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)

Young (3-month-old) male Wistar rats showed a relative decrease in heart rate to a sudden silence superimposed on low intensity background noise. This bradycardia was accompanied by immobility behavior. In 26-month-old rats the magnitude of the heart rate response was reduced while immobility behavior remained in the same order of magnitude as in young controls. In the aged rats a shift in autonomic regulation of heart rate in the direction of increased sympathetic influence was indicated by the results obtained by blocking the autonomic input with atropine methyl-nitrate (0.5 mg/kg) or atenolol (1 mg/kg) given subcutaneously (SC) 30 min prior to testing. Pretest (30 min) administration of amphetamine (0.5 mg/kg SC) reinstated the bradycardiac response in aged rats to a level seen in young ones. Arginine-vasopressin (AVP, 10 micrograms/kg SC), administered 60 min before the experiment, markedly facilitated the cardiac response in young animals but failed to restore cardiac responses in aged ones. The immobility behavior in the peptide-treated aged rats was also absent. The present findings suggest that a diminished central aminergic drive in aged rats is causing a reduction of the parasympathetic cardiac response to stress of sudden silence. The results also indicate an age-related vasopressinergic modulation of behavioral and cardiac responses to mild stress.
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PMID:Behavioral and cardiac responses to mild stress in young and aged rats: effects of amphetamine and vasopressin. 155 32

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

AVP maintains ethanol (EtOH) tolerance after cessation of chronic EtOH treatment. However, the acute interaction of AVP and EtOH has not been well characterized. Rats were trained on a moving belt and the EtOH dose-response relationship (range 1.0-2.0 g/kg) was determined after pretreatment with saline, AVP (2.5-40 micrograms SC or 10 ng ICV), the AVP-V1 receptor antagonist [Des-Gly9,d(CH2)5(1),O-Et-Tyr2, Val4,Arg8]-vasopressin (10 ng ICV), or AVP in combination with the V1 antagonist. AVP produced a 16% decrease in the EtOH ED50 when given either SC or ICV; this decrease, which appears to represent true potentiation rather than additivity, was prevented by the preadministration of the V1 antagonist. Other rats were made EtOH-tolerant by 7 daily injections of either EtOH alone (1.8 g/kg IP) or EtOH (1.5 g/kg IP) + AVP (10 micrograms SC), followed by a practice session on the moving belt. In both sets of tolerant animals, AVP potentiation of acute EtOH effects was still seen on day 6. The mechanism of AVP potentiation of EtOH-induced impairment is unknown, but the failure of the V1 antagonist alone to alter the effect of EtOH suggests that endogenous AVP is not involved directly in modulating EtOH intoxication.
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PMID:Arginine-8-vasopressin potentiates acute ethanol intoxication. 157 31

Experiments were designed to characterize the mechanism of vasopressin action in small arteries of brain stem and cerebrum and to determine the role of L-arginine pathway in reactivity of these vessels to vasopressin. Secondary branches of canine basilar arteries (425 +/- 63 microns ID, n = 6) and middle cerebral arteries (466 +/- 30 microns ID, n = 6) were dissected and mounted on glass microcannulas in organ chambers. Changes in intraluminal diameter of the pressurized arteries were measured using a video dimension analyzer. Vasopressin caused endothelium-dependent relaxation in the brain stem arteries [-log half-maximal effective concentration (EC50) = 9.2 +/- 0.4, n = 5] but not in the branches of middle cerebral arteries. In contrast, bradykinin caused identical endothelium-dependent relaxations in arteries of both regions (-log EC50 = 8.0 +/- 0.2, n = 5, and 7.7 +/- 0.1, n = 4 for brain stem and cerebrum, respectively). Relaxations to vasopressin (but not to bradykinin) were reduced in the presence of V1-vasopressinergic antagonist [1-(beta-mercapto-beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin [d(CH2)5-Tyr(Me)AVP;10(-7) M], pertussin toxin (100 ng/ml), and NG-monomethyl-L-arginine (L-NMMA; 10(-4) M). The inhibitory effect of L-NMMA was prevented by L-arginine (3 x 10(-4) M) but not D-arginine (3 x 10(-4) M). These studies suggest that vasopressin causes endothelium-dependent relaxation in canine brain stem arteries. The effect of the neuropeptide appears to be mediated by activation of endothelial V1-vasopressinergic receptors coupled to nitric oxide synthase. This signal transduction pathway is not functional in endothelial cells of branches of middle cerebral arteries.
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PMID:Endothelial L-arginine pathway and regional cerebral arterial reactivity to vasopressin. 159 Apr 60

