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)

In vitro and in vivo experiments have provided indirect evidence that some of the central actions of angiotensin II (ANG II) involve catecholaminergic pathways in the brain. In this study in conscious rats we investigated the effect of stimulation of periventricular ANG II receptors on blood pressure and on catecholamine release (microdialysis and HPLC) from the paraventricular nucleus (PVN), a hypothalamic area thought to be instrumental in the central pressor responses to ANG II through the release of vasopressin into the blood. Intracerebroventricular (i.c.v.) injections of pressor doses of ANG II (1 ng and 100 ng) led to significant dose-dependent increases of the noradrenaline (NA) release in the PVN (1 ng: 30.95 +/- 6.01 to 47.38 +/- 6.79 pg/sample, P less than or equal to 0.01; 100 ng: 32.93 +/- 5.38 to 73.18 +/- 11.4 pg/sample, P less than or equal to 0.01). These changes coincided in extent and duration with the respective pressor responses. A subpressor dose of ANG II (100 pg) did not release catecholamines from the PVN. Dopamine (DA) and the NA and DA, metabolites 3,4-dihydroxyphenylethylglycol and 3,4-dihydroxyphenylacetic acid, were not influenced by i.c.v. injections of ANG II at any dose. Pretreatment with the novel non-peptide ANG II-AT 1 receptor antagonist DuP 753 (5 micrograms, i.c.v.) abolished the effect of 100 ng ANG II on blood pressure and on NA release. Our results show for the first time in vivo that stimulation of periventricular ANG II-AT 1 receptors induces a selective NA release in the PVN. They further support the hypothesis that ANG II engages a noradrenergic pathway in the PVN to release vasopressin.
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PMID:Angiotensin II evokes noradrenaline release from the paraventricular nucleus in conscious rats. 161 72

The effects of a Ca2+ entry blocker CD-349 and an intracellular Ca2+ release inhibitor TMB-8 on renal vasoconstriction induced by angiotensin II (ANG II) and arg-vasopressin (AVP) were examined in anesthetized dogs. Intrarenal bolus injection of ANG II (3-10 ng/kg), AVP (5-20 ng/kg) or a Ca2+ entry promotor Bay K 8644 (0.1-0.4 micrograms/kg) produced a dose-dependent decrease in renal blood flow (RBF). Intrarenal infusion of CD-349 (0.03-0.3 micrograms/kg/min) suppressed the RBF responses to ANG II, AVP, and Bay K 8644. The RBF responses to ANG II and AVP were augmented slightly by intrarenal infusion of Bay K 8644 (0.3 micrograms/kg/min). Intrarenal infusion of TMB-8 (0.03-0.1 mg/kg/min) also suppressed the RBF responses to ANG II and AVP, whereas it did not affect the RBF response to Bay K 8644. These results suggest that vasoconstriction induced by ANG II or AVP is mediated both by the influx of Ca2+ through dihydropyridine-sensitive Ca2+ channels and the release of Ca2+ from TMB-8-sensitive Ca2+ pools in the in vivo dog kidney.
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PMID:Effects of a novel Ca2+ entry blocker, CD-349, and TMB-8 on renal vasoconstriction induced by angiotensin II and vasopressin in dogs. 170 91

