Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sodium and the renin-angiotensin system (RAS) participate in the regulation of cardiovascular function, in part via activation of central nervous system (CNS) mechanisms. Because intraventricular (IVT) administration of either hypertonic sodium chloride (NaCl) or angiotensin II (ANG II) elicits similar effects (i.e., natriuresis, hypertension, increased drinking, and enhanced vasopressin release) a common and final pathway may be involved. With this in mind, we measured the effect of an IVT injection (third or lateral ventricle) of 0.6 M NaCl on postganglionic renal nerve activity (RNA) and blood pressure in morphine-pentobarbital-anesthetized dogs before and after blockade of the brain RAS with either captopril or [Sar1,Ile8]ANG II. Both vagus and carotid sinus nerves were cut to avoid impingement of the baroreceptor reflex on the measured variables. IVT injection of 0.6 M NaCl produced a prominent hypertensive response and tachycardia associated with a 59 +/- 9% increase in RNA. These changes were statistically significant (P less than 0.001), correlated with each other, and were abolished by administration of hexamethonium chloride (10 mg/kg iv). Blockade of central ANG II receptors with [Sar1,Ile8]ANG II was without effect. However, in dogs given IVT SQ 14,225, there was a slight increase in baseline RNA before injection of 0.6 M NaCl; in addition, both the pressor and heart rate responses to the stimulus of hypertonic NaCl were further augmented. These results demonstrate that central administration of hypertonic NaCl in baroreceptor-denervated dogs produces marked activation of sympathetic nerve activity via mechanisms other than activation of the brain RAS.
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PMID:Lack of interaction between a hypertonic NaCl stimulus and the brain renin-angiotensin system. 683 51

This is a report about a 14-year old girl who, following chemotherapy for malignant teratoma, developed a clinical state of SIADH (syndrome of inappropriate secretion of antidiuretic hormone). The causative agent was most likely vincristine (VCR). The important feature in this case was that the urinary kallikrein activity was high when she was affected by SIADH and decreased when her hyponatremia improved. Sodium clearance was significantly correlated with the increase in urinary kallikrein activity. It is considered that the kallikrein-kinin system may in part participate in the excessive natriuresis of SIADH.
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PMID:Increased renal kallikrein excretion in SIADH after vincristine therapy. 692 Feb 97

1. The mechanisms of central angiotensin II blood pressure effects in conscious dogs on normal or sodium-deficient diets were examined. 2. The biosynthesis of brain angiotensin II in cerebrospinal fluid from its local precursor angiotensinogen was induced in vivo by injection of 0.5 unit of hog kidney renin through a chronically implanted cannula into the third brain ventricle in conscious dogs. 3. Intracerebroventricular administration of renin induced an increase of arterial blood pressure and a marked drinking response under both dietary regimens. Sodium restriction had no effect on the magnitude of the central angiotensin pressor response. 4. Plasma concentrations of renin and angiotensin II decreased, and plasma antidiuretic hormone, noradrenaline, adrenaline and corticosterone increased, in both groups of dogs. 5. Simultaneous intraventricular administrations of captopril with renin inhibited the central renin effects. Intracerebroventricular injections of [Sar1, Val5, Ala8] angiotensin II alone increased plasma renin and angiotensin II concentrations. 6. It is concluded that endogenous brain angiotensin II participates in central mechanisms of blood pressure regulation by the stimulation of the release of antidiuretic hormone, adrenocorticotrophic hormone, adrenaline and noradrenaline.
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PMID:Brain angiotensin II stimulates release of pituitary hormones, plasma catecholamines and increases blood pressure in dogs. 700 37

