (VRC). During hypotension (mean arterial pressure decreased approximately 20%) combined with ANG II receptor blockade, VE, heart rate, and arginine vasopressin increases were attenuated compared within unblocked studies. With ANG II receptor blockade during hypotension, alveolar ventilation and arterial PCO2 (PaCO2) were unchanged, which contrasted with a doubling of alveolar ventilation and a decrease of 4.8 +/- 1 Torr in PaCO2 in unblocked studies. During hypercapnia, the slope of the VRC was not affected by ANG II receptor blockade, but with 6.5% inspired CO2 fraction, VE and PaCO2 were lower than in unblocked studies. These results indicated that ANG II contributed to the respiratory response to a modest hypotension but did not affect respiratory sensitivity to CO2.
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PMID:Renin-angiotensin system stimulates respiration during acute hypotension but not during hypercapnia. 848 61

In normoxic conscious dogs, increased angiotensin II (ANG II), or activation (disinhibition) of the renin-angiotensin system by vasopressin (AVP) V1-receptor block, increases ventilation and decreases arterial PCO2. Both hormones can be increased during hypoxia and might modulate ventilatory drive. Six conscious dogs were studied before and during hypocapnic, isocapnic, and hypercapnic hypoxia. To study potential hormonal effects during hypocapnic hypoxia, experiment 1 included three protocols in which 12.8% O2 was breathed for 60 min: protocol 1, control studies without block; protocol 2, AVP V1 receptors were blocked at the onset of hypoxia; and protocol 3, ANG II receptors were blocked 20 min before hypoxia. To study potential effects of acid-base changes during acute hypoxia, experiment 2 included two protocols (with and without AVP V1-receptor block). A 40-min period of hypocapnic hypoxia was followed by two successive 20-min periods with hypoxia maintained but inspired CO2 progressively increased. Neither hormonal block affected respiration during the hypoxic conditions. Unlike normoxia in conscious dogs, during acute hypoxia, respiratory control by ANG II is not modulated by AVP and acid-base effects on receptors do not account for this difference.
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PMID:Respiration during acute hypoxia: angiotensin- and vasopressin-receptor blocks. 896 41

Changes in renal sympathetic nerve activity (SNA) are postulated to influence renal function in selective ways, such that different levels of activation produce particular renal responses, initially in renin release, then sodium excretion, with changes in renal hemodynamics occurring only with much greater stimulus intensities. The aim of this study was to determine the renal hemodynamic and excretory responses to graded physiological increases in renal SNA induced by breathing different hypoxic gas mixtures. Experiments were performed in seven conscious rabbits subjected to four gas mixtures (14% O2, 10% O2, 10% O2 + 3% CO2, and 10% O2 + 5% CO2) and instrumented for recording of renal nerve activity. After a 30-min control period, rabbits were subjected to one of the four gas mixtures for 30 min, and then room air was resumed for a further 30 min. The four gas mixtures increased renal SNA by 14, 38, 49, and 165% respectively, but arterial pressure (thus renal perfusion pressure) was not altered by any of the gas mixtures. The greatest level of sympathetic activation produced significant falls in glomerular filtration rate (GFR), renal blood flow, sodium and fluid excretion, and significant increases in plasma renin activity. These returned to levels not significantly different from control conditions in the 30-min period after the gas mixture. When the changes to the various gas mixtures were analyzed within each rabbit, a significant linear relationship was found with all variables to the increase in SNA. Renal denervation in a separate group of seven rabbits completely abolished all of the above responses to the different gas mixtures. Thus graded activation of renal nerves induced by changes in inspired gas mixtures resulted in graded decreases in renal blood flow, GFR, and sodium excretion and graded increases in renin activity, with the changes occurring across a similar range of nerve activities; there was no evidence for a selective change in any renal variable.
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PMID:Functional response to graded increases in renal nerve activity during hypoxia in conscious rabbits. 899 44

This study examined the possible contribution of the brain renin-angiotensin system on the sympathetic activation induced by hypoxia in conscious rabbits. Blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded under conditions of normoxia and hypoxia (10% O2 + 3% CO2) before and after fourth ventricular administration of either losartan (10 micrograms in 25 microliters), enalaprilat (500 ng in 25 microliters) or Ringer's (25 microliters). Hypoxia increased the RSNA by 113% and slightly decreased HR without changing BP. It also increased the variability of BP or HR in the 0.2-0.4 Hz frequency domain. Losartan and enalaprilat did not change the resting BP or HR but elevated the RSNA increase seen during hypoxia. Our results suggest that central angiotensin is involved in mediating response to chemoreceptor activation.
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PMID:Effect of central endogenous angiotensin II on sympathetic activation induced by hypoxia. 924 64

The aim of this study was to investigate the haemodynamic and endocrinological effects of noninvasive positive pressure ventilation (NIPPV). Eleven patients with oedema and recent hypercapnic and hypoxaemic worsening of a chronic respiratory insufficiency were included. Echocardiography, cardiac radionuclide assessment, blood catecholamines, salt and water handling hormones were measured at admission and discharge (long study (LS)). To discriminate between the action of NIPPV and other treatments, measurements were performed on the fourth day, for 4 h without NIPPV and 4 h with NIPPV (short study (SS)). NIPPV entailed a correction of P(a,CO2) and an increase of P(a,O2) in LS and SS. Oedema disappeared. Body weight decreased (from 85+/-42 to 81+/-40 kg) during LS. Systolic and mean pulmonary arterial pressure decreased in LS and SS. Right ventricular ejection fraction increased in LS. Left ventricular ejection fraction did not change. Cardiac index was normal on admission and then decreased. Natriuretic peptides and catecholamines were increased on admission, whereas plasma renin activity, aldosterone and vasopressin were normal. We suggest that in these patients, oedema can occur independently of renin-angiotensin-aldosterone-vasopressin and with a normal cardiac output. Noninvasive positive pressure ventilation allowed a correction of blood gases, associated with the resolution of oedema, a decrease in pulmonary arterial pressures and an increase in right ventricular ejection fraction.
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PMID:Haemodynamic and endocrinological effects of noninvasive mechanical ventilation in respiratory failure. 942 94

