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)

Angiotensin-(1-7) is a bioactive component of the renin-angiotensin system that is endogenously formed in the circulation and various tissues by several enzymatic pathways from either angiotensin (Ang) I or Ang II. Initial studies indicated that Ang-(1-7) mimicked some of the effects of Ang II, including stimulation of release of prostanoids and vasopressin. However, Ang-(1-7) is devoid of the vasoconstrictor, central pressor, or thirst-stimulating actions associated with Ang II. In fact, new findings reveal depressor, vasodilator, and antihypertensive actions that may be more apparent in hypertensive animals or humans. Thus, increasing evidence suggests that Ang-(1-7) may oppose the actions of Ang II directly or as a result of increasing prostaglandins or nitric oxide. In this review, we examine recent studies to address whether the kidney is a target organ for antihypertensive actions of Ang-(1-7).
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PMID:Differential actions of angiotensin-(1-7) in the kidney. 983 74

In summary, the prevailing concept is that brain Ang II increases blood pressure by activating AT1 receptors, and that these have a neuromodulating effect to increase the activity of autonomic nervous system. Pathways for Ang II stimulating thirst and blood pressure, increased vasopressin release and sympathetic activation have been outlined. Brain RAS synthesis, while incompletely understood, is active in the absence of a peripheral RAS. Angiotensin elicits specific receptor mediated signals in neurons, particularly in the hypothalamus and brainstem. These actions are due to neuronal membrane ionic currents and the regulation of transcription factors. The areas to be explored further are characterization and functional roles of the other AT receptor subtypes, such as AT4, AT(1-7) and nuclear AT-R. Their interactions with other peptides and transmitters, and their signaling pathways need to be investigated. The story that began 100 years ago with renin is certainly not ended and will continue to unfold as further investigations with new techniques progress.
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PMID:Angiotensin II in central nervous system physiology. 987 41

We previously demonstrated that the Ren-2 transgenic (TG) rat is sensitive to salt, showing a sodium-induced pressor response. The present studies determined the effect of central stimulation with hypertonic saline (HS) and angiotensin II (Ang II) on mean arterial pressure (MAP), heart rate (HR), and plasma vasopressin. HS (1 mol/L NaCl, 5 microL) or Ang II (100 ng, 5 microL) was injected into the lateral ventricle of conscious male TG and control rats. The pressor responses to HS and Ang were greater in TG than in control rats, increases of 42+/-4 and 41+/-4 mm Hg versus 25+/-3 and 18+/-2 mm Hg (HS and Ang II and TG and control rats, respectively). The TG rats also showed an increased vasopressin response to Ang II, peak levels of 14+/-3 versus 28+/-3 pg/mL (control versus TG rats). HS increased plasma vasopressin levels, although the group responses were not different. HR was not significantly altered by either stimulus. Results demonstrate an increased responsiveness to intraventricular HS and Ang II in Ren-2 transgenic rats, suggesting a relationship between the enhanced angiotensinergic drive and central cardiovascular and vasopressin responses.
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PMID:Increased central angiotensin and osmotic responses in the Ren-2 transgenic rat. 993 Nov 34

Mammalian brain contains high densities of angiotensin II (Ang II) type 1 (AT1) receptors, localized mainly to specific nuclei within the hypothalamus and brainstem regions. Neuronal AT1 receptors within these areas mediate the stimulatory actions of central Ang II on blood pressure, water and sodium intake, and vasopressin secretion, effects that involve the modulation of brain noradrenergic pathways. This review focuses on the intracellular events that mediate the functional effects of Ang II in neurons, via AT1 receptors. The signaling pathways involved in short-term changes in neuronal activity, membrane ionic currents, norepinephrine (NE) release, and longer-term neuromodulatory actions of Ang II are discussed. It will be apparent from this discussion that the signaling pathways involved in these events are often distinct.
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PMID:Angiotensin II type 1 receptor-modulated signaling pathways in neurons. 1032 70

