UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin II (AII)-immunoreactive cell bodies were found in all parts of the paraventricular nucleus of the hypothalamus (PVH) in the normal, colchicine-treated rat. The greatest concentration of cells was found in the posterior part of the magnocellular division of the nucleus, while scattered cells were found in all 5 parts of the parvocellular division. In comparison, the Brattleboro rat showed similar cell staining in parvocellular parts of the PVH, although a substantial decrease in the number of AII-stained cells was found in the magnocellular division. In the normal animal, fiber staining was evident in both laminae of the median eminence. This immunostaining was selectively enhanced in the internal lamina following water deprivation, and was selectively enhanced in the external lamina following adrenalectomy. The Brattleboro rat was similar to the normal animal with regard to staining of the external lamina, but, consistent with the diminished number of immunoreactive magnocellular neurons, little immunostaining in the internal lamina was detected. Unilateral lesions of the PVH selectively diminished staining of fibers and varicosities in the ipsilateral external lamina, while bilateral lesions virtually eliminated staining on both sides. The findings in the Brattleboro rat indicate that specific subpopulations of both parvocellular and magnocellular neurons in the PVH contain an antigen that is immunologically similar to synthetic AII and unrelated to vasopressin or its prohormone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The distribution of angiotensin II-immunoreactive cells and fibers in the paraventriculo-hypophysial system of the rat. 389 94

A rise in cytosolic free calcium ([Ca2+]i) is thought to be the principal mediator in vascular smooth muscle contraction. Quantitative changes of [Ca2+]i in response to two vasoconstrictor peptide hormones, angiotensin II and vasopressin, were directly measured in monolayers of adherent cultured rat aortic smooth muscle cells loaded with the fluorescent calcium indicator Quin 2. Angiotensin II induced rapid, concentration-dependent rises in [Ca2+]i from 1.53 +/- 0.27 X 10(-7) (n = 16) up to 1.2 X 10(-6) M, with ED50 of 0.45 X 10(-9) M, an effect which was blocked by the antagonist analogue [Sar1, Ala8]angiotensin II. Vasopressin also elicited transient rises in [Ca2+]i to peak levels of about 8 X 10(-7) M, with ED50 of 1.05 X 10(-9) M, and this response was completely abolished by a vasopressor antagonist. In calcium-free medium, basal [Ca2+]i levels fell to 0.92 +/- 0.24 X 10(-7) M (n = 4), and both hormones were still able to raise [Ca2+]i, although to a lesser extent. Readdition of extracellular calcium following the [Ca2+]i transient induced a second, slower [Ca2+]i rise. In calcium-containing medium, lanthanum ion (2 X 10(-5) M) reduced peptide-evoked [Ca2+]i rises to the values observed in calcium-free medium. Stimulation with each peptide completely desensitized the smooth muscle cells to a subsequent identical challenge, with little crosstachyphylaxis. Potassium ion (50 mM) only minimally affected [Ca2+]i levels. The calcium channel blocker nifedipine (10(-6) M) did not prevent the [Ca2+]i rises induced by angiotensin II, vasopressin, or potassium. These findings indicate that the two physiologically important vasoconstrictor hormones angiotensin II and vasopressin rapidly raise [Ca2+]i in cultured vascular smooth muscle cells, in part by mobilizing calcium from intracellular pools and in part through activation of receptor-operated calcium channels.
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PMID:Cytosolic free calcium levels in monolayers of cultured rat aortic smooth muscle cells. Effects of angiotensin II and vasopressin. 400 79