Studies using the urinary bladder of the toad to elucidate the mechanism of transepithelial ion transport are reviewed. Sodium ions are reabsorbed from bladder urine across the granular cells, accounting for all the electrical activity of this epithelium. Sodium ions enter the granular cells passively through selective sodium channels down an electrochemical gradient, mix in the intracellular "active transport pool," and are pumped actively out of the cell across the basolateral plasma membrane. The concentration of sodium within the active transport pool is normally low, 10-14 mM, with Ringer solution bathing both surfaces. The apical plasma membrane is the major resistance barrier; both vasopressin and aldosterone stimulate sodium transport across the tissue by increasing the permeability of this barrier. The apical plasma membrane is impermeable to chloride ions and they are reabsorbed passively, in response to the transepithelial electrical potential established by active sodium transport, through paracellular channels. The bladder reabsorbs 18 sodium ions per molecule of suprabasal oxygen consumed. The relatively high apical membrane resistance buffers the basolateral active transport system from changes in osmotic work in pumping sodium out of the cell over the physiologic range of transepithelial potentials.
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PMID:From toad bladder to kidney. 703 40

Many aspects of the physiological adaptation to chronic vasopressin and hypotonic fluid administration remain unclear. We therefore infused vasopressin [either 1-desamino-8-D-arginine vasopressin (DDAVP) at 0.112 ng/h or arginine vasopressin (AVP) at 2.4 mU/h] and hypotonic fluid (0.22% NaCl at 3.1 ml/h) into conscious unrestrained rats for 4-6 days. To determine if a decrease in the hydrosmotic effect of vasopressin occurred, urinary osmolality, flow rate, and free water reabsorption were measured sequentially in vasopressin-treated and control animals (receiving 0.22% NaCl alone). Progressive increases in urine flow and decreases in urine osmolality and free water reabsorption occurred in vasopressin-treated animals. This decreased hydrosmotic effect was noted with both DDAVP and AVP and could be dissociated from hormonal degradation and urinary prostaglandin E2 excretion. Sodium and water balance were measured to assess the determinants of the hypotonic state following chronic vasopressin and hypotonic fluid. In DDAVP-treated animals, sodium balance remained constant and hyponatremia resulted from water retention alone. In AVP-treated animals, a greater degree of hyponatremia was observed and resulted from combined positive water balance and negative sodium balance. The difference in sodium balance observed when DDAVP- and AVP-treated animals were compared could not be attributed to differences in either magnitude of water retention or filtered load of sodium.
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PMID:Effects of DDAVP and AVP on sodium and water balance in conscious rat. 713 81

To elucidate and to try to reverse the antinatriuretic mechanisms in liver cirrhosis, atrial natriuretic peptide (ANP) was given as a pharmacological bolus dose (2 micrograms per kg body weight) to 14 cirrhotic patients, and as a control to 14 healthy subjects. The nine patients with ascites had baseline values of glomerular filtration rate (GFR), effective renal plasma flow (ERPF) and blood pressure (BP) similar to controls. Their distal tubular fractional reabsorption of sodium (DFRNa), estimated by the lithium clearance technique, was higher than in controls, and so were plasma values of aldosterone (564 vs. 119 pmol l-1 medians), endothelin (1.23 vs. 0.63 pmol l-1), ANP (7.5 vs. 3.6 pmol l-1) and cyclic GMP (8.8 vs. 4.6 nmol l-1); p < 0.01 for all. The five patients without ascites had higher GFR and ERPF, and lower plasma angiotensin II than controls. After ANP injection, similar plasma levels of ANP and cyclic GMP were reached in all groups. Urinary sodium excretion rate increased in controls (0.23 to 0.52 mmol min-1, p < 0.01), while GFR increased (108 to 117 ml min-1, p < 0.05), and DFRNa decreased (93 to 89%, p < 0.01). In cirrhotics with ascites sodium excretion was unaltered (0.12 to 0.11 mmol min-1), and so was GFR (84 to 83 ml min-1). Proximal tubular fractional reabsorption of sodium increased after 90 min, whereas DFRNa decreased immediately (97 to 96%, p < 0.01) though less markedly than in controls. Sodium excretion increased in four of five patients without ascites (0.23 to 0.27 mmol min-1, medians). In patients with ascites, endothelin in plasma decreased after ANP (p < 0.05). Plasma levels of angiotensin II, aldosterone and vasopressin were unchanged in all groups. In conclusion, although hyper-reabsorption of sodium occurred in the distal rather than the proximal part of the nephron in cirrhotic patients with ascites, ANP had no natriuretic effect. This was most probably due primarily to the lack of increase of GFR and blunted inhibition of DFRNa, attributed to high aldosterone. The effect of ANP in suppressing the high endothelin did not seem to improve sodium excretion.
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PMID:Effects of high dose atrial natriuretic peptide on renal haemodynamics, sodium handling and hormones in cirrhotic patients with and without ascites. 756 29

