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)

It is now becoming apparent that the medullary circulation in the kidney can be regulated separately from overall renal blood flow. This characteristic of the medullary circulation plays an important role in the kidney's ability to excrete a dilute or concentrated urine in concert with changes in water and sodium transport in the distal nephron secondary to the action of vasopressin, prostaglandins, the renal nerves, and other hormones without significant other renal hemodynamic changes. There is strong evidence that renal autocoids such as angiotensin II and prostaglandins uniquely affect regional blood flow in the inner medulla because of the special structure and organization of the microvasculature in this region. There is also evidence that this regional blood flow is in part regulated by circulating hormones, such as vasopressin and atrial natriuretic peptide, which are released in response to changes in extracellular fluid volume or osmolality. In addition, data are emerging to suggest that the kallikrein-kinin system, acetylcholine, the renal nerves and adenosine participate in this regulation. In addition to the role of the medullary circulation in the urinary concentrating operation, there are data to suggest that the medullary circulation either directly (by changes in physical forces) or indirectly (by regulating medullary toxicity) may influence sodium excretion in a variety of conditions. In this regard, activation of the renin-angiotensin system locally reduces blood flow in the papilla which may be necessary before sodium retention is fully expressed in salt retaining states. Future research looking at the microvasculature of the medulla and papilla and those factors that control the contractility of these vessels are necessary before a clearer picture emerges. Nevertheless, from the data already available it seems reasonable to suggest that the medullary circulation may be as important to kidney function during physiological and pathophysiological states as is the cortical circulation.
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PMID:Renal medullary circulation: hormonal control. 213 85

The peptide hormone, arginine-vasopressin[( Arg8]vasopressin, AVP), stimulates efflux of the bile salts taurocholate and glycocholate from the rat hepatocyte in suspension via its association with the V1 receptor on the hepatic cell membrane. At a concentration ratio of 5:1 (antagonist to hormone), the V1 vasopressin antagonist, (dCH2)5Tyr(Me)AVP, inhibits the vasopressin induced efflux of taurocholate by approximately 82%, and of glycocholate, by approximately 85%. In contrast, the V2 antagonist (d(CH2)5[D-Ile2,Ala4]AVP, does not interfere with the stimulation of taurocholate and glycocholate efflux by vasopressin. In the isolated perfused rat liver, vasopressin (5 X 10(-10) M) causes an immediate increase of 55 +/- 12% over baseline in [14C]taurocholate secretion and a corresponding increase in bile flow. A more gradual and prolonged increase in [14C]taurocholate secretion, reflecting an increased biliary concentration of [14C]taurocholate, is observed beginning 6 min after vasopressin, reaching a plateau of 23 +/- 12% over baseline by 14 min and returning to baseline by 30 min. The mean rate of 14C secretion during the 30 min following administration of vasopressin (non-steady state) is increased by 14.3 +/- 6.4% over pre-infusion steady-state baseline (P less than 0.05). Prior administration of the V1 receptor antagonist d(CH2)5Tyr(Me)AVP attenuates these effects of vasopressin. The combination of these in vitro and in vivo findings suggest that vasopressin may play a role in regulating bile salt efflux. Furthermore, these studies in the isolated hepatocyte and the intact liver may provide a unique approach for defining biochemical changes associated with bile salt transport from the hepatic cell.
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PMID:Receptor-mediated stimulation of taurocholate efflux from the rat hepatocyte and the ex vivo perfused rat liver. 213 86

It is clear from the extant literature that various fish groups face chronic osmoregulatory problems that depend on the surrounding salinity. Their physiologic and hormonal responses are largely those seen in the mammals, but their terrestrial descendants have lost osmoregulatory structures such as gills and rectal glands and depend primarily on renal function. A data base is now emerging that strongly suggests that a putative atriopeptin plays a role in osmoregulation in fishes. This conclusion is supported by the fact that heterologous AP produces relevant physiologic responses (e.g. natriuresis, vasodilation, stimulation, or inhibition of Na+ secretion by intestine, gills, and rectal gland) in both teleosts and elasmobranchs. Moreover, cardiac and brain extracts from fish can produce similar effects in both fishes and mammals, and these tissues from various fish groups contain immunoreactive AP, as does plasma. Both physiologic and immunologic evidence suggests that the ventricle may be a significant source of AP in fishes, contrary to the situation in mammals. Finally, osmotic perturbations result in a change in plasma and tissue APir levels. The finding that plasma APir levels increase in sea water, and that heterologous AP stimulates salt secretion by the teleost gill and shark rectal gland, and inhibits salt uptake by the teleost intestine, suggests that AP may primarily play a role in salt, rather than fluid, secretion in fishes. The fact that in mammals AP inhibits prolactin secretion, but is itself stimulated by cortisol, supports this conclusion, since prolactin is generally considered to be the dominant osmoregulatory hormone in freshwater fishes, and cortisol serves this function in marine fishes. In addition, if AP inhibits brain AVT release in fishes, as it apparently inhibits vasopressin release in mammals, this also would be adaptive in marine fishes since AVT in fishes is diuretic, rather than antidiuretic. Interactions between AP and these hormones (prolactin, cortisol, and ATV) have not been studied in fishes to date, but these theoretical interactions do lend support to the hypothesis that AP may function primarily in salt homeostasis in fishes. At least one potential hormonal interaction counters this argument, however. Atriopeptin is known to inhibit the production and effects of angiotensin II in mammals, and since this hormone is apparently dipsogenic in fishes, it may play a critical role in osmoregulation in sea water. Finally, it is of some historical interest that in Keys' (67) original description of the eel heart-gill perfusion system in 1931 he commented that gill resistance remained constant for hours only if the heart itself was perfused.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:An emerging role for a cardiac peptide hormone in fish osmoregulation. 213 57