To clarify a possible mechanism whereby the perception of thirst may be associated with diabetes mellitus, we measured plasma levels of vasopressin (AVP), angiotensin II (ANG II), atrial natriuretic peptide (ANP) and plasma renin activity (PRA) in non-insulin-dependent (NIDDM) diabetic patients with or without thirst. Thirteen male NIDDM patients complaining of thirst had a significantly high blood hematocrit, plasma urea nitrogen and creatinine concentrations and plasma osmolality, indicating a reduction in plasma volume. In addition, the patients had a significantly high mean plasma concentrations of AVP (3.20 +/- 1.27 pmol/l) ANG II (33.8 +/- 31.4 pmol/l) and PRA, but a low mean plasma ANP concentration (8.9 +/- 4.5 pmol/l). After treatment with diet and/or sulfonylurea, plasma levels of AVP, ANG II and PRA decreased with a concomitant increase in plasma volume and disappearance of thirst. In contrast, 13 NIDDM patients (9 females and 4 males) without thirst had normal plasma urea nitrogen and creatinine concentrations, and the hematocrit did not change significantly after treatment. Plasma AVP (0.95 +/- 0.34 pmol/l), ANG II (14.7 +/- 8.8 pmol/l) and ANP (10.7 +/- 4.9 pmol/l) concentrations, and PRA were normal in this group of patients. There was no significant difference between the two groups of patients, however, in fasting glucose concentration and HbA1c. We conclude from these results that a reduction in plasma volume may be the major factor responsible for the induction of thirst sensation and for increased AVP secretion in NIDDM patients. The mechanism underlying a reduction in plasma volume remains unclear.
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PMID:Thirst and plasma levels of vasopressin, angiotensin II and atrial natriuretic peptide in patients with non-insulin-dependent diabetes mellitus. 182 24

The present studies were performed to examine the vasoconstrictor effect of angiotensin II (ANG II), angiotensin III (ANG III), and vasopressin in isolated afferent arterioles of the rabbit kidney. Afferent arterioles were dissected together with their glomerulus and perfused with a pressure head of 120 cmH2O. Changes in vasomotor tone were assessed as diameter changes on videotaped recordings. Afferent arterioles responded to the angiotensins and vasopressin with dose-dependent reductions in vascular diameters with half-maximum responses being observed at concentrations between 10(-9) and 10(-8) M. Responses to ANG II and III were inhibited by saralasin. Contractile responses to ANG II and vasopressin were not altered by prior occlusion of the efferent arteriole, suggesting that afferent vasoconstriction does not represent a myogenic reaction to an increase in efferent resistance. The vasoconstrictor response to ANG II was largely eliminated by removal of the glomerulus and the distal-most portion of the afferent arteriole, whereas the response to vasopressin remained intact. Our data are consistent with the notion that the juxtaglomerular apparatus (JGA) and/or glomerulus may control proximal afferent arteriolar contractility by electrotonic or myogenic coupling mechanisms or by producing cofactors that modulate vasomotor responses.
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PMID:Vasoconstrictor effect of angiotensin and vasopressin in isolated rabbit afferent arterioles. 187 51

We examined the effect of platelet-activating factor (PAF) on renal vascular reactivity in the pentobarbital sodium-anesthetized male Wistar rat. Intrarenal infusion of C16-PAF at hypotensive (2.5 ng.min-1.kg-1) or nonhypotensive (0.5 ng.min-1.kg-1) doses caused renal vasodilation and dose dependently antagonized the renal vasoconstrictor responses of intrarenal boluses of angiotensin II (ANG II) greater than norepinephrine (NE) greater than vasopressin (AVP). PAF infusion at the high dose did not alter non-receptor-mediated renal vasoconstriction induced by intrarenal KCl injection. The inhibitory effect of PAF on agonist-induced renal vasoconstriction was accentuated by eicosanoid synthesis inhibition (indomethacin or dexamethasone), unaffected by dopamine-receptor blockade (haloperidol) but was totally abolished by PAF receptor antagonism (L-659,989). In contrast, intrarenal infusion of a calcium channel antagonist (nimodipine) or an intracellular calcium channel antagonist (TMB-8) equally inhibited the renal vasoconstrictor responses of ANG II, NE, and AVP. Thus PAF can cause renal vasodilation in the rat kidney and dose-dependently antagonizes the renal vasoconstrictor responses of ANG II greater than NE greater than AVP. The inhibitory effect of PAF on renal vasoconstrictor responses is mediated by PAF receptors and does not appear to be due to a nonspecific membrane effect, reduction in calcium mobilization, or the release of vasodilatory eicosanoids or dopamine.
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PMID:Selective inhibition of vasoconstrictor responses by platelet-activating factor in rat kidney. 190 4

