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)

1. The renal vascular responses to the peptide hormones angiotensin II (ANG II), arginine-vasopressin (AVP) and bradykinin (BK) were studied in anaesthetized rats with flow-meter techniques. The contribution of prostaglandins (PG) to their renal vascular effects was assessed with the aid of the PG-synthesis inhibitor indomethacin. 2. ANG II and AVP induced a dose-dependent increase in renal vascular resistance (RVR). The renal vasoconstrictor effects of both peptides were significantly augmented in rats pretreated with indomethacin. Indomethacin alone induced an increase in RVR, but not in mesenteric vascular resistance (MVR). 3. BK in low doses (1 micrograms/kg . min) tended to decrease RVR but increased RVR in high doses (20 micrograms/kg . min). MVR was reduced after all doses. The renal vasoconstrictor effect of BK was not affected by the ANG II-antagonist saralasin but almost completely blocked by indomethacin. 4. These results suggest that in the rat, as in other animal species and in man, renal PG's attenuate the renal effects of vasoconstrictor hormones such as ANG II and AVP. Although it has no such effect in other species. BK in high doses induces renal vasoconstriction in the rat, which appears also to be mediated by PG's. This response might be peculiar to the rat, since PG's act as renal vasodilators in other species.
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PMID:Renal vascular effects of angiotensin II, arginine-vasopressin and bradykinin in rats: interactions with prostaglandins. 682 26

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

1. By immunoperoxidase technique, immunoreactive angiotensin II (ANG II) was located in the cell bodies of many magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus and their pathways to median eminence and posterior pituitary gland in the rat. 2. Like vasopressin and its neurophysin, but not oxytocin, ANG II was also found in parvocellular neurons in the suprachiasmatic nucleus. 3. Analysis of these peptides in the same magnocellular neurons reveals that ANG II is localized primarily in vasopressin cells. 4. Like vasopressin and its precursor, ANG II is deficient in homozygous Brattleboro rats with diabetes insipidus. 5. In adrenalectomized rats increases in vasopressin and its neurophysin in median eminence are associated with increases in ANG II. 6. The data suggest that the ANG II demonstrated shares antigenic determinants with the vasopressin precursor, or is regulated in a similar way to vasopressin in the same neurons.
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PMID:Immunocytochemical localization of angiotensin II and vasopressin in rat hypothalamus: evidence for production in the same neuron. 700 38

In chronically cannulated conscious chickens, Gallus gallus, native chicken angiotensin II ([Asp1,Val5]ANG II) caused biphasic blood pressure responses, a depressor followed by a pressor response. The pressor response appears to be mediated primarily by catecholamines. The depressor responses increased with increasing doses and were accompanied by tachycardia. The onset of the depressor action of [Asp1,Val5]ANG II (2.49 +/- 0.22 s) was nearly as quick as that of acetylcholine or histamine. Replacement of aspartic acid in position 1 with sarcosine or asparagine reduced both depressor and pressor potencies, whereas there was no difference either in depressor or pressor potencies between [Asp1,Val5] and [Asp1,Ile5]ANG II. The depressor response to [Asp1,Val5]ANG II was not inhibited by atropine, a vasopressin antagonist, prostaglandin synthetase inhibitors, methysergide, or propranolol but was blocked markedly by [Sar1, Ile8]ANG II and partially by [Sar1,Thr8]ANG II. The results suggest that the vasodepressor action of ANG II is mediated by angiotensin receptors and may possibly be a direct action on the vascular smooth muscle.
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PMID:Vasodepressor action of angiotensin in conscious chickens. 711 76

