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)

Conscious Merino ewes were given an intravenous hypertonic sodium chloride load of 4 mmol.min-1 for 100 min. This resulted in increases in urine flow, sodium and potassium excretion and plasma sodium concentration and osmolality. Urinary vasopressin output and solute-free water reabsorption increased and plasma renin activity declined. Renal plasma flow and glomerular filtration rate (GFR) rose, as did the solute clearance. The change in urinary osmolality was related to the initial urine osmolality such that when the initial urine osmolality was high the urine became more dilute, and vice versa. Tubular sodium reabsorption increased but the fractional reabsorption rate fell. It is suggested that the increase in GFR was at least partly due to the increase in AVP and that the electrolyte loss can be accounted for by the increase in GFR without necessarily involving AVP or other hormonal effects at the tubular level.
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PMID:The effect of intravenous hypertonic saline infusion on renal function and vasopressin excretion in sheep. 25 75

The effect of furosemide on plasma renin, vasopressin (AVP), and aldosterone concentrations was studied in 10 control and 6 nephrectomized lambs during the 1st 2 wk of life. In a separate study in 10 newborn lambs, 1-sarcosine-8-alanine-angiotensin II (saralasin acetate, 5 mug/kg per min) was infused alone for 40 min, after which furosemide 2 mg/kg i.v. was injected in association with continuing saralasin acetate infusion. Plasma renin activity increased from a mean (+/-SEM) of 21.3+/-3.4 ng/ml per h in the 10 control lambs to 39.4+/-8.2 ng/ml per h at 8 min (P < 0.001) and remained high through 120 min after furosemide. Plasma AVP and aldosterone concentrations increased from respective mean values of 2.1+/-0.4 muU/ml and 12.8+/-2.5 ng/dl to 9.8+/-2.0 muU/ml (P < 0.01) and 23.0+/-7.7 ng/dl (P < 0.05) at 35 min and 13.8+/-2.1 muU/ml and 23.0+/-4.4 ng/dl at 65 min after furosemide (each P < 0.01). There was an insignificant AVP response in the 10 lambs treated with angiotensin inhibitor: from a mean base line of 4.7+/-0.9 to 8.3+/-2.0 muU/ml at 35 min, and 7.4+/-2.0 muU/ml at 65 min after furosemide. There was no increase in AVP in the anephric lambs. The mean increment AVP response from base line in the newborn lambs without saralasin, Delta 10.8+/-2.0 muU/ml, was greater than in the lambs with saralasin, Delta4.0+/-1.9 (P < 0.05), and greater than in the anephric lambs, Delta3.3+/-2.1 muU/ml (P < 0.05). The mean blood pressure fell 6 mm Hg in the 10 control lambs (P < 0.05), 7 mm Hg in the anephric lambs (P < 0.05), and 16 mm Hg in the lambs treated with angiotensin inhibitor (P < 0.05) by 35 min after furosemide. However, the changes in plasma AVP were not related to the fall in blood pressure. These data support the view that the observed AVP response to furosemide in the newborn lamb was mediated through the renin-angiotensin system.
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PMID:Endogenous angiotensin stimulation of vasopressin in the newborn lamb. 42 54

The thermal dehydration test was performed in 12 patients with renal transplant and in 20 healthy subjects. The study was aimed at the evaluation of the effect of volume regulating hormones on electrolyte composition of thermal sweat in patients with renal transplant. Blood plasma renin activity (PRA) as well as plasma concentrations of aldosterone (ALD), vasopressin (AVP) and atrial natriuretic peptide (ANP) were determined before and after thermal dehydration in all the subjects studied. In all the subjects sweat was also collected after 15 and 45 minutes of exposition to heat and the concentrations of sodium, potassium and chloride were determined in all sweat samples. Significantly elevated PRA and ANP concentrations and significantly lowered plasma AVP concentrations but normal ALD levels were found before thermal dehydration test in all the patients with renal transplant. After the exposition to heat lasting 1 hour the direction of changes was similar, their magnitude was, however, different in renal transplant patients than in healthy subjects. In addition, lower concentrations of sodium and chloride in thermal sweat and lower total concentration of sweat solids were found in renal transplant patients than in healthy controls. No significant correlation was found between the plasma concentrations of the hormones determined and the electrolyte concentrations of thermal sweat both in the renal transplant patients and in healthy subjects. The results suggest that the volume regulating hormones have no effect on the electrolyte composition of thermal sweat induced by short exposition to heat both in renal transplant patients and in healthy subjects.
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PMID:[Effect of thermal dehydration on blood levels of hormones regulating volume and electrolyte content of sweat in patients with kidney transplantation]. 134 26

