Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The brain is one of the organs where an intrinsic renin-angiotensin system (RAS) has been described. Stimulation of circumventricular or brainstem angiotensin II (Ang II) receptors engenders a distinct pattern of cardiovascular, endocrine, and behavioral responses featuring blood pressure increase, attenuation of the baroreceptor reflex, drinking, release of pituitary hormones such as vasopressin, oxytocin, and ACTH, and natriuresis. In contrast to most of the other central actions of Ang II, the natriuretic effect cannot be elicited by Ang II as a circulating hormone. Recently, we have shown that stimulation of Ang II AT-1 receptors in the circumventricular organs causes a selective release of norepinephrine (NE) in the paraventricular nucleus (PVN) and in the supraoptic nucleus (SON). As vasopressin is also released from the PVN and SON, it is possible that the Ang II-NE interaction is involved in the release of vasopressin, thereby contributing to central blood pressure regulation and volume control. Finally, a substantial body of results suggests that an overactivity of the brain renin-angiotensin system is one of the contributors to genetic hypertension. However, this idea needs further confirmation.
 ...
PMID:Role of brain angiotensin in cardiovascular regulation. 138 68

Hypothalamic and neurophypophyseal levels of catecholamines and peptides were measured in spontaneous and deoxycorticosterone (DOCA)/salt hypertension. Catecholamines, norepinephrine, epinephrine and dopamine were measured by electrochemical detection while the peptides, vasopressin, oxytocin, luteinizing hormone-releasing hormone (LHRH), the enkephalins and somatostatin (SRIF) were measured by radioimmunoassay. Blood pressure was significantly elevated in both groups as compared to their controls. Marked changes in central neural peptides were observed in the SHR, while no differences were seen in DOCA/salt hypertension. Hypothalamic vasopressin, oxytocin, LHRH and SRIF were significantly decreased. In the posterior pituitary, enkephalins were increased twofold in the SHR. With regard to catecholamines, there was no change in hypothalamic content. However, a dramatic decrease in neurohypophyseal dopamine was observed in SHR. Plasma levels of vasopressin were significantly elevated in both types of hypertension while oxytocin was increased only in the DOCA/salt model. These result show that (1) a wide spectrum of neuroendocrine changes are associated with genetic hypertension, (2) there are CNS differences between DOCA/salt and spontaneous hypertension, and (3) central aminergic changes may be involved in th neuroendocrine alterations seen in the SHR.
 ...
PMID:Central neural peptides and catecholamines in spontaneous and DOCA/salt hypertension. 611 62

To investigate the role of arginine vasopressin (AVP) in genetic hypertension, we measured 24-h urinary volume, osmolality, and 24-h AVP excretion, as well as pituitary and pineal AVP and oxytocin levels, in genetically hypertensive (LH), normotensive (LN), and low blood pressure (LL) 5-and 45-week-old female rats of the Lyon strains. We also determined vascular sensitivity to AVP, norepinephrine, and angiotensin II in 6- and 21-week-old rats. AVP secretion was increased in both LH and LL rats compared with LN controls. Previous reports of increased AVP secretion in spontaneously hypertensive rats have suggested that AVP might play a role in high blood pressure. The existence of a similar increase in LL rats indicates that genetic hypertension of LH rats is not related directly to their increased AVP secretion. Furthermore, the vascular sensitivity to AVP was not specifically enhanced in 21-week-old LH rats compared with LN and LL controls. This study provides evidence against a major role of vasopressin in the genesis and maintenance of high blood pressure in this model of experimental hypertension, and emphasizes that the choice of controls in such investigations is of crucial importance.
 ...
PMID:Vasopressin and oxytocin in genetically hypertensive rats of the Lyon strain. 619 19

MK 421, at the dose of 25 mg/kg, administered daily by gavage to spontaneously hypertensive rats (SHRs) from their 4th to 15th weeks of age almost completely inhibited development of genetic hypertension. Since heart rate and cardiac and systolic indexes were not affected by the drug, prevention of genetic hypertension development was solely related to an early, potent and long-lasting reduction of the progressive increase of the peripheral resistance which generally develops in SHRs during ageing. MK 421 reduced body growth but did not modify fluid intake, plasma NA+ and urine volume, thus water and salt retention did not develop. MK 421 enhanced vascular responsiveness to norepinephrine and angiotension II and reduced myocardial hypertrophy. Plasma renin concentration was increased and urinary antidiuretic hormone did not change. Finally, MK 421's preventive effects against genetic hypertension development persisted up to 10 weeks after discontinuation of treatment.
 ...
PMID:MK 421 and prevention of genetic hypertension development in young spontaneously hypertensive rats. 628 98