Intracerebroventricularly (i.c.v.) administered angiotensin II (ANG II) at a dose of 100 ng caused a large increase in plasma oxytocin levels in Long Evans (LE) rats and in rats heterozygous for hypothalamic diabetes insipidus (HZ). In rats homozygous for diabetes insipidus (DI) even 100 fold higher doses of ANG II i.c.v. exerted only marginal effects on oxytocin release. The impaired responsiveness in DI rats was fully restored by prolonged treatment with a vasopressin (AVP) analogue. These data show that the decreased sensitivity of ANG II receptors in DI rats is due to the AVP defect and its metabolic consequences and can be reversed by AVP substitution.
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PMID:Angiotensin stimulates oxytocin release: imparied response in rats with genetic hypothalamic diabetes insipidus. 712 94

The cardiovascular effects of opioid peptides have been studied. Leucine-enkephalin (Leu-ENK) produced blood pressure (BP) increases following administration into the lateral brain ventricles (i.v.t.), into the cisterna magna (i.c.i.), and following intravenous (i.v.) administration. Heart rate (HR) increases were observed following all routes of administration (threshold for BP and HR effects at 0.3 nmole, maximum at 360 nmoles). The cardiovascular effects were independent of generalized seizures, which may occur at higher doses of enkephalins (ENK). D-alanine-enkephalin (D-Ala-ENK) attenuated the vagal component of the baroreceptor reflex in cats. This was indicated by the findings that HR did not decrease following D-Ala-ENK-induced BP increases and that the compensatory decreases in HR following i.v. pressor doses of angiotensin II (ANG II) were markedly attenuated in cats treated with i.v.t. D-Ala-ENK. Naloxone inhibited the BP and HR effects following i.c.i. and i.v., but not following i.v.t., administration of Leu-ENK. The i.v.t. Leu-ENK effect were inhibited by beta-adrenergic receptor blockade. Bratteboro rats homozygous for hereditary diabetes insipidus with total absence of antidiuretic hormone (ADH) synthesis responded with BP decreases following i.v.t. Leu-ENK, while BP increases were observed in control Long-Evans rats. Blood pressure increases to i.v.t. Leu-ENK were markedly greater in spontaneously hypertensive rats of the stroke-prone strain (SHR-sp) than in normotensive control rats; SHR-sp exhibit a humoral pattern of increased ADH, ACTH, and catecholamines, presumably due to central peptidergic stimulation. The known effects of opioid peptides on these hormones and the observed cardiovascular responses suggest a possible participation of this peptide system in the maintenance of high BP in the SHR-sp.
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PMID:Enkephalin effects on blood pressure, heart rate, and baroreceptor reflex. 739 23

Experiments were carried out in male Sprague-Dawley rats. 3'-end digoxigenin-labeled 26 bp oligonucliotide probe was used to detect the vasopressin (AVP) mRNA in the hypothalamus. Dot blotting technique was used in the investigation of AVP gene transcription level. The results showed that continuous intracerebroventricular administration (i.c.v.) of angiotensin II at a rate of 0.2 nmol/h for 2 days by using a miniosmotic pump resulted in a significant increase in daily water intake. An increase of AVP gene transcription level in the hypothalamus was also observed, but statistically insignificant. When daily water intake was limited (25 ml/d), continuous i.c.v. infusion of ANG II caused a significant increase in hypothalamic AVP gene transcription. It was also observed that hypothalamic AVP gene transcription level increased after salt loading and dehydration. However, intraperitoneal application of angiotensin converting enzyme inhibitor captopril (5 mg/(kg.d)) or i.c.v. nonpeptide angiotensin II receptor antagonist Dup753 (0.9 nmol/h) did not attenuate the increase of AVP gene transcription level induced by salt loading or dehydration. It is therefore suggested that the administration of ANG II enhances AVP gene transcription in the hypothalamus, especially when water intake is limited. However, this increase does not involve the participation of endogenous ANG II.
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PMID:[Effect of angiotensin II on vasopressin gene transcription in the hypothalamus of rats]. 748 79

