Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

During episodes of blood loss, several apparently redundant mechanisms are activated to maintain arterial blood pressure. This study was designed to examine one such compensatory mechanism involving enhanced vasopressin release during hemorrhage when the autonomic nervous system (ANS) is pharmacologically blocked. First, to confirm that this compensatory mechanism exists in canines, conscious dogs were hemorrhaged under normal conditions and during ANS blockade. In dogs with intact cardiac nerves (intact, n = 7), hemorrhage at 0.8 ml/kg/min increased plasma vasopressin (PAVP) from 3.0 +/- 0.7 to 6.6 +/- 2.4 and 78 +/- 50 pg/ml at blood losses of 10 and 20 ml/kg, respectively. At the same amount of blood loss during hemorrhage with ANS blockage, PAVP was enhanced significantly from 33 +/- 17 to 230 +/- 90 and 610 +/- 270 pg/ml. ANS blockade did not, however, alter the hemorrhage-induced increases in plasma renin activity. Next, to examine the afferent mechanisms responsible for the enhanced PAVP response, cardiac-denervated dogs (CD, n = 9) were hemorrhaged with and without ANS blockade. Without blockade, PAVP increased from 3.7 +/- 0.9 to 5.2 +/- 0.8 and 26 +/- 11 pg/ml at blood losses of 10 and 20 ml/kg. PAVP was significantly higher in response to hemorrhage with ANS blockade, increasing from 17 +/- 6 to 76 +/- 18 and 330 +/- 80 pg/ml. The rise in PAVP in the CD dogs suggested that peripheral baroreceptors were involved in eliciting vasopressin release under these conditions. Therefore, the influence of arterial baroreceptors was examined by infusing norepinephrine during hemorrhage in order to maintain blood pressure constant. Under these conditions, PAVP increased significantly in the intact dogs at 10 ml/kg blood loss, but did not change in the CD dogs. These results demonstrate that the enhanced release of AVP during hemorrhage with ANS blockade can be mediated either by cardiac or arterial baroreceptors; however, the maximum response is elicited only when both sets of receptors are functioning normally.
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PMID:Contribution of cardiac and arterial baroreceptors to enhanced vasopressin release during hemorrhage with autonomic blockade. 770 Aug 84

There are inherent complications associated with chronic indwelling venous catheters for use as bleed catheters in long term hemorrhage experiments in conscious animals. As an alternative we have developed a protocol for bleeding conscious rabbits using a disposable catheter in the central ear artery. Previously we had bled rabbits through a catheter chronically implanted in the inferior vena cava (IVC); thus, we were interested in any potential differences in the hormonal (vasopressin and renin) and cardiovascular profile during hemorrhage between the IVC and ear artery bleeds. Rabbits underwent two bleeds, 1 week apart, one using the indwelling IVC catheter and the other with an ear artery (EA) catheter. We compared the mean arterial pressure (MAP), heart rate (HR), plasma vasopressin (AVP), and plasma renin activity (PRA) before and during hemorrhage. Baseline cardiovascular and hormonal values were the same, regardless of choice of bleed site. In addition there were no differences between bleed sites in the rate of fall of MAP (slope: IVC, 0.24 +/- 0.05; EA, 0.26 +/- 0.04) and the rate of rise of HR (slope: IVC, -1.37 +/- 0.22; EA, -1.20 +/- 0.19). Finally the AVP and PRA values associated with a MAP of 50 mmHg (1 mmHg = 133.3 Pa) (close to peak levels achieved during the hemorrhage) were also not different between IVC and EA bleeds. Given that the profiles of the bleeds were not different and that surgical implantation, possible infection, and daily flushing were avoided by the use of the EA catheter, we concluded that use of the EA as a site for bleeding conscious rabbits was justified.
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PMID:Hemorrhage from the inferior vena cava versus the ear artery: a comparison of cardiovascular and hormonal responses in conscious rabbits. 795 3