This study assessed whether the angiotensin-II (Ang II)-induced contractile responsiveness of resistance arteries is altered during the development of hypertension in spontaneously hypertensive rats (SHR). Structural parameters and Ang II-stimulated contraction were determined in small mesenteric arteries from 6-week-old (phase of developing hypertension) and 21-week-old SHR (phase of established hypertension), compared with age-matched Wistar-Kyoto rats (WKY). To ascertain whether effects were specific for Ang II, contractile responses to another vasoactive agonist, vasopressin (AVP), were also determined. Systolic blood pressure was measured in conscious rats by the tail-cuff method. Segments of third-order mesenteric arteries (approximately 200 microm in diameter and 2 mm in length) were mounted in a pressurized system with the intraluminal pressure maintained at 45 mm Hg. Blood pressure was significantly increased in SHR (P < .001) and was higher in adult than in young SHR (P < .001). Ang II dose-dependently increased contraction, with responses significantly greater (P < .05) in SHR than in age-matched WKY. SHR, in the early phase of hypertension, exhibited significantly augmented contractile responses (Emax = 70 +/- 5%), compared with SHR with established hypertension (Emax = 33 +/- 5%). These effects were not generalized, as responses to AVP were not significantly different between young and adult SHR. Functional Ang II-elicited alterations were associated with structural modifications: 6-week-old SHR had smaller media to lumen ratio compared with 21-week-old SHR (8.1% +/- 0.17% v 10.6% +/- 0.20%, P < .01). In young SHR vessels the media cross-sectional area was unchanged relative to age-matched WKY rats, suggesting eutrophic remodeling (remodeling index 101.4% v 93.3% young v adult), whereas the cross-sectional area of adult vessels was increased in comparison to WKY rats, suggesting mild hypertrophic remodeling (growth index -1.0% v 15.2%, young v adult). In conclusion, the present study demonstrates that in SHR with early hypertension and slight medial thickening, Ang II-mediated vascular contractile responsiveness is significantly augmented compared with SHR with established hypertension and more severe vascular structural changes. These findings indicate attenuation, as hypertension progresses, of the initially enhanced vascular reactivity to Ang II that is present during the development of hypertension in SHR.
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PMID:Altered angiotensin II-induced small artery contraction during the development of hypertension in spontaneously hypertensive rats. 1041 69

The possibility of the brain-specific expression of a component of the renin-angiotensin system was evaluated in the present study. We used the hemagglutinating virus of Japan-liposome complex to transfect human angiotensin-converting enzyme (ACE) cDNA, driven by the cytomegalovirus enhancer and beta-actin promoter, into the lateral cerebroventricle of male Sprague-Dawley rats. We evaluated the time course of hemodynamics, the tissue levels of angiotensin (Ang) II and vasopressin, and ACE activity. Intracerebroventricular transfection of the human ACE gene increased both blood pressure and heart rate. Transfected rats exhibited higher concentrations of brain Ang II and increased brain ACE activity. This activation of the brain angiotensin system was accompanied by increased vasopressin production. The increases in blood pressure and heart rate were abolished by intracerebroventricular administration of an ACE inhibitor or Ang II type 1 receptor antagonist. The expression of the transgene was widely distributed in the periventricular cell layer, the cortex, the hypothalamic nuclei, and the brain stem. Expression in the neuronal cells persisted for up to 14 days. Thus, this hemagglutinating virus of Japan-liposome method is a highly efficient system for gene delivery and is extremely useful for functional gene transfection. This novel hypertensive model may enable characterization of the functions of the renin-angiotensin system in the brain and determination of its role in the pathogenesis of hypertension.
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PMID:Activation of the brain angiotensin system by in vivo human angiotensin-converting enzyme gene transfer in rats. 1045 58

The present study aimed to investigate the reactivity of cultured pituicytes from adult neurohypophysis to various bioactive substances using Ca2+ indicator dye Fura-2. A transient increase of intracellular Ca2+ [Ca2+]i was observed when pituicytes were treated with nucleotides (ATP, ADP, UTP, and UDP) and amines (5-HT2 and alpha2-agonist). Treatment with peptides such as endothelin-1 (ET-1), endothelin-3 (ET-3), bradykinin (BK), vasopressin (AVP), and angiotensin II (Ang II) also induced [Ca2+]i increase in pituicytes. Prostaglandin E2 (PGE2) and F2alpha (PGF2alpha) increased [Ca2+]i, but amino acids of GABA, glutamate (Glu), and taurine had no effect. Serum-free culture condition augmented [Ca2+]i responses to ATP, Ang II and 5-HT within 24 h. These results indicate that pituicytes express many of receptors for neurotransmitters or neuromodulators.
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PMID:Intracellular Ca2+ responses to nucleotides, peptides, amines, amino acids and prostaglandins in cultured pituicytes from adult rat neurohypophysis. 1046 4