To clarify the cardiovascular effects of central vasopressin (AVP), a chronic intracerebroventricular (ICV) infusion of AVP was performed in conscious Wistar normotensive rats. Animals were divided into 3 groups: 1) AVP 1 ng/hr (Low), 2) AVP 100 ng/hr (High), and 3) saline (control) ICV infusion. After a 6 day control period, AVP or saline was continuously infused into the lateral cerebroventricle at a rate of 1 microliter/hr using osmotic minipump for 7 days. As a result, a dose-related elevation of AVP concentration in CSF was achieved. Systolic blood pressure in both Low and High AVP infusion was slightly (7-12 mmHg) but significantly higher than that in control. ICV infusion of AVP did not alter urine volume, electrolytes excretion or osmolality, and AVP vascular antagonist injected intravenously failed to affect mean arterial pressure. Furthermore, plasma catecholamines and renin activity did not differ significantly among the groups. Thus, chronic ICV infusion of AVP induced the elevation of blood pressure, which is due to centrally mediated effect of AVP.
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PMID:Chronic cardiovascular effects of central vasopressin in conscious rats. 135 44

The present study aims to answer the following questions: 1. do secretion of volume related hormones in patients with EH pre- and post treatment with propranolol 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 propranolol influence sweat electrolytes in EH patients. In 15 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 propranolol therapy. In all subjects the 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 propranolol 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 propranolol 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 posttreatment between ANP and sweat potassium concentration respectively, and significant negative correlation between PRA and sweat sodium and chloride concentration. From results obtained in this paper it seemed, 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:[Effect of thermal dehydration on blood levels of volume- regulating hormones and sweat electrolytes in patients with essential hypertension treated with propranolol]. 138 27

Activation of the renin-angiotensin system induced by feeding a low NaCl, K-free (LS) diet is associated with polydipsia and a chronic reduction in effective plasma osmolality (efPosm). We have recently shown that converting enzyme inhibition with enalapril (EP) abolishes polydipsia. The present study was designed to test the hypothesis that the osmotic threshold for vasopressin is reset in rats fed the LS diet and to examine the effect of EP on ambient and osmotically stimulated plasma vasopressin levels (PAVP). Animals were fed the LS diet or a control salt diet and treated with vehicle or the lowest dose of EP sufficient to prevent polydipsia (7.5 mg.kg-1.day-1) in rats fed the LS diet. PAVP and efPosm were measured under ambient conditions and after osmotic loading. Urine osmolality (Uosm) was measured under ambient conditions and after water loading. The chronic reduction in efPosm in LS rats was associated with the excretion of a Uosm 1-2 times greater than the corresponding Posm, PAVP similar to controls (LS, 2.27 +/- 1.08 vs. control, 1.19 +/- 0.22 pg/mL) and the ability to excrete a water load. Following osmotic loading, efPosm and PAVP increased significantly and similarly in both LS and control rats. EP administration had no effect on water intake, ambient efPosm and PAVP, and the AVP response to osmotic loading in rats fed the control diet. EP prevented polydipsia in LS rats, however it had no significant effect on ambient or osmotically stimulated PAVP or efPosm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reset of the osmotic threshold for vasopressin in rats fed a low NaCl, K-free diet. 142 6

A 32-year-old man was diagnosed as having pseudo-Bartter syndrome due to surreptitious habitual vomiting and to maldigestion related to decayed teeth. His chief complaints were muscle pain and weakness. In this case, metabolic alkalosis, hypokalemia, hypochloremia, increased plasma renin activity and aldosterone levels were noticed with marked decreases in urinary chloride excretion. Creatinine clearance (GFR) and renal plasma flow (RPF) were also decreased. Blood pressure was normal, but the pressor response to angiotensin II was attenuated. Before treatment with 0.9% saline infusion, plasma vasopressin (AVP) was not suppressed sufficiently by lowering the plasma osmolality (Posm) with an oral water load (WL), but it normally responded to a rise in Posm due to hypertonic saline infusion. Moreover, plasma AVP was normally suppressed by WL after the replenishment of saline. Plasma atrial natriuretic peptide (ANP) was low before WL, but increased normally in response to WL. However, inconsistent with the normal response in this case, decreases in plasma AVP failed to dilute urinary osmolality and to increase urine flow, irrespective of the levels of plasma ANP. These results indicate that chronic inanition due to surreptitious vomiting causes impaired renal diluting ability through decreases in GFR and RPF, irrespective of the levels of plasma AVP and ANP.
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PMID:Impaired water diuresis in a patient with pseudo-Bartter syndrome. 153 41

