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)

New findings from this laboratory suggest that fragments of angiotensin derived from the amino (N-)terminus are biologically active end products of the renin-angiotensin system. In vitro and in vivo experiments revealed that the heptapeptide angiotensin-(1-7) [Ang-(1-7)] is a major endogenous product of the renin-angiotensin system cascade in the brains of rats and dogs. Additional studies with enzyme inhibitors showed that Ang-(1-7) is produced directly from angiotensin I by an enzyme other than the angiotensin converting enzyme. Immunocytochemical fibers within the hypothalamo-neurohypophyseal vasopressinergic system of the rat. Although Ang-(1-7) is as potent as angiotensin II (Ang II) in stimulating release of vasopressin from superperfused hypothalamo-neurohypophyseal explants, the heptapeptide has no dipsogenic or vasoconstrictor activity. In contrast, Ang-(1-7) mimics the effects of Ang II in augmenting the intrinsic discharge rate of neurons within the vagal-solitary complex and in causing monophasic depressor responses after microinjection into the medial region of the nucleus tractus solitarii. The evidence obtained in these experiments suggests novel mechanisms for the generation of angiotensin peptides in the brain. Additionally, the findings suggest that some of the biological actions ascribed to Ang II might be conveyed by the endogenous production of other angiotensin peptides that are generated by enzymatic pathways alternate to those described in the peripheral circulation.
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PMID:Pathways of angiotensin formation and function in the brain. 240 55

Differences in responsiveness of various vascular beds to pressor hormones have been reported. In our study, we have examined the effects of angiotensin II (Ang II) and vasopressin (AVP) on cytosolic free Ca2+ concentration [( Ca2+]c), protein kinase C (PKC) activity, and prostacyclin (PGI2) production in cultured aortic and mesenteric smooth muscle cells obtained from female Wistar rats. [Ca2+]c was determined using the Ca2+ fluorescent probe fura-2. PKC activity was assessed by the measurement of the phosphorylation of histone III-S, in the presence or absence of phospholipids, both in the cytosolic and particulate fractions. PGI2 production was estimated by a specific radioimmunoassay of its stable metabolite, 6-keto-PGF1 alpha. Our results demonstrate that basal production of PGI2 was higher in mesenteric than in aortic smooth muscle cells. In mesenteric cells, the [Ca2+]c, PKC activity, and PGI2 responses to AVP were higher than those induced by Ang II. This situation is the opposite of that observed in aortic smooth muscle cells. These results indicate different sensitivities to AVP and Ang II between vascular smooth muscle cells originating from two types of vessels.
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PMID:Comparison of the effects of angiotensin II and vasopressin on cytosolic free calcium concentration, protein kinase C activity, and prostacyclin production in cultured rat aortic and mesenteric smooth muscle cells. 247 23

