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 present experiments were designed to determine whether blockade of endogenous opiate receptors with naloxone would suppress renin release induced by circulating epinephrine or by reductions of renal perfusion pressure. In the first series of experiments, anesthetized dogs were prepared with a flow probe around the left renal artery and a catheter in the left renal vein, permitting measurement of renin secretion before, during, and after 15-min infusions of epinephrine (50 ng.kg-1.min-1 iv). The epinephrine infusions were conducted either before or after blockade of opiate receptors with naloxone (1 mg/kg iv). Naloxone failed to alter the renin secretory response to intravenous epinephrine infusion. In a second series of experiments, anesthetized dogs were uninephrectomized and prepared with a constrictor cuff around the left renal artery and a renal arterial catheter distal to the cuff. After control measurements of renal perfusion pressure and plasma renin activity (PRA), the cuff was constricted at 15-min intervals to produce controlled stepwise reductions of renal perfusion pressure ranging from 15 to 90 mmHg. One-half of the animals was pretreated with naloxone (1 mg/kg iv). Naloxone pretreatment had no effect on the PRA response to reduced renal perfusion pressure at any pressure. The data fail to support the hypothesis that endogenous opioid peptides are modulators in the control of renin release.
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PMID:Effects of an opiate receptor antagonist on renin release in dogs. 131 Feb 18

Experimental and clinical studies seem to prove that both endogenous opioids and atrial natriuretic peptide (ANP) are involved in blood pressure regulation. This raised the question, whether these two factors are functionally interrelated to each other. We tried to answer this question by assessing plasma ANP levels in 15 patients with II degrees essential hypertension and in 15 healthy subjects under water immersion (WI) conditions. In all subjects two WI tests were performed--one without pretreatment with naloxone, and a second one after blockade of opioid receptors by this opioid receptor antagonist. Parallel to ANP, plasma renin activity (PRA), aldosterone (ALD) and vasopressin (AVP) were assessed. In hypertensive patients significantly higher basal plasma ANP levels were found than in control subjects. WI induced a significant increase of plasma ANP in both examined groups which became markedly reduced after blockade of opioid receptors by naloxone. Naloxone did not influence the WI induced decrease of PRA, ALD and AVP respectively. From results presented in this study we conclude, that a.) opioid receptors seem to influence regulation of ANP secretion both in healthy normotensive subjects and patients with essential hypertension, and b.) that WI induced alterations of ANP on the one side and of PRA, ALD and AVP on the other side are not interrelated.
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PMID:Do opioid receptors participate in the regulation of atrial natriuretic peptide (ANP) secretion in hypertensive patients? 133 Mar 91

The effects of naloxone on the development of hypertension were studied in unilaterally nephrectomized rats implanted with deoxycorticosterone acetate (DOCA; 200 mg/kg) and given saline to drink. Intraperitoneal (i.p.) infusion of naloxone at 150 micrograms/hr significantly lowered systolic blood pressure (SBP) compared to rats not receiving naloxone, (135 +/- 4.4 vs 158 +/- 5.9 mmHg on day 16). IP infusion of naloxone at 300 micrograms/hr produced the same reductions of SBP as that at 150 micrograms/hr in DOCA-salt treated rats. In other experiments intracerebroventricular (i.c.v.) infusion of naloxone at 7 micrograms/hr also significantly attenuated the DOCA-salt hypertension. The same dose given i.p. had no effect on the development of hypertension. Naloxone had no effect on plasma renin activity (PRA), plasma atrial natriuretic peptide (ANP), or concentrations of Na+ and K+ in plasma. The present data demonstrate that naloxone significantly attenuates the development of hypertension in rats given DOCA and fed a high salt diet. The attenuation of blood pressure could not be associated with the changes in PRA or plasma ANP. These results imply that the central opiate receptors play an important role in the pathogenesis of this model of hypertension.
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PMID:Naloxone attenuates development of hypertension in DOCA-salt hypertensive rats. 202 70