The contribution of the autonomic nervous system, angiotensin II (ANG II), and arginine vasopressin (AVP) to the control of blood pressure (BP) was examined in 12 chronically instrumented tethered monkeys. The vasopressin antagonist, [d(CH2)5AVP] (Manning Compound, MC), the ANG II antagonist, saralasin (SAR), and the ganglionic blocking drug, hexamethonium (Hx), were injected in a random sequence into the left atrium (LA) while BP and heart rate (HR) were monitored. When given as the first antagonist, MC caused a slight decrease in BP; SAR did not significantly decrease BP regardless of the sequence of administration, whereas Hx caused a consistent decrease in blood pressure of 35-50 mmHg. Seven (4 intact and 3 with renal denervation) additional animals were involved in hemorrhage experiments. Blood pressure was reduced to 50-60 mmHg by hemorrhage and then allowed to return spontaneously. Ten to 15 min after the end of the hemorrhage, MC was given. When blood pressure had stabilized, SAR was given. Blood pressure returned to 80-90 mmHg after the hemorrhage. MC did not affect the blood pressure recovery; however, saralasin reduced it to the post-hemorrhage levels. We would conclude that the sympathetic nervous system is the primary controlling mechanism for BP in the conscious primate, with AVP making a minor contribution. The release of renin would appear to be primarily under the control of the sympathetic nervous system.
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PMID:Neural and hormonal control of blood pressure in conscious monkeys. 196 11

In order to investigate the physiological role of angiotensin II (ANG II) in the control of vasopressin (VP) secretion, the VP responses to hypotension induced by hemorrhage (20 ml/kg, n = 10) or nitroprusside infusion (1-10 micrograms/kg.min, n = 9) were studied with or without blockade of ANG II formation by the converting enzyme inhibitor captopril in conscious rabbits. Administration of captopril (5 mg/kg, iv) caused a small decrease in mean arterial pressure but did not enhance the hypotensive response to subsequent hemorrhage or nitroprusside infusion. The renin response to both stimuli was enhanced by captopril, whereas the increase in plasma ANG II concentration was attenuated. Plasma VP (PAVP) concentration increased during hemorrhage (2.0 +/- 0.2-113.6 +/- 47.7 pg/ml, P less than 0.01) and nitroprusside infusion (2.1 +/- 0.3-5.1 +/- 1.0 pg/ml, P less than 0.01). Captopril did not change basal plasma PAVP, nor did it attenuate the VP responses to hemorrhage or nitroprusside. Indeed, captopril tended to enhance the VP responses to hemorrhage (2.3 +/- 0.3-147.1 +/- 65.9 pg/ml) and nitroprusside infusion (1.9 +/- 0.2-15.4 +/- 6.0 pg/ml). The relationship between log PAVP and mean arterial pressure during hemorrhage and nitroprusside infusion in the presence of captopril was not different than in the absence of captopril. These results indicate that in conscious rabbits, the renin-angiotensin system does not contribute to the increase in VP secretion during hypotension induced by hemorrhage or nitroprusside infusion.
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PMID:Role of endogenous angiotensin II in the control of vasopressin secretion during hypovolemia and hypotension in conscious rabbits. 198 18