We examined the response to hemorrhage in conscious normotensive and hypertensive rabbits under control conditions and during efferent blockade of 1) the hormones vasopressin (AVP) and angiotensin II (ANG II), 2) the autonomic nervous system, and 3) autonomic and hormonal inputs. We recorded mean arterial pressure, heart rate, and hindlimb conductance. The response to hemorrhage was unchanged with hormonal blockade alone. Blockade of the autonomic nervous system caused a faster rate of blood pressure decline, but the rate of decrease in hindlimb conductance was maintained at control levels. Blocking the autonomic nervous system and the hormones resulted in rapid blood pressure decline and an increase in hindlimb conductance. Although the three types of efferent blockade had a similar pattern of effects in normotensive and hypertensive rabbits, hypertensive rabbits exhibited less cardiovascular support during hemorrhage than normotensive rabbits. During hemorrhage, hypertensive rabbits had an attenuation of hindlimb vasoconstriction, a reduction in the heart rate-mean arterial pressure relationship, and reduced ability to maintain blood pressure compared with normotensive rabbits.
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PMID:Control of blood pressure and hindlimb conductance during hemorrhage in conscious renal hypertensive rabbits. 761 81

The role of brain angiotensin II (ANG II) in mediating cardiovascular, vasopressin, and renin responses to hemorrhage was assessed in conscious spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto (WKY) and Wistar rats. Intracerebroventricular administration of losartan (10 micrograms) and saralasin (1 microgram.microliter-1.min-1) produced a markedly greater fall in blood pressure and a reduced tachycardia during and after hemorrhage (15 ml/kg) compared with the artificial cerebrospinal fluid control in SHR and Wistar rats but not in WKY rats. Vasopressin release after hemorrhage was also impaired, but renin release was enhanced by intracerebroventricular ANG II antagonists in SHR and Wistar rats but not in WKY rats. Losartan and saralasin produced remarkably similar effects on the cardiovascular, vasopressin, and renin responses to hemorrhage. These data suggest that brain ANG II acting through AT1 receptors plays an important physiological role in mediating rapid cardiovascular regulation and vasopressin release in response to hemorrhage. The relative importance of brain angiotensin system may vary in different strains of rate.
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PMID:Central ANG II-receptor antagonists impair cardiovascular and vasopressin response to hemorrhage in rats. 761 27

We have previously shown that restriction of water intake decreased stool frequency and stool weight in volunteers. The aim of this study was to investigate whether these effects of thirst could be mediated by an action of systematically released hormones on colonic smooth muscle. Using isolated colonic smooth muscle strips the effect of arginine-vasopressin (AVP), angiotensin II (ANG II) and aldosterone on rat colonic motility in vitro was investigated. AVP (10(-12)-10(-10) mol/l) and aldosterone (3 x 10(-10)-3 x 10(-8) mol/l) and physiological hormonal concentrations of ANG II (10(-13)-10(-10) mol/l) had no effect on either basal activity, direct stimulation of colonic smooth muscle or neurally stimulated contractions using carbachol 10(-7)-3 x 10(-5) mol/l or neurally stimulated contractions using electrical field stimulation at various stimulation frequencies (1-10 pps, 1 ms, 40 V). ANG II in higher concentrations (10(-7)-10(-6) mol/l) increased basal activity and neurally mediated contractions. Accordingly, ANG II (10(-6) mol/l) caused a prestimulation but did not increase the maximum contractile effect of carbachol. The response to ANG II was not affected by atropine (10(-6) mol/l). TTX (10(-6) mol/l) and N-nitro-L8-arginine (L-NNA) (3 x 10(-4) mol/l) stimulated basal muscular activity but did not affect the maximum contractile effect of ANG II. Systemic serum concentrations of AVP, aldosterone and ANG II are presumably not involved in thirst-induced colonic motility changes. The ANG II effect in higher concentrations is mediated by a direct stimulatory smooth muscle effect and/or by facilitating neuronal liberation of acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of hormones and peptides involved in water balance on rat colonic motility in vitro. 762 62


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