As it has been suggested that parathyroid hormone (PTH) is implicated in the pathophysiology of essential hypertension, the effects of PTH(1-34) were assessed during infusion over 120 min in ten men with essential hypertension and in ten healthy men. Ionized calcium was kept constant by a clamping technique. Mean arterial blood pressure fell slightly in the patients (116 mm Hg, median, before, and 108 mm Hg during the infusion, P < .01), but remained unchanged in the controls (median 87 mm Hg). The pulse rate rose to a similar extent in the two groups, but cardiac output, measured by the CO2 rebreathing technique, was unchanged. The glomerular filtration rate (GFR) was slightly lower in the hypertensives than in the controls at baseline (92 v 109 mL/min, P < .02), but it increased similarly during PTH infusion in both groups (+13% v +9%, medians), as did the effective renal plasma flow (+50% v +38%). The urinary rate of sodium excretion, which was similar at baseline, increased more in the patients than in the controls (+191% v +46%, P < .05); this was mainly attributable to a reduction in the tubular reabsorption of sodium. Calculations based on lithium clearance indicated that mainly the proximal tubular reabsorption of sodium decreased during PTH infusion. Baseline plasma PTH(1-84) was higher in the patients than in the controls (20.5 ng/L v 16.5 ng/L, P < .05). The baseline plasma values of renin, aldosterone, atrial natriuretic peptide, endothelin, and noradrenaline were similar in the two groups. During infusion of PTH, renin increased less in the patients than in the controls (P < .02), and aldosterone increased only in the controls (P < .01). The other hormonal values remained unchanged. In conclusion, the patients with essential hypertension had increased baseline PTH values, but nevertheless PTH had more marked vasodilative and natriuretic effects than in the controls. PTH thus seems to counteract rather than aggravate elevation of blood pressure in these patients.
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PMID:Effects of PTH(1-34) on blood pressure, renal function, and hormones in essential hypertension: the altered pattern of reactivity may counteract raised blood pressure. 944 71

A role for vitamin D in the pathophysiology of essential hypertension has frequently been suggested, but acute direct effects on blood pressure, cardiac output, renal hemodynamics, or hormones have not previously been demonstrated. The rapid effects of 1,25-dihydroxycholecalciferol (1,25-D) were assessed over 120 min after a bolus injection (0.02 microg/kg body weight) in eight men with essential hypertension and in nine healthy men. A placebo group of 10 healthy men was also included. Ionized calcium was monitored closely during the study, and was kept constant with a clamping technique. In the hypertensive patients, a transient increase in blood pressure and a reciprocal fall in cardiac output measured by a CO2 rebreathing technique (-15%, P < .05) were observed after 1,25-D injection. In the control group, both blood pressure and cardiac output remained unchanged. The glomerular filtration rate, effective renal plasma flow, and urinary sodium and water excretions were unchanged in both groups. Plasma levels of atrial natriuretic peptide at baseline were higher in the hypertensive patients than in the control subjects (P < .02); plasma levels of renin, aldosterone, norepinephrine, endothelin, and parathyroid hormone(1-84) were similar in the two groups. None of these hormones was affected during the observation time after the injection of 1,25-D. In conclusion, acute administration of 1,25-D caused a fast and likely nongenomic-mediated decrease in cardiac output in patients with essential hypertension, which together with a transient BP increase implies a 1,25-D-induced increase in total peripheral resistance. These data suggest an enhanced cardiovascular responsiveness to 1,25-D in hypertensive compared to healthy normotensive subjects.
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PMID:Acute cardiovascular effect of 1,25-dihydroxycholecalciferol in essential hypertension. 1019 37

We tested the hypothesis that angiotensin II (ANG II) contributes to ventilatory and acid-base adaptations during 3-4 h of hypoxia (partial pressure of O2 in arterial blood approximately 43 Torr) in the conscious dog. Three protocols were carried out over 3-4 h in five dogs: 1) air control, 2) 12% O2 breathing, and 3) 12% O2 breathing with ANG II receptors blocked by infusion of saralasin (0. 5 microg . kg-1 . min-1). After 2 h of hypoxia, expired ventilation and alveolar ventilation progressively increased, and the partial pressure of CO2 in arterial blood and the difference between the arterial concentrations of strong cations and strong anions ([SID]) decreased. When the hypoxic chemoreceptor drive to breathe was abolished transiently for 30 s with 100% O2, the resultant central apneic time decreased between 0.5 and 2.5 h of hypoxia. All these adaptive responses to hypoxia were abolished by ANG II receptor block. Because plasma ANG II levels were lower during hypoxia and hypoxic release of arginine vasopressin from the pituitary into the plasma was prevented by ANG II receptor block, the brain renin-angiotensin system was likely involved. It is possible that ANG II mediates ventilatory and acid-base adaptive responses to prolonged hypoxia via alterations in ion transport to decrease [SID] in brain extracellular fluid rather than acting by a direct neural mechanism.
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PMID:Angiotensin II modulates respiratory and acid-base responses to prolonged hypoxia in conscious dogs. 968 73


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