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)

The natriuretic peptide system consists of three endogenous ligands, i.e., atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), and at least three subtypes of receptors. All of the peptides and receptors exist in the central nervous system (CNS). ANPs in the brain are N-terminally truncated forms: ANP (4-28) and ANP (5-28). The primary structure of BNP varies considerably among species, whereas that of CNP is highly conserved. ANP, BNP, and CNP are distributed in discrete brain regions, although the distribution varies in different species. Few immunohistochemical studies have so far been performed on BNP and CNP. There are three subtypes of receptors: ANP-A and ANP-B, which are bioactive, and the C receptor, which does not seem to be directly related to bioactivity. In the rat, the major subtype of ANP receptor in the CNS is the ANP-B receptor, based on the results of Northern blotting. Since the ligand for ANP-B receptor is CNP, the CNP-ANP-B receptor system may be most important, at least in rat brain. It is still unknown whether or not a specific receptor for BNP exists in central or peripheral tissues. Further studies should clarify the exact localization of ANP, BNP, and CNP and the three receptor subtypes in the CNS. Although natriuretic peptides and their receptors are distributed widely in the CNS, the AV3V regions, basal medial hypothalamus, brainstem, and circumventricular organs are the most prominent sites. This suggests an important physiological role of the natriuretic peptide system in the central control of cardiovascular homeostasis. The natriuretic peptide system seems to be involved in the regulation of water and salt intake, blood pressure, and secretion of vasopressin in the direction of reducing body fluid and lowering blood pressure. Such actions of natriuretic peptides are antagonistic to the central actions of angiotensin II (AII). In fact, the distribution of ANP and AII and their receptors in the CNS overlaps considerably. It is highly likely, therefore, that the central natriuretic peptide system and the renin-angiotensin system play important roles in the central control of cardiovascular and body fluid homeostasis in opposite directions. The natriuretic peptide system may also be involved in neuroendocrine control and some other CNS functions, although the physiological significance of these actions is less clear at the present time. It is now clear that there is considerable plasticity in the regulation of natriuretic peptides and their receptors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The natriuretic peptide system in the brain: implications in the central control of cardiovascular and neuroendocrine functions. 133

The endolymphatic sac (ES) is believed to absorb the endolymphatic fluid produced by the stria vascularis and vestibular dark cells. Recent studies have implied that the function of the ES may be controlled by circulating hormones, suggesting that hormone receptors should exist there. In the present study, the expression of genes encoding receptors for aldosterone, atrial natriuretic peptide (ANP) and vasopressin in the ES was examined by reverse transcription-polymerase chain reaction (RT-PCR). Next, the cellular localization of the expression of these genes was investigated by in situ hybridization. RT-PCR indicated that aldosterone. ANP-A and vasopressin V1a receptor genes were expressed in the ES. In contrast, neither ANP-B nor vasopressin V2 receptor gene expression was detected. In situ hybridization experiments demonstrated aldosterone receptor gene expression in epithelial cells of the intermediate potion of the ES, while expression of ANP-A or V1a receptor genes was not detected. The present results suggested that aldosterone may play a specific role in the function of the ES. However, we could not conclude that ANP and vasopressin play physiological roles in the ES because receptors for these hormones were detected only by highly sensitive PCR.
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PMID:Expression of mRNAs encoding hormone receptors in the endolymphatic sac of the rat. 1021 85

1. The renal medulla plays an important role in regulating body sodium and fluid balance and blood pressure homeostasis through its unique structural relationships and interactions between renomedullary interstitial cells (RMIC), renal tubules and medullary vasculature. 2. Several endocrine and/or paracrine factors, including angiotensin (Ang)II, endothelin (ET), bradykinin (BK), atrial natriuretic peptide (ANP) and vasopressin (AVP), are implicated in the regulation of renal medullary function and blood pressure by acting on RMIC, tubules and medullary blood vessels. 3. Renomedullary interstitial cells express multiple vasoactive peptide receptors (AT1, ETA, ETB, BK B2, NPRA and NPRB and V1a) in culture and in tissue. 4. In cultured RMIC, AngII, ET, BK, ANP and AVP act on their respective receptors to induce various cellular responses, including contraction, prostaglandin synthesis, cell proliferation and/or extracellular matrix synthesis. 5. Infusion of vasoactive peptides or their antagonists systemically or directly into the medullary interstitium modulates medullary blood flow, sodium excretion and urine osmolarity. 6. Overall, expression of multiple vasoactive peptide receptors in RMIC, which respond to various vasoactive peptides and paracrine factors in vitro and in vivo, supports the hypothesis that RMIC may be an important paracrine target of various vasoactive peptides in the regulation of renal medullary function and long-term blood pressure homeostasis.
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PMID:Renomedullary interstitial cells: a target for endocrine and paracrine actions of vasoactive peptides in the renal medulla. 1087