Inhibitors of nitric oxide (NO) synthesis increase blood pressure and decrease regional blood flow. We investigated whether blockade of the renin-angiotensin, sympathetic nervous, prostaglandin or vasopressin systems attenuates the effects of the NO synthesis inhibitor NG-nitro-L-arginine (L-NOARG) on mean arterial pressure and renal blood flow in anesthetized male Sprague-Dawley rats. Treatment with L-NOARG (10 mg kg-1, i.v. bolus plus infusion at 20 mg kg-1 hr-1) increased mean arterial pressure from 113 +/- 2 to 133 +/- 4 mm Hg, decreased renal blood flow from 7.7 +/- 0.6 to 4.3 +/- 0.6 ml min-1 g-1 and increased renal vascular resistance from 15.8 +/- 1.8 to 36.9 +/- 6.1 mm Hg/ml min-1 g-1. These effects were attenuated in rats pretreated with L-arginine to interfere with the inhibitory action of L-NOARG on NO synthesis, but not in rats pretreated with D-arginine. Acetylcholine did not relax aortic rings taken from rats treated with L-NOARG, consistent with inhibition of NO-mediated vasorelaxation. The pressor and renal vasoconstrictor effects of L-NOARG were not impaired in rats separately pretreated with either chlorisondamine, captopril, prazosin, indomethacin or d(CH2)5Tyr(Me)AVP, or in rats pretreated with chlorisondamine, captopril and indomethacin in combination. Collectively, these data argue against significant contribution of the sympathetic nervous system, the renin-angiotensin system, vasopressor prostanoids or vasopressin to the mechanisms of L-NOARG-induced elevation of mean arterial pressure and renal vasoconstriction in anesthetized rats.
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PMID:Pressor and renal vasoconstrictor effects of NG-nitro-L-arginine as affected by blockade of pressor mechanisms mediated by the sympathetic nervous system, angiotensin, prostanoids and vasopressin. 156 Mar 71

This study simultaneously evaluated multiple circulating neurohormones, osmolality, thirst, and fluid balance in eight actively drinking, alcoholic males and seven controls before and 12 hr after an ethanol challenge. Basal levels of serum osmolality and thirst were significantly higher in alcoholics compared with controls, yet actively drinking alcoholics at the start of the study had normal vasopressin (AVP) levels, plasma angiotensin II (Ang II), plasma renin activity, plasma aldosterone (Aldo), and plasma catecholamines. In response to ethanol, serum osmolalities rose significantly higher while plasma AVP levels became significantly suppressed in alcoholics. After the ethanol stimulus, plasma Ang II levels of alcoholics were significantly higher than those of controls at 11 AM (12.15 +/- 4.49 vs. 1.83 +/- 0.6 pg/ml, p less than 0.02) and 12 noon (14.93 +/- 6.81 vs. 1.37 +/- 0.17 pg/ml, p less than 0.04). Neither plasma renin activity nor Aldo changed in accordance with the elevated plasma Ang II in alcoholics. Diuresis in the alcoholics, assessed by the sum of urine output following the challenge dose, was significantly less than that of controls. Thirst scores and fluid intakes after the ethanol challenge did not differ between alcoholics and controls. The lack of an Ang II-mediated increase in plasma Aldo or thirst response suggests that ethanol may have a specific blunting effect on Ang II receptors. This study demonstrates that ethanol can be used as a provocative test in chronic alcoholics to uncover aberrant hormonal responses for two systems, namely, Ang II and AVP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuroendocrine, fluid balance, and thirst responses to alcohol in alcoholics. 159 May 44

The present study has aimed to answer the following questions: 1) to what extent does the profile of volume related hormones in patients with chronic renal failure (CRF) differ from that of healthy subjects, and 2) do volume related hormones influence the electrolyte composition of thermal sweat? Twelve hemodialyzed patients with CRF and 20 healthy subjects were examined before and after one hour exposition to humid heat. In all examined subjects the following parameters were assessed before and after thermal dehydration: plasma renin activity (PRA) and plasma aldosterone (Ald), vasopressin (AVP) and atrial natriuretic peptide (ANP) concentrations. In addition sodium, potassium, and chloride were estimated in thermal sweat collected after 15 and 45 minutes respectively of thermal exposition. Patients with CRF showed significantly higher values of PRA, Ald, AVP and ANP before thermal dehydration. After one hour of heat exposition a significant increase in PRA, Ald and AVP but a significant decrease of plasma ANP level were noticed in both healthy subjects and patients with CRF. The magnitude of plasma Ald and ANP alterations induced by thermal dehydration was significantly more marked in patients than in healthy subjects. A similar electrolyte composition of thermal sweat was found in both examined groups. No significant correlation was found between the plasma profile of volume related hormones and electrolyte composition of sweat both in patients and normals. Results presented in this paper suggest, that volume related hormones do not influence the electrolyte composition of thermal sweat both in healthy subjects and patients with CRF.
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PMID:[Influence of thermal dehydration on blood values of hormones which regulate volume and composition of electrolytes in sweat of patients with ic renal failure treated with hemodialysis]. 181 85


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