Cytosolic free Ca2+ concentrations [( Ca2+]i) were measured in smooth muscle cells (SMC) from spontaneously hypertensive rats (SHR) and age and sex matched Wistar-Kyoto rats (WKY). Resting levels of [Ca2+]i were 114 +/- 6 nM and 116 +/- 5 nM in SMC from WKY and SHR, respectively. Angiotensin II (AII) induced a dose-dependent large increases in [Ca2+]i in SMC. There were no significant differences in resting or AII-stimulated levels of [Ca2+]i when SMC from WKY and SHR were compared. Arg-vasopressin (AVP) caused a similar but smaller [Ca2+]i increase than AII in SMC. AVP caused larger [Ca2+]i increases in SMC from SHR than in SMC from WKY. Although concentrations of AVP higher than those ordinarily detected in plasma were necessary to obtain different responses between SHR and WKY, these differences may be related to the pathogenesis of hypertension.
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PMID:Vasopressin-induced calcium increases in smooth muscle cells from spontaneously hypertensive rats. 402 31

Investigations into the site of vasodilator and antivasoconstrictor activity of calcium antagonists previously performed in cats were extended to a second species, barbiturate-anaesthetized rabbits, and a second vasoconstrictor agent, vasopressin. The dihydropyridine derivative darodipine (code name PY 108-068; 10, 30 and 100 micrograms kg-1 i.v.) showed systemic haemodynamic effects comparable to those seen in cats at half these doses. Darodipine effected regional vasodilatation (measured with tracer microspheres) in the heart, brain and skeletal muscles as in cats. Only the vessels of the adrenals (dilated in rabbits but not in cats), and the kidneys and skin (constricted in rabbits but not in cats) responded differently to darodipine. Angiotensin II (A II; 0.15 and 1.5 micrograms kg-1 min-1) constricted the same vascular beds in rabbits as in cats, namely the heart, kidneys, small intestine, pancreas, spleen, skin and arterio-venous shunts (inferred from microspheres reaching the lungs), the only exceptions being the vessels of the stomach and liver (constriction only in cats) and the adrenals (constriction only in rabbits). Darodipine (30 and 100 micrograms kg-1) attenuated the A II-induced vasoconstriction in the same vascular beds in rabbits as in cats including the kidneys, which were constricted after administration of the antagonist alone. These results indicate surprisingly small species differences for the vasodilator effects of darodipine as well as the attenuation of the vasoconstrictor effects of A II. Lysine-vasopressin (2 and 50 mu kg-1 min-1) did not increase blood pressure in anaesthetized rabbits but dose-dependently lowered heart rate, cardiac output, total peripheral conductance and myocardial contractile force (measured with a strain gauge). Vasopressin constricted all peripheral vascular beds dose-dependently, except for those of the kidney and liver. The effects of vasopressin persisted in the animals infused with placebo solution. Darodipine (30 and 100 micrograms kg-1), but not verapamil (300 and 1000 micrograms kg-1) reversed the vasopressin-induced cardiac depression and decrease in cardiac output. This probably also explains most of the apparent differences between the effects of the two calcium antagonists on the peripheral circulation. Both calcium antagonists diminished the vasopressin constriction in most vascular beds except those of the spleen, skin and arterio-venous shunts. Most of the effects were dose-related but not strictly competitive, as far as this can be judged based on two doses of agonist and antagonist. 9 As with A II the effects of vasopressin were diminished in vascular beds not normally dilated by calcium antagonists. 10 Calcium antagonists display two typical patterns of activity. The vasodilator pattern consists of dilatation of the vesels of the heart, brain and, to a degree varying with the agents, skeletal muscle. The antivasoconstrictor effects occur in some but not all of the vessels constricted by the constrictor agent, vasoconstriction of the spleen, skin and arterio-venous shunts being resistant to the action of calcium antagonists. The pattern of antivasoconstrictor activity appears to depend on the constrictor compound used, inasmuch as such agents constrict different vascular beds.
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PMID:Modification of vasopressin- and angiotensin II- induced changes by calcium antagonists in the peripheral circulation of anaesthetized rabbits. 402 74