The aim of the study was to examine regional changes in sympathetic nerve activity (SNA) and baroreceptor function and arterial plasma catecholamines, arginine vasopressin (AVP) and plasma renin activity during morphine withdrawal in chloralose-anesthetized rats. Dependence was induced by s.c. morphine base pellets. Adrenal, renal and splanchnic SNA and SNA from the lumbar sympathetic chain were recorded before and after i.v. injections of naloxone. Baroreceptor function was examined with phenylephrine-induced increases in mean arterial pressure. In separate experiments, arterial plasma norepinephrine, epinephrine, dopamine, plasma renin activity and AVP were measured before and after naloxone-precipitated withdrawal. Naloxone administration elicited an increase in mean arterial pressure and heart rate. Although renal SNA was inhibited by approximately 50%, adrenal SNA and lumbar SNA increased by approximately 400 and 80%, respectively. Splanchnic SNA did not change significantly. The baroreceptor-mediated inhibition of adrenal SNA was facilitated while that for renal SNA was attenuated. The arterial plasma level of norepinephrine was doubled and epinephrine increased almost 20-fold. AVP increased about 15-fold, whereas plasma renin activity showed only a minor increase after naloxone. This study shows that a marked differentiation of the SNA response occurs during morphine withdrawal in rats, which suggests an interaction between opioid receptors and the control of regional sympathetic output. Furthermore, large amounts of AVP and epinephrine are released, which probably contribute to the cardiovascular changes seen in the withdrawal phase.
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PMID:Regional changes in sympathetic nerve activity and baroreceptor reflex function and arterial plasma levels of catecholamines, renin and vasopressin during naloxone-precipitated morphine withdrawal in rats. 218 76

On isolated heart preparation, it was found that Leu5-Enkephalin (Leu5-ENK) did not influence the cardiac function. On the other hand, Leu5-ENK induced a specific dose-related inhibition, in the cardiac perfusate, of the activities of kininase II (KII) and angiotensin converting enzyme (ACE) (but not of kininase I-KI). Instead no detectable alterations of the above enzymatic activities with the used concentrations of Leu5-ENK were observed in vitro. This opioid also increased specifically the effects induced by some of the autacoids, related to both renin-angiotensin and kallikrein-kinin systems, on the KII and ACE activities. A specific correlation between these Leu5-ENK-induced modifications and the functional responses of the heart to the same autacoids was observed. Naloxone (NAL) and more significantly ICI 174864 (ICI) opposed or reversed the inhibitory effect of the used opioid whereas they had neither inhibitory nor synergic effect on both KII and ACE activity by themselves. The possible physiologic role of the enkephalins in regulating cardiovascular function by acting peripherally on some humoral systems through modulatory mechanism was discussed.
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PMID:Physiologic role of the peripheral enkephalinergic system in regulating cardiovascular homeostasis: evidence of interactions with the renin-angiotensin and kallikrein-kinin systems. 255 18

Naloxone reverses hemorrhagic hypotension in the conscious guinea-pig. Captopril and saralasin impede this naloxone effect, suggesting that angiotensin II is involved in naloxone action. This is compatible with previous work which has shown that B-endorphin inhibits the centrally mediated pressor action of angiotensin II, and that naloxone blocks this effect. Naloxone may be interacting with the postulated brain renin-angiotension II system or may be blocking the action of shock-induced circulating angiotensin II on a centrally located area such as the hypothalamus.
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PMID:Naloxone reversal of hemorrhagic hypotension in the conscious guinea-pig is impeded by inhibition of the renin-angiotensin II system. 281 78

Plasma levels of some hormones, implicated in the pathogenesis of hypovolemic shock (ACTH, corticosterone, plasma renin activity, aldosterone, prostaglandins, vasopressin and beta-endorphin) were examined on rats with hemorrhagic shock. The animals were treated with the specific opioid antagonist, naloxone (1 mg/kg body weight, i. v.). The results demonstrated that during the first, compensated stage of hypovolemic shock, an increase of ACTH, corticosterone, vasopressin, and stimulation of renin-angiotensin-aldosterone system was evident, that is, an activation of hormonal mechanisms responsible for blood pressure and blood volume restoration occurred. beta-Endorphin and prostaglandin E-release during hemorrhagic shock might contribute to the cardiodepressor changes. Naloxone treatment prevented the development of shock into a progressive stage by several eventual mechanisms: An antagonism of opiate receptors. Stimulation of ACTH secretion, followed by an increased secretion of glucocorticoids or a direct effect on adrenocortical function. Stimulation of aldosterone secretion by ACTH or directly.
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PMID:Hormone changes and beta-endorphin in the pathogenesis of hemorrhagic shock. 293 Sep 96