The extracellular Ca2+ dependence of agonist stimulation of vascular smooth muscle (VSM) has been investigated in rat cultured aortic smooth muscle cells (SMCs) and isolated mesenteric resistance vessels (MRVs). Agonists such as [Arg8]vasopressin (AVP), angiotensin II (Ang II), and adenosine-5'-triphosphate (ATP) stimulated 45Ca2+ entry into the SMCs that was (a) independent of the extent to which the membranes were polarized, and (b) was not inhibited by organic Ca2+ channel antagonists. Measuring the intracellular Ca2+ concentration [( Ca2+]i) after stimulation with agonists revealed a rapid increase of [Ca2+]i, which was followed by a sustained rise that was insensitive to Ca2+ antagonists. In Ca2+-free medium, only the initial peak of [Ca2+]i was still observed, but the sustained response to the agonists disappeared completely. This observation indicates that the sustained elevation seen in Ca2+-containing medium was the consequence of agonist-induced Ca2+ entry. In MRVs, a corresponding Ca2+-antagonist-insensitive, agonist (norepinephrine and AVP)-induced tonic tension was also identified. Moreover, agonists were able to induce sustained tension in the MRVs regardless of whether the membrane was normally polarized or was previously depolarized (80 mM K+) upon their administration. The agonist-stimulated 45Ca2+ entry in the SMCs could be blocked by the multivalent cations La3+, Cd2+, Mn2+, Co2+, Ni2+, and Mg2+ (in this order of potency). Depolarization-induced 45Ca2+ influx was inhibited by these cations in the same order of potency, but was significantly more sensitive to Cd2+ and significantly less sensitive to La3+ than that stimulated by agonists. Treatment with 2-nitro-4-carboxyphenyl-N,N-diphenyl-carbamate (NCDC, a proposed inhibitor of phospholipase C) reduced both the agonist-induced 45Ca2+ influx and the sustained elevation of [Ca2+]i in the SMCs. NCDC also abolished both contraction and depolarization induced by agonists in the MRVs. The kinase C stimulator phorbol-12-myristate-13-acetate (PMA) inhibited the agonist-induced 45Ca2+ influx and sustained increase in [Ca2+]i in the SMCs, whereas the kinase C inhibitor staurosporine had no effect. In the MRVs, in contrast, PMA had no influence on agonist-induced contractions. Staurosporine (1 microM), however, completely prevented these contractions, as did NCDC, but, unlike NCDC, it did so without affecting the agonist-induced depolarization. These data support an important role of receptor-operated Ca2+-permeable channels in VSM activation by agonists and suggest that these channels may be controlled by intracellular enzymic pathways and second messenger systems.
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PMID:Receptor-operated calcium-permeable channels in vascular smooth muscle. 247 25

The contractile responses to various endogenous vasoactive agents were investigated in isolated human uteroplacental arteries from normotensive (NT) patients and patients with pre-eclampsia (PE) undergoing caesarian section. Tissue samples were obtained from the uterine incision and from macroscopically normal cotyledons. Vascular ring preparations of intramyometrial and stem villous arteries (length 1.0-1.3 mm, outer diameter 400-600 microns) were dissected and mounted in organ baths and isometric tension was recorded. Concentration-response relationships for vasopressin (VP), oxytocin (OX), angiotensin II (Ang II), noradrenaline (NA), 5-hydroxytryptamine (5-HT), prostaglandin F2 alpha (PGF2 alpha) and prostaglandin E2 (PGE2) were assessed. For each compound, the mean maximum contractile effect (Emax) and the drug concentration producing half-maximal response (EC50) were determined. In intramyometrial arteries from NT and PE patients, VP, Ang II, NA, 5-HT and PGF2 alpha induced contraction while OX and PGE2 produced weak or no responses. Preparations from PE patients showed higher Emax values, while no differences in EC50 were found between the two groups. In fetal stem villous arteries, Ang II, 5-HT, PGF2 alpha and PGE2 induced contractions, while VP, NA and OX produced weak responses. No differences in Emax or EC50 values were found between the fetal vessels of PE and NT patients. No qualitative differences were demonstrated in response to the agents tested between the vessels (fetal and maternal) from NT women at term and PE patients. However, the results may reflect quantitative differences, suggesting increased contractility of maternal uteroplacental arteries from women with PE.
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PMID:Effect of endogenous vasoconstrictors on maternal intramyometrial and fetal stem villous arteries in pre-eclampsia. 276 Apr 57