The renin-angiotensin system (RAS) is one of the oldest known hormone systems. Its effector hormone, angiotensin (Ang) II, acts through 2 receptor subtypes, AT(1) and AT(2). Most physiologic effects of Ang II, including vasoconstriction, renal salt and water retention, aldosterone and vasopressin release, and sympathetic facilitation, are mediated by AT(1). Recent data, however, suggest that Ang II also contributes to cell proliferation, left ventricular hypertrophy, vascular media hypertrophy, neointima formation in atherosclerosis, and nephrosclerosis by stimulation of AT(1) receptors. AT(2) receptors are associated with antiproliferation, cell differentiation and development, tissue regeneration, and apoptosis. They also antagonize AT(1) receptor-mediated effects, which suggests that the ratio of angiotensin receptors expressed on a particular cell can determine the net effect of Ang II. Selective AT(1) receptor antagonists ("sartans") have been used to treat several million hypertensive patients worldwide. These agents offer a powerful therapeutic alternative to angiotensin-converting enzyme (ACE) inhibitors, which reduce the generation of Ang II. Conversely, AT(1) receptor antagonists block the RAS by acting on cellular angiotensin receptors and do not interfere with the breakdown of kinins. These medications inhibit the RAS more completely than do the ACE inhibitors because their action is independent of Ang II-generating pathways. At the same time, early, preliminary data suggest that AT(1) receptor antagonists offer target-organ protection similar to that provided by the ACE inhibitors. Because AT(2) receptors are left unopposed and Ang II levels are increased with AT(1) receptor antagonist treatment, it is important to understand the function of AT(2) to fully appreciate the mechanisms of action of AT(1) receptor antagonists, especially their potential for target-organ protection.
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PMID:Neurohormonal modulation in cardiovascular disease. 1061 81

The purpose of this investigation was to test the hypothesis that peripheral vasoconstriction and orthostatic tolerance are associated with increased circulating plasma concentrations of noradrenaline, vasopressin and renin-angiotensin. Sixteen men were categorized as having high (HT, n=9) or low (LT, n=7) tolerance to lower body negative pressure (LBNP) based on whether the endpoint of their pre-syncopal-limited LBNP (peak LBNP) exposure exceeded -60 mmHg. The two groups were matched for age, height, weight, leg volume, blood volume and maximal oxygen uptake, as well as baseline blood volume and plasma concentrations of vasoactive hormones. Peak LBNP induced similar reductions in mean arterial pressure in both groups. The reduction in leg arterial pulse volume (measured by impedance rheography), an index of peripheral vascular constriction, from baseline to peak LBNP was greater (P<0.05) in the HT group (-0.041 +/- 0.005 ml 100 ml-1) compared to the reduction in the LT group (-0. 025 +/- 0.003 ml 100 ml-1). Greater peak LBNP in the HT group was associated with higher (P<0.05) average elevations in plasma concentrations of vasopressin (pVP, Delta=+7.2 +/- 2.0 pg ml-1) and plasma renin-angiotensin (PRA, Delta=+2.9 +/- 1.3 ng Ang II ml-1 h-1) compared to average elevations of pVP (+2.2 +/- 1.0 pg ml-1) and PRA (+0.1 +/- 0.1 ng Ang II ml-1 h-1) in the LT group. Plasma noradrenaline concentrations were increased (P<0.05) from baseline to peak LBNP in both HT and LT groups, with no statistically distinguishable difference between groups. These data suggest that the renin-angiotensin and vasopressin systems may contribute to sustaining arterial pressure and orthostatic tolerance by their vasoconstrictive actions.
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PMID:Vasoactive neuroendocrine responses associated with tolerance to lower body negative pressure in humans. 1079 10

The effects of cold-restraint stress, repeated over 3 days, and treatment of rats with vasoactive intestinal peptide (VIP) on the contractile responses of isolated aorta to vasoconstrictors, and on aortic adventitial mast cells were investigated. Stress significantly reduced the contractile response of rat aorta smooth muscle to norepinephrine (NE), angiotensin II (Ang II) and vasopressin (VP). Decreased sensitivity to NE, Ang II and VP may result from decreased receptor density, and affinity or reduced effector efficacy. Stress induced degranulation, decreased the number and changed the granular content of mast cells; all degranulated mast cells were stained with alcian blue, and the percentage of safranin staining cells was decreased. Given prior to stress, VIP reversed the reduced contractile responses and sensitivity of aorta to NE and Ang II but had no effect on VP subsensitivity. VIP also inhibited stress-induced degranulation of mast cells, and after VIP only alcian blue-stained mast cells were seen. When VIP was given to non-stressed rats, the contractile response of the aorta to NE, but not Ang II or VP, was increased compared with control. Mast cell count was decreased in the adventitia of non-stressed VIP treated rats. The results indicate that stress decreases the heparin content of mast cells and VIP has an additive effect. In conclusion, VIP modulates both stress-induced mast cell activity and reduced sensitivity of aorta smooth muscle to NE and Ang II. It can be suggested that VIP may moderate some effects of stress on vascular pathophysiology.
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PMID:The effect of stress and in vivo vasoactive intestinal peptide (VIP) treatment on the response of isolated rat aorta to norepinephrine, angiotensin II and vasopressin, and adventitial mast cells. 1134 95


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