The current study examined three pressor systems which might support mean arterial pressure (MAP) after lesions of the rostral ventrolateral medulla (RVLM). In two protocols, bilateral electrolytic lesions or sham lesions were placed in the RVLM of rats anesthetized with sodium pentobarbital. In the first protocol, the following drugs were given sequentially after placement of the lesions: captopril (5 mg/kg) and d-pentamethylene methylated tyrosine (30 micrograms/kg), a vascular arginine-vasopressin antagonist (AVPX). A final procedure consisted of spinal-cord transection. The second protocol was identical to the first except that the order of drug administration was reversed. In the first protocol, RVLM lesions caused a slight, but statistically significant, decrease in MAP from 118 +/- 3 mmHg to 103 +/- 5 mmHg. After captopril and AVPX, MAP further decreased to 87 +/- 5 mmHg and 62 +/- 4 mmHg, respectively. The MAP fell to 38 +/- 2 mmHg after spinal-cord transection. In the sham-lesion group, MAP rose slightly from 127 +/- 6 mmHg to 134 +/- 7 mmHg after placement of the sham lesions. A significant reduction in MAP was not seen until after administration of AVPX, which decreased MAP to 103 +/- 6 mmHg. Spinal-cord transection substantially lowered MAP to 36 +/- 4 mmHg. In the second protocol, RVLM lesions had no effect on MAP. Administration of AVPX had little effect on MAP (before: 117 +/- 5 mmHg; after: 102 +/- 7 mmHg). In contrast, sequential administration of captopril substantially decreased MAP to 55 +/- 5 mmHg. Spinal cord transection lowered MAP to 33 +/- 1 mmHg. A decrease in MAP in the companion sham-lesion group was not seen until after administration of captopril (before: 109 +/- 8 mmHg; after: 89 +/- 11 mmHg). The greatest fall in MAP followed spinal cord transection (to 39 +/- 6 mmHg). These results demonstrate normotension after RVLM lesions despite a marked reduction in sympathetic vasomotor activity. They also indicate that, after RVLM lesions, arterial pressure is maintained mainly by activity of the renin-angiotensin system and by AVP secretion.
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PMID:Pressor systems involved in the maintenance of arterial pressure after lesions of the rostral ventrolateral medulla. 812 Mar 44

The unifying hypothesis of body fluid volume regulation explains the renal handling of sodium and water in health and in various disease states associated with edema formation and no intrinsic renal parenchymal disease. According to this hypothesis, underfilling of the arterial vascular compartment, resulting from either a decrease in cardiac output or peripheral arterial vasodilation, initiates a sequence of events that results in activation of the sympathetic nervous and renin-angiotensin-aldosterone systems and the nonosmotic release of AVP. Activation of these neurohormonal vasoconstrictor systems causes diminished renal hemodynamics and renal sodium and water retention that persist despite an increase in total extracellular and blood volume. In edematous patients, a vasoconstrictor-mediated increase in proximal tubular sodium reabsorption results in diminished sodium delivery to the distal tubular sites of action of aldosterone and ANP; this explains the failure of such patients to escape from the sodium-retaining effects of aldosterone and the resistance to the natriuretic and diuretic effects of ANP. In pregnancy, an early decrease in systemic vascular resistance associated with activation of the neurohormonal vasoconstrictor systems precedes the normal expansion of blood and plasma volumes and is consistent with the arterial underfilling hypothesis. The loss of this peripheral vasodilatory response in some pregnancies may contribute to the development of preeclampsia and eclampsia.
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PMID:Body fluid volume regulation in health and disease. 814 Sep 55

The present study aimed to answer the following questions: 1. do secretion of volume related hormones in patients with EH pre and post treatment with captopril differ from normotensive subjects if examined in thermal dehydration conditions; 2. is the electrolyte composition of thermal sweat related to the plasma profile of volume related hormones? and 3. does treatment by captopril influence sweat electrolytes in EH patients. In 16 patients with EH and in 20 healthy subjects a thermal dehydration test was performed. In patients with EH this test was done twice: before treatment and after 6 weeks of captopril therapy. In all subjects plasma renin activity (PRA), aldosterone (Ald) AVP and ANP were measured before and after thermal dehydration. In sweat samples collected after 15' and 45' of thermal dehydration the concentration of Na, K and Cl was assessed. In hypertensive patients before captopril treatment significantly higher values of PRA, ALD and ANP were found, while sweat concentrations of Na and Cl were significantly lower than in controls. After captopril treatment sweat electrolytes concentrations showed a tendency to normalize. No significant correlation was found between the plasma hormonal profile and sweat Na, K and Cl concentrations respectively both in controls and patients with EH pretreatment. A significant positive correlation was noticed only in hypertensive patients post-treatment between plasma aldosterone and sweat Na and Cl concentration respectively. Results obtained in this study show, that volume related hormones (Ald, AVP, ANP) do not seem to influence markedly the electrolyte composition of thermal sweat both in healthy subjects and in hypertensive patients.
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PMID:[Hormones regulating volume and electrolytes of sweat in patients with essential hypertension. Effect of thermal dehydration and treatment with captopril]. 823 Sep 93