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 [3H]arginine-vasopressin ([3H]AVP) binding site in rat, rhesus and human liver and nonpregnant human uterus was characterized and contrasted. [3H]AVP bound with high affinity (Ki values, 0.2-0.6 nM) to preparations of all tissues studied. Competition binding studies using a series of compounds from three structural classes indicate a marked species difference between the rat and primate liver AVP-V1 site. This site in rhesus and human liver however, is essentially identical, indicating that the rhesus liver is an appropriate surrogate for human tissue. These studies also indicate that the AVP-V1 site of nonpregnant human uterus and human liver is equivalent.
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PMID:Radioligand binding studies reveal marked species differences in the vasopressin V1 receptor of rat, rhesus and human tissues. 159 23

The hemodynamic responses and the role of renal nerves in the physiopathogenesis of acute (45 min) aortic coarctation hypertension were studied in conscious rats. The hemodynamic responses elicited by aortic constriction in intact and bilaterally nephrectomized rats were analyzed by means of miniaturized pulsed-Doppler flow probes. Anephric rats presented a smaller increase in mean carotid pressure (MCP) and calculated aortic resistance during aortic coarctation than did intact animals. Reflex bradycardia throughout the experiment did not differ significantly between the two groups. The pressor response following aortic coarctation in untreated renal-denervated rats was similar to that found in intact subjects. Renal-denervated rats previously treated with V1-vascular arginine vasopressin antagonist [d(CH2)5Tyr(Me)AVP] showed the same hypertensive response as control renal-denervated rats. Previous treatment of renal-denervated rats with saralasin (an angiotensin II antagonist) produced a significant reduction in the hypertensive response throughout the experiment when compared to untreated renal-denervated rats. Similarly, rats treated with the vasopressin antagonist plus saralasin showed a blunted hypertensive response following aortic coarctation. The results for rats previously treated with vasopressin antagonist plus saralasin did not differ from those obtained with saralasin alone. Overall, the results of aortic coarctation hypertension obtained in the present study indicate that: 1) Anephric rats showed a blunted hypertensive response due to the lack of neuro-humoral release of vasopressor substances (e.g. angiotensin II and vasopressin) triggered by the kidneys, when only the mechanical factor of constriction was present; 2) The lack of afferent feedback from the kidneys in renal-denervated rats for vasopressin release from the central nervous system allowed angiotensin II to play the major physiopathological role associated with the mechanical factor in the hypertensive response.
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PMID:Mechanical and neuro-humoral factors in acute aortic coarctation hypertension. 160 37

In the present study we compared the effects of Des Leu Angiotensin I (Des Leu AI) with Angiotensin II (AII) on the secretion of vasopressin (AVP) from the isolated hypothalamoneurohypophyseal system (HNS) and isolated posterior pituitary gland of the rat. Administration of 10(-6)M, 10(-5) M and 10(-4) M Des Leu AI was without significant effect on AVP secretion from the HNS. A similar phenomenon was seen in the posterior pituitary with 10(-6) M and 10(-5) M Des Leu AI, although 10(-4) M significantly increased AVP release. Administration of 10(-6) M AII was without significant effect in either preparation, although 10(-5) M and 10(-4) M AII caused significant dose-dependent increases in AVP secretion over control release that were similar in both the HNS and posterior pituitary gland. These results suggest that Des Leu AI is not a physiologically relevant stimulus of AVP secretion when restricted to this area of the rat brain. They are also consistent with the presence of receptors sensitive to AII in the pituitary gland of the rat.
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PMID:Comparative effects of Des Leu Angiotensin I and Angiotensin II on AVP secretion from the hypothalamoneurohypophysis and pituitary of the rat. 161 85