The involvement of endogenous opioid peptides in the antihypertensive action of acutely administered clonidine, a centrally acting adrenergic agonist, was studied in humans. Eight hypertensive subjects received clonidine 0.2 mg orally, naloxone 8 mg i.v. followed by a 0.13 mg/min infusion, and both drugs together on separate days. Clonidine resulted in a significant decrease in mean blood pressure, which was not affected by concomitant treatment with naloxone. Naloxone alone or with clonidine caused significant elevations in plasma aldosterone, not mediated by increased plasma renin activity. Plasma beta-endorphin was not increased after clonidine administration. In humans, the antihypertensive effects of acute clonidine administration do not appear to be mediated by the release or action of endogenous opioids.
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PMID:Endogenous opioid peptides: do they mediate the acute antihypertensive action of clonidine in humans? 293 15

To assess the role of endogenous opioids in the secretion of pituitary and adrenal hormones, we injected intravenously the antagonist naloxone (1 mg/kg) into six dogs, euhydrated or dehydrated. Plasma renin activity (PRA), osmolality, and concentrations of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, vasopressin, Na+, and K+ were measured. Dehydration elevated (P less than 0.05) PRA, vasopressin, osmolality, and Na+. Thirty minutes after injection of naloxone, osmolality, Na+, K+, hematocrit, and plasma protein were not altered. Naloxone-induced elevations of ACTH (25 +/- 10 and 22 +/- 4 pg/ml) and cortisol (4.8 +/- 1.0 and 5.1 +/- 1.0 micrograms/dl) were similar during euhydration and dehydration, respectively. The increase in aldosterone due to naloxone was greater after euhydration (7.7 +/- 3 ng/dl) than during dehydration (2.3 +/- 0.8 ng/dl). Naloxone increased vasopressin by (5.3 +/- 2.8 microU/ml) during dehydration but not during euhydration. Intravenous hypertonic saline infusions showed that naloxone potentiates the osmotic release of vasopressin. Our results indicated that dehydration did not alter the inhibitory role of opioids in regulation of ACTH and cortisol but suppressed the inhibition of aldosterone secretion. Our findings also showed that opioids inhibit secretion of vasopressin during dehydration by decreased responsiveness to osmotic stimulation.
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PMID:Pituitary and adrenal hormone responses to naloxone in euhydrated and dehydrated dogs. 300 81

It has been reported that endogenous opioid antagonism through naloxone (NAL) blunts the hypotensive effect of captopril (CAP) in normal man. For this reason a study was carried out to determine whether NAL interacts with the antihypertensive effect of CAP in patients with mild-to-moderate essential hypertension (n = 6; age 22-43 years). Patients received, according to a randomized code, placebo (PL) during saline infusion, CAP (25 mg orally) during saline infusion, PL + NAL (0.4 mg as a bolus followed by a continuous infusion of 4.0 mg/h for 2 h) and CAP + NAL at the same doses. Three-day intervals elapsed between each phase of the study. Blood pressure (BP) and heart rate (HR) were recorded before (-20 to 0 min) and every 15 min for the next 2 h after drug administration. Blood samples for plasma renin activity (PRA), noradrenaline (NA) and aldosterone (ALD) were collected before (time 0) and 120 min after drug administration. Neither PL nor NAL changed any of the parameters examined, while CAP alone reduced mean BP to a highly significant extent. Naloxone did not change the hypotensive effect of CAP to any significant extent. Captropril, either alone or associated with NAL, tended to reduce plasma ALD and increase PRA (P less than 0.05) without changing HR or plasma NA. These data indicate that, at least under the experimental conditions used, endogenous opioid antagonism does not interfere with the haemodynamic and humoral effect of CAP in essential hypertensive man. This suggests that endogenous opioids do not mediate the pharmacological actions of CAP.
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PMID:Naloxone does not modify the antihypertensive effect of captopril in essential hypertensive patients. 300 98


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