This study examined whether angiotensin II (ANG II) influences the pressure-natriuretic (PN) response by altering renal cortical or medullary hemodynamics. Studies were performed in Inactin-anesthetized rats that were acutely volume expanded to maintain plasma renin activity and ANG II levels in the physiological range. Neural influences on the kidney were eliminated by renal denervation, and plasma levels of norepinephrine, vasopressin, cortisol, and aldosterone were fixed by intravenous infusion. In control rats (n = 8), sodium excretion increased from 3 to 17 microeq.min-1.g kidney wt-1 as renal perfusion pressure (RPP) was elevated from 96 to 141 mmHg (n = 8). Captopril (2 mg/kg, n = 9) reduced plasma levels of ANG II from 48 +/- 5 to 18 +/- 2 pg/ml, but it did not alter the PN relationship. Infusion of ANG II (20 ng.kg-1.min-1, n = 9) increased plasma levels of ANG II to 232 +/- 42 pg/ml and shifted the PN relationship to the right by 14 mmHg. Captopril increased renal blood flow, and infusion of ANG II returned it to control. Captopril had no effect on glomerular filtration rate (GFR) or glomerular capillary pressure (Pglom); however, subsequent ANG II infusion decreased Pglom from 56 +/- 2 to 48 +/- 2 mmHg and reduced GFR by 30%. Neither captopril nor ANG II altered papillary bloodflow or vasa recta capillary pressure at normal levels of RPP. These results indicate that the shift of the PN relationship during infusion of ANG II is due to a decrease in filtered load and enhanced tubular reabsorption of sodium. Acute blockade of the renin-angiotensin system had little effect on the PN response in volume-expanded rats despite affecting renal hemodynamics, because either the plasma and/or intrarenal levels of ANG II were already suppressed below those needed to influence tubular function or volume expansion inhibits tubular reabsorption in the nephron segments normally influenced by ANG II.
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PMID:Influence of angiotensin II on pressure natriuresis and renal hemodynamics in volume-expanded rats. 205 47

The diabetogenic agent streptozotocin (STZ) was injected intraperitoneally in Long-Evans and arginine vasopressin (AVP)-deficient Brattleboro rats. Twenty-eight days later both strains had a bradycardia and systolic hypotension; STZ-treated Brattleboro rats also had diastolic hypotension. The vasopressin (V1-receptor) antagonist, d(CH2)5[Tyr(Et)]DAVP, had no effect on resting blood pressure (BP) or heart rate (HR) in either strain of rat, indicating the relative maintenance of diastolic BP in STZ-treated Long-Evans rats was not dependent on acute vascular actions of AVP. Captopril caused a modest hypotension in all groups of rats, indicating that BP was not differentially dependent on the renin-angiotensin system in the different groups. In the presence of captopril and the ganglion blocker, pentolinium tartrate, the AVP-mediated recovery in BP was impaired in STZ-treated Long-Evans rats. During administration of d(CH2)5[Tyr(Et)]DAVP and pentolinium, the angiotensin II (ANG II)-mediated BP recovery was smaller in both groups of STZ-treated rats, indicating that this abnormality was not likely to be caused by inhibition of renin release by AVP. The abnormalities in ANG II- and AVP-mediated recovery were prevented by insulin treatment.
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PMID:Blood pressure in streptozotocin-treated Brattleboro and Long-Evans rats. 213 47

The polydipsic inbred mice, STR/N, are known to possess an extremely strong appetite for drinking but no abnormality in the vasopressin system and renal functions. In brain slice preparations the sensitivity of neurons in the anteroventral region of the third ventricle (AV3V) and the subfornical organ (SFO) to angiotensin II (ANG II) was investigated using extracellular recordings in the STR/N and its control, Swiss/Webster (S/W) mice. In the AV3V, less proportion of neurons (15 out of 168; 9%) of the STR/N than that in the S/W (49/206; 24%) was excited by ANG II added to the medium. In the SFO, a proportion of neurons excited by ANG II was again lower in the STR/N (27/104; 26%) than in the S/W mice (64/118; 54%). The threshold concentration of ANG II for excitation of the AV3V and SFO neurons was, however, similar for both strains, 10(-9) M or less. Only one neuron in the SFO of a S/W mouse was inhibited by ANG II application. The excitatory effect of ANG II on AV3V and SFO neurons of both strains of mice persisted under synaptic blockade and was reversibly antagonized by an ANG II antagonist, saralasin. Such differences in sensitivity to ANG II of neurons in the SFO and AV3V, the regions thought to be involved in drinking behavior, suggest the involvement, at least in part, of the central angiotensin system in the polydipsia of the STR/N mice.
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PMID:Sensitivity to angiotensin II of neurons in the circumventricular organs of polydipsic inbred mice. 229 1

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