The neurohormonal contribution to high blood pressure was investigated in 9 conscious two-kidney, two-clip Goldblatt (2K2C) hypertensive dogs during evolution of the benign and malignant phases after application of bilateral renal clips (BRC). Serial measurements were taken of the plasma renin activity (PRA), plasma angiotensin I-immunoreactivity (Ang I-ir), plasma angiotensin II-ir (Ang II-ir), renin substrate (RS) catecholamines [epinephrine (Epi) and norepinephrine (NE)] and vasopressin (AVP). Immediately after BRC, the elevation of the blood pressure (86 +/- 3 to 110 +/- 3 mmHg, p less than 0.01) was associated with an increase in heart rate (93 +/- 3 to 114 +/- 9 beats/min, p less than 0.01). These hemodynamic changes were accompanied by increases in PRA, Ang I-ir, Ang II-ir, Epi, NE and AVP. The renin angiotensin system was activated throughout the 3 week period following BRC, as indicated by increases in PRA, Ang I-ir and Ang II-ir. Catecholamines were elevated immediately after BRC, followed by a return toward the control values. AVP underwent a slight but not significant elevation after BRC, which was sustained during the 3 weeks. Production of malignant hypertension was affected by occlusion of one of the adjustable renal clips 3 weeks after BRC. A marked elevation of the blood pressure was associated with significant increases in PRA, Ang I-ir, Ang II-ir, Epi, NE and AVP, compared with the pre-occlusion values. In addition, pharmacologic experiments were performed in 6 of 9 dogs. Administration of angiotensin I converting enzyme inhibitor (SQ 14225) reduced the blood pressure both in the benign and malignant phases of 2K2C renovascular hypertension, and a ganglionic blocking agent (hexamethonium) also decreased the blood pressure. However, a specific, vascular acting AVP antagonist failed to reduce the blood pressure significantly. From this study, it seems likely that severe renal ischemia caused by renal clipping caused the activation of the renin-angiotensin and the sympathetic nervous system and elevation of serum vasopressin. However, there are no apparent differences between the benign and malignant phases of renovascular hypertension, except for the marked elevation of neurohormone levels in malignant hypertension.
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PMID:Characterization of neurohormonal changes following the production of the benign and malignant phases of two-kidney, two-clip Goldblatt hypertension. 288 73

The cardiovascular responses to selective alpha 1- and alpha 2-adrenoceptor antagonism (with prazosin and idazoxan, respectively) were assessed in rats 4 weeks after unilateral nephro-adrenalectomy, contralateral adrenal enucleation and the provision of a 1% NaCl solution as drinking fluid (AEN rats) and in sham-operated (SON) rats. Measurements were made between 0700 and 1000 h and between 1400 and 1700 h, since we have previously shown that resting blood pressures (BPs) in AEN rats are higher in the morning than in the afternoon. Following prazosin administration (morning or afternoon), BP fell to similar levels in both SON and AEN rats. Idazoxan, given 20 min after the start of prazosin infusion, caused similar transient falls in BP in all four groups of rats. Following the subsequent additional antagonism of angiotensin II (Ang II) production (with captopril) and vasopressin (V1) receptors [with d(CH2)5DAVP], BP in AEN rats studied in the morning was higher than in SON rats at that time of day, and higher than in AEN rats studied in the afternoon. These findings suggest than an additional underlying mechanism capable of increasing BP exists in AEN rats studied in the morning.
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PMID:The cardiovascular responses to sequential inhibition of alpha-adrenoceptors, the renin-angiotensin system and vasopressin in rats with adrenal regeneration hypertension. 289 90

Administration of angiotensin II (Ang II) into the cerebral ventricles (icv) of rats elicits vasopressin release and an increase in blood pressure. The effect of atrial natriuretic factor (ANF) on these actions of ANG II was studied in conscious spontaneously hypertensive rats. The magnitude and time course of the blood pressure increase following ANG II (50 and 100 ng) were not altered by ANF, icv. However, vasopressin levels which were stimulated from 10.8 +/- 1.5 to 62.1 +/- 6.4 pq/ml by ANG II (100 ng) were significantly suppressed by combined administration of ANG II (100 ng) and ANF (3 ug/kg) (33.0 +/- 4.3 pg/ml). The injection of ANF alone into the cerebral ventricles had no effect on resting blood pressure or vasopressin levels. Peripheral administration of ANF was unable to attenuate the ANG II-induced vasopressin release. These data suggest that there exists a central interaction of ANF and ANG II within the brain which cannot be mimicked by peripheral administration of ANF.
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PMID:Angiotensin II-induced vasopressin release is attenuated by central atrial natriuretic factor. 295 10