The contribution of the sympathetic nervous system and vasopressin to the maintenance of arterial pressure was investigated in high sodium-fed rats 4 weeks after the induction of one-kidney, figure-8 renal wrap hypertension. Arterial pressure was significantly greater in renal-wrapped rats than in sham-operated animals. The contribution of the sympathetic nervous system was assessed functionally by measuring the arterial pressure response to ganglionic blockade and estimating the apparent rate of release of norepinephrine. The contribution of vasopressin was assessed by administration of the vascular antagonist d(CH2)5Tyr(Me)-AVP. Whole-animal vascular responsiveness and cardiac baroreceptor reflex sensitivity were determined by graded intravenous bolus injections of angiotensin II, vasopressin, and phenylephrine. Hypertensive rats demonstrated an exaggerated reduction in arterial pressure to autonomic blockade before and after blockade of vascular vasopressin receptors. There was a significant 27% increase in the apparent rate of release of norepinephrine into the plasma. Administration of d(CH2)5Tyr(Me)-AVP did not affect arterial pressure when given alone. However, after ganglionic blockade, inhibition of the vasopressin system elicited similar falls in blood pressure in both normotensive and hypertensive rats. Arterial pressure dose-response effects of phenylephrine, angiotensin II, and vasopressin were similar between renal-wrapped and sham-operated animals; however, cardiac baroreceptor reflex sensitivity was suppressed in the hypertensive rats. These studies indicate that the maintenance of arterial pressure in chronic, high sodium renal-wrap hypertension is associated with an augmented sympathetic nervous system function.
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PMID:Sympathetic nervous system in high sodium one-kidney, figure-8 renal hypertension. 161 57

Urea transport across the terminal inner medullary collecting duct (IMCD) is mediated by a urea transporter that is stimulated by vasopressin (AVP) or hyperosmolarity. To determine whether hyperosmolarity stimulates urea transport by an adenylyl cyclase-dependent or -independent mechanism, terminal IMCDs were perfused with 10 microM forskolin followed by an increase in osmolality or with increasing osmolality followed by 10 nM AVP. In both protocols, stimulating adenylyl cyclase caused an additive increase in urea permeability (Purea) to that stimulated by hyperosmolarity. Next, we investigated whether hyperosmolarity stimulates the same urea transporter as AVP by studying the inhibitor profile and IMCD subsegment response of hyperosmolarity-stimulated urea transport and comparing it to properties already demonstrated for AVP-stimulated urea transport. In terminal IMCDs, luminal phloretin (250 microM) reversibly inhibited Purea by 63%. Thiourea (100 mM) inhibited Purea by 73% at two different levels of osmolality, 690 and 290 mosmol/kgH2O. The half-maximal inhibitory concentration (K1/2) for thiourea at 690 mosmol/kgH2O was not significantly different from the K1/2 value at 290 mosmol/kgH2O, suggesting that stimulation by hyperosmolarity is related to an increase in the Vmax for the urea transporter. Finally, we found that hyperosmolarity did not stimulate Purea in the initial IMCD. In summary, the data suggests that hyperosmolarity stimulates urea transport by an adenylyl cyclase-independent mechanism. However, the inhibitor profile and the IMCD subsegment response for hyperosmolarity-stimulated and AVP-stimulated Purea are similar, suggesting that both hyperosmolarity and AVP stimulate the same urea transporter.
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PMID:Characteristics of osmolarity-stimulated urea transport in rat IMCD. 162 10


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