This study explored the possibility that the nucleus reticularis parvocellularis (NRP) acts in concert with the rostral ventrolateral medulla (RVLM) in the maintenance of mean arterial pressure (MAP). Bilateral electrolytic or chemical lesions (kainic acid) were placed in three groups of rats anesthetized with sodium pentobarbital. In the different groups, lesions were placed only in the NRP or RVLM or in both the NRP and RVLM (NRPRVLM). Captopril (5 mg/kg, i.v.) and an arginine vasopressin antagonist (AVPX), d-pentamethylene methylated tyrosine (30 micrograms/kg, i.v.), were sequentially administered. A final procedure consisted of spinal cord transection. The RVLM lesions did not significantly alter MAP (before: 116 +/- 3 mmHg; after: 106 +/- 5 mmHg). Sequential administration of captopril and AVPX each reduced MAP to 87 +/- 5 mmHg and 62 +/- 4 mmHg, respectively. Spinal-cord transection lowered MAP to 38 +/- 2 mmHg. Lesions of the NRP also did not alter MAP (before: 113 +/- 4 mmHg; after: 118 +/- 5 mmHg). Captopril reduced MAP to 109 +/- 7 mmHg, AVPX had no effect, and spinal-cord transection decreased MAP to 31 +/- 3 mmHg. In contrast to the lack of effect of lesions of the RVLM or NRP on MAP, profound hypotension was observed after NRPRVLM lesions (before: 113 +/- 3 mmHg; after: 51 +/- 3 mmHg). Subsequent administration of captopril decreased MAP to 39 +/- 2 mmHg, and AVPX lowered MAP to 32 +/- 1 mmHg. Spinal-cord transection reduced MAP to 23 +/- 1 mmHg. Several conclusions can be drawn from this study. First, lesions of the RVLM do not decrease MAP because of compensation by the renin-angiotensin system and AVP secretion which is mediated by the NRP. Second, lesions of the NRP do not affect MAP because the intact RVLM can maintain sympathetic tone. Third, the profound hypotension observed after NRPRLVM lesions occurred because of the simultaneous impairment of sympathetic vasomotor activity and the neuroendocrine vasoconstrictor effects of the renin-angiotensin system and AVP secretion.
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PMID:Cardiovascular effects of lesions of the rostral ventrolateral medulla and the nucleus reticularis parvocellularis in rats. 831 11

CHF is a common, complex and life-threatening clinical syndrome. It is widely accepted that enhanced peripheral vascular tone plays a major role in the pathophysiology of CHF. Increased activity of the sympathetic nervous system is one of the most important factors responsible for the increased afterload in CHF. This increase in sympathetic activity occurs early in the course of development of CHF. Efferent sympathetic activity is distributed in a non-uniform way in CHF, with significant increases to the heart and kidney but normal activity to some other organs such as the lung. Increased renal sympathetic activity contributes significantly to altered neural haemodynamics, sodium and water retention, and modulation of the actions of other vasoactive hormones. The regional alteration in sympathetic activity may be largely responsible for the changes in resting regional blood flow to different organs in CHF and the maldistribution of blood flow that occurs during the stress of exercise. Disordered function of cardiovascular reflexes is observed in CHF and may contribute to disordered sympathetic function. In CHF there are significant interactions between the sympathetic nervous system and other humoral systems such as the renin-angiotensin system, AVP, ANP, endothelin and renal DA. The various drugs used in the treatment of CHF have different effects on sympathetic activity: digitalis and ACE inhibitors tend to suppress activity while diuretics may have the opposite effect. Following cardiac transplantation, there is a prompt return of sympathetic function towards normal, although the heart may remain significantly denervated for a long time, with gradual reinnervation. Cyclosporin therapy tends to increase sympathetic activity and this may contribute to post-transplant hypertension.
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PMID:Sympathetic dysfunction in heart failure. 848 86