ANP stimulates a profound natriuresis and diuresis by a series of concerted actions along the nephron, including stimulation of glomerular filtration and inhibition of net salt and water reabsorption in the cortical and inner medullary collecting ducts. Several actions of ANP contribute to its natriuretic and diuretic effects in the collecting duct. These include reductions in aldosterone secretion, increases in hydrostatic pressures opposing Na+ reabsorption, possible stimulation of medullary washout, and direct inhibition of salt and water transport. In both CCD and IMCD, ANP antagonizes the hydroosmotic actions of vasopressin, which leads to diuresis. The mechanisms by which ANP inhibits response to vasopressin remain unclear, although in IMCD, cGMP can duplicate the response to ANP. In CCD, ANP can inhibit Na+ reabsorption via cGMP; the transport pathway regulated by ANP is unknown. In IMCD, ANP acting via cGMP inhibits a conductive Na+ or cation channel, which appears to be on the luminal membrane.
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PMID:Renal actions of atrial natriuretic peptide: regulation of collecting duct sodium and water transport. 213 59

Three experiments tested whether the subfornical organ (SFO) could be a site of action for the antidipsogenic effects of atrial natriuretic peptide (ANP) in rats. Pretreatment with 100, 230, or 500 pmol ANP in the SFO reduced drinking induced by 10 pmol angiotensin II in the SFO. Drinking in response to water deprivation was reduced by ANP in rats having cannulas in or near the SFO, but not in rats having cannulas distant from the SFO or in the ventricles. Finally, ANP had no effect on eating or drinking after food deprivation, suggesting that the rats in the other experiments were not acutely incapacitated. The SFO may mediate the central effects of ANP on drinking induced by angiotensin or in response to water deprivation and could play a similar role in the central effects of ANP on salt appetite, diuresis, vasopressin secretion, and blood pressure.
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PMID:Atrial natriuretic peptide in the subfornical organ reduces drinking induced by angiotensin or in response to water deprivation. 214 Jun 87

Atrial natriuretic factor (ANF) is widely distributed in the preoptic area and the hypothalamus, it is present there both in cell bodies and nerve terminals. Effect of experimental alterations in the salt and water balance was examined on preoptic-hypothalamic ANF levels measured in ten microdissected nuclei. Immunohistochemical analysis was also performed to confirm radioimmunological results. Following interventions were performed in adult male rats: adrenalectomy (5 days), daily 0.9% NaCl, aldosterone (5 micrograms/100 g) and dexamethasone (2 micrograms/ml drinking water) treatments in both intact and adrenalectomized groups, and in rats with diabetes insipidus (Brattleboro rats) and DOC-salt hypertension. Although no appreciable alterations were observed in the intensity of ANF-like immunoreactivity in sections of the preoptic-hypothalamic region, ANF levels altered markedly in the periventricular structures (organum vasculosum laminae terminalis, preoptic and periventricular nuclei). Little or no changes were measured in ANF levels of other hypothalamic nuclei (except the perifornical nucleus). Adrenalectomy depleted ANF levels which were restored by NaCl drinking. Aldosterone elevated ANF concentrations both in intact and adrenalectomized animals while dexamethasone treatment was without any significant effect on ANF levels in the periventricular preoptic nucleus. Diabetes insipidus or DOC-salt hypertension had little or no effect on ANF levels in this brain area. Unchanged ANF concentrations were also measured in the vasopressin-containing supraoptic nucleus following adrenalectomy or in diabetes insipidus rats.
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PMID:Atrial natriuretic factor in central nervous system regulatory mechanisms: effect of experimental alterations in water and salt homeostasis and blood pressure. 214 14