Studies were performed to determine the primary signal transduction mechanism that mediates adenosine stimulation of electrogenic sodium transport in renal epithelial cells. Experiments were performed on cultured amphibian A6 cells with an adenosine analogue that preferentially binds to the A1 receptor, cyclohexyladenosine (CHA). Sodium transport was assessed by the equivalent short circuit current (Ieq). CHA was found to stimulate Ieq via activation of an A1 receptor because (1) the threshold concentration was 1 nM compared to that of 10 microM for the specific A2 agonist CGS21680, (2) CHA inhibited vasopressin (AVP)-stimulated cAMP production by a pertussis toxin-sensitive mechanism, and (3) the action of CHA was inhibited by the A1 antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). CHA increased intracellular Ca2+ ([Ca2+]i) and stimulated phosphoinositide turnover at concentrations that increased Ieq and in a time course that paralleled the increase in Ieq. Ion transport was stimulated by a Ca(2+)-dependent mechanism because the CHA induced increase in Ieq was inhibited by chelating [Ca2+]i with 5,5'dimethyl BAPTA in a dose-dependent manner, with a Ki of approximately 10 microM. The increase in Ieq was also dose-dependently inhibited by the specific PKC inhibitors dihydroxychlorpromazine and chelerythrine, and by trifluoperazine which inhibits PKC and calmodulin. Further studies indicated that CHA-stimulated Ieq was independent of cAMP generation because CHA did not induce an increase in cAMP accumulation parallel to the increase in Ieq in a dose-response analysis, and the adenylate cyclase inhibitor 2',5' dideoxy-adenosine (DDA) did not affect the CHA-induced increase in Ieq.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adenosine stimulation of Na+ transport is mediated by an A1 receptor and a [Ca2+]i-dependent mechanism. 764 26

The pressure-natriuresis curve of transgenic rats harboring an extra mouse renin gene [TGR(mRen-2)27] is shifted rightward compared with controls; however, whether intrarenal angiotensin II effects are responsible for the rightward shift is unknown. To clarify this issue we infused the converting enzyme inhibitor captopril or the angiotensin II receptor blocker CV 11974 into transgenic and normotensive Sprague-Dawley Hannover control rats. We eliminated any other neural or endocrine regulatory differences between transgenic and control rats by renal denervation and infusion of vasopressin, aldosterone, corticosterone, and norepinephrine in sufficient quantities to occupy all receptors. Sodium excretion increased from 3.4 +/- 1.2 to 10.1 +/- 0.5 mumol/min per gram kidney weight in transgenic rats when renal perfusion pressure was increased from 158 to 201 mm Hg. Captopril (4 mg/kg) and CV 11974 (0.1 mg/kg) shifted the pressure-natriuresis curve of transgenic rats leftward, so that sodium excretion was threefold higher at similar renal perfusion pressures (150 to 160 mm Hg). Similarly, fractional sodium and water excretion curves were shifted leftward, so that values for transgenic and control rats were no longer different. Over the pressure range, renal blood flow in transgenic rats ranged from 3.1 +/- 0.7 to 4.4 +/- 0.5 mL/min per gram kidney weight and increased (P < .05) with both captopril and CV 11974 to ranges from 4.8 +/- 0.9 to 6.8 +/- 0.6 or from 4.5 +/- 0.7 to 6.9 +/- 1.0 mL/min per gram kidney weight, respectively. Glomerular filtration rate in transgenic rats, on the other hand, was not increased. Transgenic kidneys showed severe hypertension-induced nephrosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of captopril and angiotensin II receptor blockade on pressure natriuresis in transgenic TGR(mRen-2)27 rats. 764 84