The potential role of central neuroendocrine changes in the development of spontaneous hypertension was evaluated. The developmental changes in blood pressure and hypothalamic and plasma levels of vasopressin (AVP) and oxytocin (OT) were determined in groups of SHR and WKY animals from 3 to 24 weeks of age. Hypothalamic OT content was significantly lower in 3-, 6-, and 12-week-old SHR rats compared to age-matched WKY animals. Hypothalamic AVP content was not different at 3 weeks of age, but was lower in the SHRs at 6 and 12 weeks. To localize strain differences in AVP and OT, specific hypothalamic nuclei were removed from 300 microns frozen brain sections, and hormone content measured. Paraventricular AVP and OT content was lower in the SHRs which had increased blood pressure (6, 12, and 24 weeks of age) but not in the prehypertensive groups (3 weeks of age). Neuropeptide content was unchanged in the supraoptic nucleus or median eminence. Plasma levels of AVP were increased in the SHR, while OT was unchanged. Thus, genetic hypertension is associated with specific and localized changes in hypothalamic AVP and OT. The fact that the peptide deficit occurred in the paraventricular nucleus, a region thought to be involved in the control of autonomic function, may have important implications in terms of the pathogenesis of hypertension.
 ...
PMID:Changes in paraventricular vasopressin and oxytocin during the development of spontaneous hypertension. 686 74

A study was performed to investigate the neurohypophyseal dopaminergic axis in terms of its biosynthetic activity and possible changes associated with spontaneous hypertension (SHR). An in vitro system was used in which isolated neuro-intermediate lobes were incubated with the catecholamine precursor, 3H-tyrosine. Dopamine (DA) content and 3H-DA were monitored using electrochemical detection coupled with high pressure liquid chromatographic separation. A time course study showed that there was significant incorporation of 3H-tyrosine into 3H-DA. In the SHR, both neurohypophyseal DA content and biosynthetic activity were reduced. Tissue levels of 3H-DA decreased from 651 to 297 dpm/posterior pituitary. A test of the effect of dehydration on neurohypophyseal dopaminergic activity revealed that water deprivation (48 hrs) caused an increase in DA biosynthesis in the hypertensive, but not the normotensive animal. This may have been due to a greater stimulation of the neurohypophyseal axis in the SHR since these animals showed significantly higher plasma vasopressin levels and hematocrits in response to dehydration. These results demonstrate that the neurohypophysis contains an active dopaminergic system which is altered in genetic hypertension.
 ...
PMID:Neurohypophyseal dopamine biosynthesis in the spontaneously hypertensive rat. 733 97

Abnormalities of the vasopressin system are found in genetic hypertension. This study compares the delayed effects of a brief period of vasopressin V1A receptor blockade and angiotensin-converting enzyme inhibition in young female and male spontaneously hypertensive rats (SHR) on the development of hypertension in adult life. In a separate study, the role of vasopressin in the maintenance of blood pressure in adult SHR was assessed. Young SHR received either the nonpeptide vasopressin V1A receptor antagonist OPC-21268, the angiotensin-converting enzyme inhibitor ramipril, or vehicle from 6 to 10 weeks of age. During the treatment period, OPC-21268 and ramipril reduced systolic blood pressure compared with control SHR (P < .001). Blood pressure in male SHR 7 weeks after treatment withdrawal was 178 +/- 1 mm Hg in ramipril-treated, 184 +/- 1 mm Hg in OPC-21268-treated, and 200 +/- 2 mm Hg in control SHR (P < .001). Similar results were seen in female SHR, although both OPC-21268 and ramipril were less effective antihypertensive agents in female compared with male SHR. The sustained attenuation in blood pressure was not associated with significant cardiovascular structural changes (left ventricular-to-body weight ratio, renal weight-to-body weight ratio, mesenteric resistance artery media-to-lumen ratio). Results of vasopressin V1A receptor binding kinetics and plasma renin or aldosterone concentrations did not suggest a lasting effect of OPC-21268 on the vasopressin system or of ramipril on the renin-angiotensin system following treatment withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Attenuation of genetic hypertension after short-term vasopressin V1A receptor antagonism. 759 Oct 25