1. Splenic arterial flow and splenic weight were recorded in cats anaesthetized with sodium pentobarbitone. The responses of the spleen to catecholamines, angiotensin and vasopressin were investigated.2. Catecholamines caused responses mediated by alpha- and beta-adrenoceptors in the arteriolar smooth muscle, but only insignificant beta-adrenoceptor responses could be elicited from the capsular smooth muscle. The difficulties in elucidating the mechanism of action of catecholamines on arteriolar smooth muscle are discussed.3. Angiotensin caused marked vasoconstriction, but contraction of the capsular smooth muscle was less marked. Vasopressin caused vasoconstriction but had no effect on capsular smooth muscle. Thus these peptides constrict the resistance vessels but produce much weaker contraction of the capsule.4. These responses are discussed in relation to the splenic responses to acute haemorrhage.
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PMID:The vascular responses of the spleen to intravenous infusions of catecholamines, angiotensin and vasopressi in the anaesthetized cat. 431 61

1. When applied directly to the brain, angiotensin II amide, as either the valine(5) octapeptide, causes rats in normal fluid balance to drink water.2. The drinking response to angiotensin injections is copious, rapid, repeatable within the same test session, and stable over months of testing in the same animal.3. The response is motivationally potent and specific. After injection the animals move directly to the source of water and drink. There is typically no preliminary hyperactivity or subsequent depression. The animals do not eat, gnaw or exhibit other behaviours that are not normally seen during spontaneous drinking. The injections rouse sleeping animals to drink and interrupt eating in animals deprived of food for two days.4. The region of the brain that is most sensitive to angiotensin includes the anterior hypothalamus, the preoptic region, and the septum including the nucleus accumbens.5. Intracranial renin elicited drinking. Bradykinin and vasopressin did not, nor did adrenaline, noradrenaline or aldosterone. In the most sensitive region, sites positive for angiotensin also yielded drinking to carbachol.6. Responses were obtained with 5 ng (ca. 5 p-mole) and occurred reliably with 50 ng angiotensin or more. The dose-response curve for amount drunk rose from 5 to 100 ng and levelled off thereafter. Angiotensin is therefore the most potent dipsogen known and is effective at doses that are reasonably within the concentration range for circulating endogenous angiotensin.7. Injections into the sensitive region of doses of angiotensin that were effective for drinking did not produce peripheral haemodynamic changes in lightly anaesthetized rats.8. This work strengthens the suggestion that angiotensin is a natural hormone of drinking behaviour that participates in extracellular thirst by its release from the kidney and subsequent direct action on a specific chemoreceptive region in the anterior diencephalon and limbic lobe.
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PMID:Drinking induced by injection of angiotensin into the rain of the rat. 432 23

1. The effect of val(5)-angiotensin II amide, noradrenaline and vasopressin, on kidney volume and intrarenal distribution of carbon particles and thioflavine S was examined in the rat.2. Angiotensin produced a dose-dependent shrinkage of the kidney coinciding with the rise in systemic blood pressure. Noradrenaline and vasopressin, however, produced reduction in kidney volume only in much higher doses than were necessary to produce a pressor effect.3. An intravenous infusion of angiotensin sufficient to produce a diuretic response resulted in a striking increase in glomerular content of injected carbon particles, and a marked reduction in filling of the capillary plexuses of the subcortex and outer medulla. The reduction in outer medullary filling was also observed using the thioflavine S technique.4. Noradrenaline infused in amounts sufficient to produce diuresis, aortic constriction above the kidney and vasopressin injection produced no measurable change in carbon particle distribution.5. The reduction in capillary blood flow produced by angiotensin may result in impaired tubular reabsorptive capacity by reducing peritubular removal of reabsorbate, or by reducing oxygen availability. Thus the vasoconstrictor effects of angiotensin may explain its diuretic action.
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PMID:The effect of angiotensin, noradrenaline and vasopressin on blood flow distribution in the rat kidney. 433 28