Saline solutions (NaCl, 2 ml, pH 7.4, 10-598 mosmol/kgH2O) were infused over 4 min in conscious rats, via tail artery catheter or intragastric tube. Intragastric infusions of hyper- and hypotonic solutions caused, within 14.4 +/- 2.2 min, a maximal increase and decrease, respectively, of plasma vasopressin (AVP) relative to time controls (r = 0.97; P less than 0.00001) without affecting systemic plasma osmolality (r = -0.09; P less than 0.92). Mean changes of plasma AVP between 11 and 21 min were also correlated with the osmolality of gastric infusion (r = 0.72; P less than 0.000001), whereas systemic osmolality was unchanged (r = 0.14; P less than 0.42). Systemic infusions caused within 9.0 +/- 2.0 min a maximal change in both plasma AVP (r = 0.82; P less than 0.00001) and systemic osmolality (r = 0.97; P less than 0.00001). However, mean changes of plasma AVP between 11 and 21 min weakly correlated with the osmolality of systemic infusions (r = 0.27; P less than 0.20), although correlations between mean changes of systemic osmolality and the osmolality of systemic infusions were significant (r = 0.72; P less than 0.00001). Lack of correlations with mean arterial pressure and heart rate suggest that hemodynamic changes did not mediate the AVP responses. Pretreatment with atropine methyl bromate (2 mg/kg) abolished the AVP response to gastric but not systemic infusions of hypertonic saline. These results indicate that a splanchnic cholinergic receptor mechanism modulates AVP secretion during a moderate gastric intake of salt or water.
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PMID:Splanchnic control of vasopressin secretion in conscious rats. 214 82

The relation between blood pressure level and extracellular fluid volume and its distribution was studied in rats subjected to the following hypertensive stimuli--1K1C and 2K1C renal artery constriction, subtotal nephrectomy-salt and DOCA-salt. In all experimental groups the blood pressure increase was accompanied by increased extracellular fluid volume which was not always distributed proportionally between intravascular (PV) and interstitial (IFV) compartments. The blood pressure rise was further potentiated by plasma volume expansion so that the increased PV/IFV ratio was associated with a more pronounced hypertensive response (1K1C vs 2K1C, DOCA-salt vs subtotal nephrectomy-salt). However, adequate expansion of interstitial fluid is a necessary prerequisite for the hypertensive response. In DOCA-salt treated DI Brattleboro rats (lacking antidiuretic vasopressin action) plasma volume expansion per se was not accompanied by severe DOCA-salt hypertension. It is concluded that the expansion of both compartments of extracellular space, i.e. plasma volume and interstitial fluid volume, was necessary for a full development of severe hypertension. The expansion of only one of these compartments was accompanied by a mild blood pressure increase or blood pressure did not change significantly.
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PMID:Body fluids and their distribution in experimental hypertension. 214 92

Atrial natriuretic peptide, ANP(99-126), is derived from cardiac atrial tissue and has potent effects on salt and water homeostasis, including the inhibition of aldosterone and vasopressin release. Recent studies have also suggested that it may suppress the pituitary-adrenal axis. In addition, N-truncated forms of ANP, such as ANP(103-126), have been identified within the central nervous system, with a prominent hypothalamic localization in the paraventricular nucleus. We have therefore investigated whether ANP(99-126) and ANP(103-126) are able to modulate the release of the principal ACTH-releasing factor, corticotrophin-releasing factor-41 (CRF-41), from the rat hypothalamus in vitro. The static incubation system has been previously described in detail. Male Wistar rats were decapitated between 09.00 and 09.30 h, their hypothalami rapidly removed, and four half-hypothalami incubated for 20-min intervals following a period of stabilization. The effect of the ANP peptides on the basal (B) and KCl (28 mmol/l)-stimulated (S) release of immunoreactive CRF-41 was studied by means of successive incubations in the absence (B1, S1) and presence (B2, S2) of the peptides. The ratios B2:B1 and S2:S1 were compared with parallel control incubations by ANOVA. Neither form of ANP had any effect on the basal release of CRF-41. ANP(99-126) caused a dose-dependent inhibition of CRF-41 release in the concentration range 1-100 nmol (P less than 0.01). ANP(103-126) also suppressed the release of CRF-41 in the concentration range 100 pmol/l-100 nmol/l (P less than 0.01), with a minimum S2:S1 ratio at 10 nmol/l, and a decrease in effect at 100 nmol/l. Finally, the stimulation of CRF-41 release induced by noradrenaline (10 nmol/l and 1 mumol/l) was non-competitively antagonized by 100 nmol ANP(99-126)/l and 10 nmol ANP(103-126)/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptides inhibit the release of corticotrophin-releasing factor-41 from the rat hypothalamus in vitro. 214 72

The failing heart is unable to provide some organs, notably the brain and the myocardium, with the amount of blood flow they require. To this myocardial inadequacy and resulting "circulatory insufficient" the body reacts by setting in action compensatory mechanisms which are "intracardiac" first (Starling's heterometric regulation, ventricular hypertrophy), then neurohormonal, with the activation of vasoconstrictor systems (noradrenergic system, renin-angiotensin-aldosterone system, arginine-vasopressin system) counterbalanced by the activation of vasodilator systems (vasodilator prostaglandins, atrial natriuretic factor and kinins). However, the vasoconstrictor systems outweigh the vasodilator systems. They create an excessive arterial and venous vasoconstriction, together with water-and-salt retention, which leads to an increase of left ventricular work during both systole and diastole and to a gradual worsening of the heart failure. The present-day treatment of heart failure aims at reducing the water-and-salt retention and at restoring the balance between the vasoconstrictor and vasodilator systems.
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PMID:[General physiopathology of chronic left ventricular insufficiency]. 214 35


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