This study was undertaken to estimate the role of AVP in the regulation of vascular tonus and blood pressure, at first, during hemodialysis hypotension and, secondly, in hypertensive patients with chronic renal failure (CRF). Study 1: among 12 patients with hemodialysis (HD) hypotension showing similar metabolic and endocrine changes except plasma AVP during HD, 6 who showed an increase in plasma AVP after HD were hemodynamically examined during HD. Gradual decreases in mean BP and cardiac index, and increases in systemic vascular resistance (SVR) and plasma AVP, with a slight time-delay, were observed and thereafter BP inversely showed a slight increase at the end of HD, whereas no significant change in HR was found throughout HD. However, the % change in SVR had a positive correlation with % change in plasma AVP levels (P < 0.01, r = 0.559), but not with that in plasma renin activity or plasma norepinephrine levels. Study 2: oral administration of 100 mg of AVP.V1-receptor antagonist, OPC21268, which completely inhibited the vasoconstriction induced by the exogenously administered AVP, did not show any changes in BP and HR of seven hypertensive CRF patients. However, OPC21268 results in a marked decrease in BP of one hypertensive CRF patient with congestive heart failure (CHF) and nephrotic syndrome. Therefore, in some patients with HD hypotension showing impaired SNS and RAS, AVP may play an important role in the maintenance of BP during HD, predominantly via its peripheral vasoconstrictive action. On the other hand, AVP might not aggressively participate in hypertension of CRF patients, even with relatively high levels of plasma AVP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of AVP in the regulation of vascular tonus and blood pressure in patients with chronic renal failure. 851 71

We examined the effect of an orally effective, nonpeptide AVP.V1-receptor antagonist, OPC21268, on urinary albumin excretion and renal hemodynamics in non-insulin dependent diabetes mellitus (NIDDM) patients (seven patients with microalbuminuria, four with overt nephropathy, and three with normoalbuminuria) and in three normal subjects. The oral administration of 100 mg of OPC21268, which is sufficient to suppress the vasoconstriction induced by exogenously infused AVP, caused a significant decrease in urinary albumin excretion only in NIDDM with microalbuminuria concomitantly with a slight decrease in filtration fraction and glomerular filtration rate (GFR). On the other hand, urinary beta 2 microglobulin excretion did not change at all during the study. Neither change in systemic blood pressure, in heart rate, nor in plasma vasoactive substance levels (ANP, renin activity, aldosterone, and AVP) was observed in all four groups. In conclusion, in NIDDM patients with microalbuminuria, an increase in the sensitivity of contraction of glomerular efferent arterioles via an activation of AVP.V1-receptor(s) is at least present, and AVP.V1-receptor antagonist causes a decrease in urinary albumin excretion due partly to decrease the intraglomerular capillary pressure. This compound may be useful for the treatment of NIDDM microalbuminuria.
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PMID:Effect of AVP.V1-receptor antagonist on urinary albumin excretion and renal hemodynamics in NIDDM nephropathy: role of AVP.V1-receptor. 857 58

The purpose of this study was to compare the fetal circulatory responses during maternal hemorrhage and fetal hemorrhage. Four pregnant goats, gestational age 131 +/- 7 days for the fetal hemorrhage and 5 goats, 132 +/- 2 days (term 145 days) for the maternal hemorrhage were used. The amounts of hemorrhage were 700ml per 2 hours for the maternal hemorrhage and 40ml per 2 hours for the fetal hemorrhage. Although fetal arterial pH decreased during both hemorrhages, fetal arterial pO2 increased during the fetal hemorrhage and decreased in the maternal hemorrhage. The fetal arginine vasopressin concentration and plasma renin activity increased during both hemorrhages, but the rates of change in the hormone concentrations were higher during the fetal hemorrhage. The fetal aldosterone concentration decreased during maternal hemorrhage but increased during fetal hemorrhage. FAP increased and FHR decreased during maternal hemorrhage. FAP and FHR were significantly correlated to the AVP concentration. These relationships were not found during fetal hemorrhage. We therefore concluded that fetal responses were completely different in pO2, FAP and FHR during the maternal and fetal hemorrhages.
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PMID:[Comparison of fetal circulatory responses during maternal bleeding and fetal bleeding]. 857 27


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