The contribution of sodium losses to the dramatic fall in blood pressure that follows cessation of a 3-h intravenous infusion of vasopressin (20 ng.kg-1.min-1) in hypertensive rats was investigated. Cessation of the vasopressin infusion was associated with a large fall in pressure below preinfusion basal levels (30-50 mmHg) in both spontaneously hypertensive rats (SHR) and deoxycorticosterone acetate (DOCA)-salt-hypertensive rats. In contrast, pressure returned to control levels in normotensive rats. Sodium excretion rates increased markedly during the infusions of vasopressin in both SHR and DOCA-salt-hypertensive rats but also in their appropriate normotensive controls. An equinatriuretic dose of furosemide failed to induce any change in pressure in SHR or normotensive controls. In contrast, furosemide decreased pressure in the DOCA-salt-hypertensive group, although the decrease was not as large as with vasopressin. Replacement of the sodium losses that occurred during the vasopressin infusion failed to return pressure toward control levels in SHR but did increase pressure in the DOCA-salt-hypertensive group. The results indicate a major difference between the SHR and DOCA-salt-hypertensive models. In SHR, sodium losses do not contribute to the antihypertensive effect of vasopressin, but in contrast these losses do contribute significantly to this antihypertensive effect in the DOCA-salt-hypertensive model.
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PMID:Renal function contributes to antihypertensive effect of vasopressin in DOCA-salt but not spontaneous hypertension. 797 14

In order to investigate the effect of chronic sodium depletion on renal proximal tubular reabsorption, studies were performed in conscious, unrestrained Brattleboro rats. Since these animals lack circulating vasopressin, fractional water reabsorption in the distal nephron can be assumed to be constant and changes in urine flow rate should therefore reflect changes in end-proximal fluid delivery. Sodium depletion was induced by placing rats on a low-sodium diet (4 mmol Na (kg dry wt)-1) and administering frusemide (40 mg (kg body wt)-1) by gavage on the first 2 days. Extracellular volume, measured after 7-9 days, was reduced by 19% (P < 0.02) as compared with that of rats maintained on a control diet. Urine flow rate, measured during days 4-7 of the low-sodium diet, was significantly lower than that of control rats (142 +/- 8 vs. 168 +/- 5 ml day-1, P < 0.01). Since renal papillary interstitial fluid osmolality was found to be reduced in the sodium-depleted rats (693 +/- 38 vs. 812 +/- 36 mosmol (kg H2O)-1, P < 0.05), it is unlikely that water reabsorption from sites beyond the proximal tubule had increased. The observed reduction in urine flow rate therefore strongly suggests a reduction in end-proximal fluid delivery. In the second part of the study, a single group of Brattleboro rats was used, in which osmotic minipumps were implanted in the peritoneal cavity for continuous infusion of [14C]inulin. After recovery from the operation, the rats were maintained on a control diet for 6 days (pre-control period), then subjected to sodium depletion (low-sodium diet for 6 days, frusemide administration on the first 2 days), and finally returned to the control diet for 6 days, with access to 0.46 M NaCl solution on the first 2 days, in order to restore sodium balance (post-control period). On the final 2 days of each phase, urine flow rate and [14C]inulin clearance (= glomerular filtration rate, GFR) were measured. Urine flow rates during the pre-control, sodium depletion and post-control periods were 169 +/- 7, 132 +/- 8 (P < 0.001) and 176 +/- 8 microliters min-1, respectively; corresponding values for fractional water excretion were 7.0 +/- 0.3, 6.0 +/- 0.5 (P < 0.01) and 7.4 +/- 0.4%. Only a small reduction GFR, of borderline statistical significance, was observed during sodium depletion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of chronic sodium depletion on renal function in conscious rats. 800


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