We profiled the concentrations of angiotensin I (Ang I), angiotensin II (Ang II), and angiotensin(1-7) [Ang(1-7)] by the combination of radioimmunoassay and high performance liquid chromatography in the blood of 14-week-old male Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) drinking either tap water or a solution containing ceranapril (30 mg/kg) or lisinopril (20 mg/kg) for 14 days. Differences in the chemical and pharmacokinetic properties of the two converting enzyme inhibitors ruled out class-related effects. Plasma renin activity, angiotensin converting enzyme (ACE) activity, and plasma levels of Ang I and Ang II were the same in vehicle-treated WKY and SHR. In contrast, plasma levels of both Ang(1-7) and vasopressin in SHR were 3.7-fold and 2.6-fold higher, respectively (p < 0.05). Angiotensin converting enzyme inhibition reduced the blood pressure of WKY and SHR, and augmented their intake of water and output of urine. These changes were associated with increases in renin activity and plasma levels of Ang I and Ang(1-7). In both WKY and SHR, lisinopril had a greater effect in inhibiting plasma and cerebrospinal fluid ACE, reducing levels of plasma angiotensinogen, and increasing the concentrations of authentic Ang II. The principal finding of this study is that plasma Ang(1-7) is the sole component of the circulating angiotensin system that is elevated in the established phase of genetic hypertension. The finding that chronic inhibition of ACE augments circulating levels of Ang(1-7) evidenced the existence of functional pathways for the alternate processing of Ang I.
 ...
PMID:Angiotensin(1-7) in the spontaneously hypertensive rat. 828 65

The amiloride-sensitive epithelial Na+ channel is formed by the assembly of three homologous subunits, alpha, beta and gamma. The channel is characterized by its sensitivity to amiloride and to some amiloride derivatives, such as phenamil and benzamil, by its small unitary conductance (approximately 5 pS), by its high selectivity for lithium and sodium, and by its slow kinetics. The alpha-, beta-, and gamma-proteins share significant identity with degenerins, a family of proteins found in the mechanosensory neurons and interneurons of the nematode Caenorhabditis elegans. They are also homologous to FaNaCh, a protein from Helix aspersa nervous tissues, which corresponds to a neuronal ionotropic receptor for the Phe-Met-Arg-Phe-NH2 peptide. All these proteins contain a large extracellular loop, located between two transmembrane alpha-helices. The NH2 and COOH terminal segments are cytoplasmic and contain potential regulatory segments that are able to modulate the activity of the channel. Accordingly, in Liddle syndrome, in which patients develop a form of genetic hypertension, mutations within the cytoplasmic COOH terminal of the beta- and gamma-chains of the epithelial Na+ channel lead to a hyperactivity of the channel. Epithelial Na+ channel activity is tightly controlled by several distinct hormonal systems, including corticosteroids and vasopressin. In kidney and colon, aldosterone is the major sodium-retaining hormone, acting by stimulation of Na+ reabsorption through the epithelium. In the distal colon from steroid-treated animals, a large increase in beta- and gamma-subunit transcription is observed, whereas the alpha-subunit remains constitutively transcribed. In kidney, RNA levels of the three subunits are not altered by aldosterone, suggesting that other mechanisms control Na+ channel activity in that tissue. In lung, the glucocorticoids are positive regulators of the channel activity, especially around birth, and act via an increased transcription of the three subunits.
 ...
PMID:Molecular biology of the amiloride-sensitive epithelial Na+ channel. 873 81

The development of hypertension in the spontaneously hypertensive rat (SHR) is associated with renal dysfunction; the observed renal vasoconstriction may reflect an imbalance of constrictor and dilator systems. The present studies evaluated renal vascular reactivity to arginine vasopressin (AVP) and mediation by V1 and/or V2 receptors. Renal blood flow (electromagnetic flowmetry) was measured in water-loaded, 8-wk-old SHR, Wistar-Kyoto rats (WKY), and Munich-Wistar rats. Injection of AVP (2 and 5 ng) into the renal artery caused dose-dependent renal vasoconstriction. The maximum blood flow response was approximately twofold larger in SHR than both normotensive strains. The strain difference was largely unaffected by indomethacin administration, although the reduction in blood flow produced by 5 ng AVP was 4-6% larger in both SHR and WKY during cyclooxygenase inhibition. The V1 receptor antagonist, [D-(CH2)5,Tyr(Me)2,Tyr(NH2)9]Arg8-vasopressin, blocked up to 90% of the renal vasoconstriction elicited by AVP. Intrarenal injection of the V1-receptor agonist [Phe2,Ile3,Org8]vasopressin produced renal hemodynamic effects similar to AVP; this agonist reduced renal blood flow, with twofold larger responses in SHR (-40 vs. -18% for 10 ng). In contrast, similar doses of the V2-receptor agonist 1-desamino-8-D-arginine vasopressin had no effect. These results indicate that AVP-induced vasoconstriction is mediated predominantly by the V1 receptor in the rat kidney. The enhanced vascular reactivity in 8-wk-old SHR may reflect an increased V1 receptor density and/or affinity or postreceptor signaling pathways, largely independent of buffering by the vascular V2 receptor or vasodilator prostaglandin activity. The strain difference in the vascular response to AVP may contribute to the renal vasoconstriction observed during the development of genetic hypertension.
 ...
PMID:Enhanced renal vasoconstriction induced by vasopressin in SHR is mediated by V1 receptors. 877 Jan 61


1 2 3 Next >>