1. Hepatic volume was recorded by a plethysmographic technique in cats anaesthetized with pentobarbitone; the hepatic artery and portal vein remained intact. Dose-response curves were obtained for intravenous infusions of adrenaline, noradrenaline, angiotensin, vasopressin and histamine.2. Adrenaline and noradrenaline decreased hepatic blood volume and did not differ significantly in potency. Up to 40% of the hepatic blood volume was expelled by doses within the range secreted by the adrenal medullae.3. Isoprenaline, infused into the hepatic artery, had no significant effect on hepatic blood volume in doses which caused maximal vasodilatation of the hepatic arterial bed. Relaxation of hepatic capacitance vessels mediated by beta-adrenoceptors did not occur.4. Angiotensin infusions in doses previously shown to cause intestinal and splenic vasoconstriction, decreased hepatic blood volume and on a molar or microgramme basis, angiotensin was the most potent of the agents tested. Doses within the probable physiological range of endogenous production decreased hepatic blood volume by up to 20%. The responses were not significantly different when the hepatic nerves were intact or sectioned.5. Vasopressin infusions produced only small decreases in hepatic blood volume. Doses within the range secreted by the posterior pituitary which constrict the intestinal and splenic resistance vessels, did not decrease hepatic blood volume by more than 10%.6. Histamine produced no change in hepatic blood volume in doses which readily produce outflow block in dogs. Either the specific hepatic venous smooth muscle involved in outflow block is absent in the cat or it has no histamine receptors.7. After the rapid change in hepatic blood volume at the onset of the infusion, hepatic volume remained steady for the duration of each infusion. There was no evidence that these agents caused net transsinusoidal fluid movements.
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PMID:Effects of infusions of catecholamines, angiotensin, vasopressin and histamine on hepatic blood volume in the anaesthetized cat. 435 9

Prostacyclin (PGI2) and prostaglandin E2 (PGE2) production by rat glomerular epithelial cells in culture were stimulated by arginine vasopressin (AVP) over a dose range of 10(-9) to 10(-6) M, but only if the cells were allowed to recover from trypsin treatment. The effect of AVP was related to its pressor activity since the antidiuretic analogue of AVP, 1-deamino-8-D-Arg-vasopressin (dDAVP) had no effect. Angiotensin II and kallidin (lysyl-bradykinin) did not affect prostaglandin production by these cells. The stimulatory effect of AVP on arachidonate metabolism was inhibited by the calcium channel antagonist, nifedipine, in a dose-dependent fashion suggesting that cellular uptake of calcium was required.
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PMID:Stimulation of prostaglandin production in rat glomerular epithelial cells by antidiuretic hormone. 608 84

Hepatic plasma membranes of female obese mice C57 BL-6 orl ob/ob (ob/ob mice) completely lack vasopressin (VP) receptors of the V1 type whereas kidney VP receptors are normally expressed and functionally coupled to adenylate cyclase. To discover if these alterations are linked to a genetic defect of the V1 receptor, we have studied the binding of VP on liver and kidney membranes of two other models, female diabetic mice C57 BL-6 orl db/db (db/db mice) and female Zucker rats Fatty/orl fa/fa (fa/fa rats), which exhibit different temporal pattern of obesity, hyperinsulinemia and insulin resistance. In addition, since VP is known to exert its vascular response through stimulation of V1 receptors, we have studied the reactivity of VP of isolated tail artery in the three different models, ob/ob and db/db mice and fa/fa rats, and in their respective controls. In all cases, VP kidney receptors and VP vascular reactivity are normal. db/db mice exhibit a marked decrease in hepatic VP receptors whereas a 50% decrease was observed in 32 week fa/fa rats. Angiotensin II and prazosin binding sites are still present as well as the adenylate cyclase response to glucagon. These results suggest that the specific alteration in liver VP receptors is not related to a defect in V1 receptor genetic expression but is specific for liver and appears to parallel the level of hyperinsulinemia and/or insulin resistance.
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PMID:Reduction in hepatic but not in renal and vascular vasopressin receptor number in hyperinsulinemic mice and rats. 609 84

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