In order to investigate the physiological role of the brain renin-angiotensin system in the regulation of vasopressin (ADH) release, angiotensin II (Ang II, 10 ng/kg/min) or 1-Sar-8-Ile-Ang II (50 ng/kg/min), an Ang II antagonist, was administered intracerebroventricularly to dogs (n = 42) anesthetized with urethane and chloralose after morphine sedation. The effects of the intravenous infusion of either 0.15 M or 2.5 M NaCl (0.1 ml/kg/min, 75 min) were also studied. In control dogs, artificial cerebrospinal fluid (ACSF) was administered at a rate of 10 microliter/min for 105 min. ACSF given intracerebroventricularly plus 0.15 M NaCl given intravenously did not affect ADH release, but 2.5 M NaCl given intravenously raised the plasma ADH level in parallel with the rise in plasma osmolality. Heart rate and blood pressure did not change significantly in ACSF along with 0.15 M NaCl, but heart rate increased significantly in ACSF along with 2.5 M NaCl. Ang II along with 0.15 M NaCl significantly raised plasma ADH and decreased heart rate without any changes in blood pressure. Ang II along with 2.5 M NaCl brought about a significant rise in plasma ADH level, arterial blood pressure, heart rate, and plasma osmolality. But simultaneous application of Ang II and 2.5 M NaCl did not result in a larger rise in plasma ADH than that expected from the effects of the two stimulations given separately. Namely, Ang II did not potentiate ADH release elicited by osmotic stimulation. Ang II antagonist given intracerebroventricularly neither affected ADH release and the cardiovascular system in 0.15 M NaCl nor inhibited ADH release in response to osmotic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of intracerebral angiotensin receptors in the regulation of vasopressin release and the cardiovascular system. 301 65

Studies of the in vivo and in vitro metabolism of angiotensin peptide precursors, and of angiotensin II (Ang II) in tissues, has revealed the possibility that some of the fragments formed through specific enzymatic pathways are bioactive. There is evidence that Ang III is as potent as Ang II in stimulating thirst and causing aldosterone secretion. New findings from this laboratory have led us to reevaluate the concept that fragments of angiotensins derived from the amino (N-) terminus are devoid of biological activity. Using in vitro and in vivo techniques, we showed that Ang-(1-7) is processed from Ang I in amounts equal to or greater than Ang II. In addition, Ang-(1-7) generation is not dependent upon Ang I converting enzyme (ACE) activity in homogenates of canine brain stem. This heptapeptide promotes release of vasopressin from perifused hypothalamo-neurohypophysial explant and stimulates neural responses when microinjected into the vagal-solitary complex. The data supporting these findings are discussed below.
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PMID:A hypothesis regarding the function of angiotensin peptides in the brain. 307 20

The production of prostaglandins by rat renal tubular cells and by rat vascular smooth muscle cells (VSMC) in response to vasoactive hormones was examined. A superfusion technique was used to stimulate collagenase-dispersed renal cortical or medullary tubular cells and trypsinized rat aortic smooth muscle cells with vasoactive hormones and ANF. All cell types responded promptly to the stimuli in a dose-dependent manner. Renal tubular cells produced mainly PGE2, less PGF2 alpha and no 6-keto-PGF1 alpha, while VSMC produced exclusively 6-keto-PGF1 alpha. This production of PG was strictly dependent on the presence of extracellular Ca2+ and was not inhibited by antagonists of voltage-dependent Ca2+-channels. Angiotensin II (Ang II) was active on cortical tubular cells and VSMC. Sar1-Ala8-angiotensin II blocked this action. Arginine-vasopressin (AVP acted on medullary tubular cells and VSMC and its effect was inhibited by selective V1-antagonists. The V2-agonist dDAVP had no effect on PG production. A clear distinction between V1-receptor mediated PG release and V2-receptor mediated cAMP extrusion was observed in medullary tubular cells. Bradykinin was a weak agonist on medullary tubular cell. The synthetic (1-24) atrial natriuretic peptide did not prevent 6-keto-PGF1 alpha release induced by Ang II or AVP in VSMC nor the PGE2 release in cortical tubular cells induced by Ang II.
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PMID:The regulation of prostaglandins by vasoactive hormones in renal tubular and vascular smooth muscle cells. 312 55

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