The binding of atrial natriuretic peptide and C-type natriuretic peptide (CNP) to the guanylyl cyclase-linked natriuretic peptide receptors A and B (NPR-A and -B), respectively, stimulates increases in intracellular cGMP concentrations. The vasoactive peptides vasopressin, angiotensin II, and endothelin inhibit natriuretic peptide-dependent cGMP elevations by activating protein kinase C (PKC). Recently, we identified six in vivo phosphorylation sites for NPR-A and five sites for NPR-B and demonstrated that the phosphorylation of these sites is required for ligand-dependent receptor activation. Here, we show that phorbol 12-myristate 13-acetate, a direct activator of PKC, causes the dephosphorylation and desensitization of NPR-B. In contrast to the CNP-dependent desensitization process, which results in coordinate dephosphorylation of all five sites in the receptor, phorbol 12-myristate 13-acetate treatment causes the dephosphorylation of only one site, which we have identified as Ser(523). The conversion of this residue to alanine or glutamate did not reduce the amount of mature receptor protein as indicated by detergent-dependent guanylyl cyclase activities or Western blot analysis but completely blocked the ability of PKC to induce the dephosphorylation and desensitization of NPR-B. Thus, in contrast to previous reports suggesting that PKC directly phosphorylates and inhibits guanylyl cyclase-linked natriuretic peptide receptors, we show that PKC-dependent dephosphorylation of NPR-B at Ser(523) provides a possible molecular explanation for how pressor hormones inhibit CNP signaling.
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PMID:Activation of protein kinase C stimulates the dephosphorylation of natriuretic peptide receptor-B at a single serine residue: a possible mechanism of heterologous desensitization. 1091 2

Vasopressin plays a primary role in the concentration of urine to maintain body fluid homeostasis. The collecting duct as well as thick ascending limb is a major target site of vasopressin. The antidiuretic action of vasopressin is mediated by the V2 receptor in the basolateral membrane of principal cells in the collecting ducts. The binding of vasopressin to V2 receptors causes an activation of adenylate cyclase and a synthesis of cAMP. Vasopressin regulates water and ion transport through V2 receptor-mediated ion channels and transporters. In contrast, the V1a receptor mainly in the luminal membrane of distal nephron regulates basolateral V2 receptor-mediated action with regard to water and ion transport through the activation of G(q/11) and phosphoinositide turnover. Guanylate cyclase forms three types of ANP receptors, although NPR-A and B (GC-A and B) are biologically active and related to the synthesis of cGMP. Urodilatin, synthesized by the kidney, causes natriuresis by binding to GC-A in the collecting ducts. ANP causes diuresis and natriuresis, at least in part by inhibiting the V2 receptor-mediated action of AVP in the collecting ducts. The site of interaction of ANP and AVP is post cAMP synthesis, at least in the collecting ducts. The roles of AVP and ANP under pathophysiological conditions have been reported.
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PMID:Physiological effects of vasopressin and atrial natriuretic peptide in the collecting duct. 1147 37

Natriuretic peptides bind their cognate cell surface guanylyl cyclase receptors and elevate intracellular cGMP concentrations. In vascular smooth muscle cells, this results in the activation of the type I cGMP-dependent protein kinase and vasorelaxation. In contrast, pressor hormones like arginine-vasopressin, angiotensin II, and endothelin bind serpentine receptors that interact with G(q) and activate phospholipase Cbeta. The products of this enzyme, diacylglycerol and inositol trisphosphate, activate the conventional and novel forms of protein kinase C (PKC) and elevate intracellular calcium concentrations, respectively. The latter response results in vasoconstriction, which opposes the actions of natriuretic peptides. Previous reports have shown that pressor hormones inhibit natriuretic peptide receptors NPR-A or NPR-B in a variety of different cell types. Although the mechanism for this inhibition remains unknown, it has been universally accepted that PKC is an obligatory component of this pathway primarily because pharmacologic activators of PKC mimic the inhibitory effects of these hormones. Here, we show that in A10 vascular smooth muscle cells, neither chronic PKC down-regulation nor specific PKC inhibitors block the AVP-dependent desensitization of NPR-B even though both processes block PKC-dependent desensitization. In contrast, the cell-permeable calcium chelator, BAPTA-AM (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, tetraacetoxymethyl ester), abrogates the AVP-dependent desensitization of NPR-B, and ionomycin, a calcium ionophore, mimics the AVP effect. These data show that the inositol trisphosphate/calcium arm of the phospholipase C pathway mediates the desensitization of a natriuretic peptide receptor in A10 cells. In addition, we report that CNP attenuates AVP-dependent elevations in intracellular calcium concentrations. Together, these data reveal a dominant role for intracellular calcium in the reciprocal regulation of these two important vasoactive signaling systems.
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PMID:Vasopressin-dependent inhibition of the C-type natriuretic peptide receptor, NPR-B/GC-B, requires elevated intracellular calcium concentrations. 1219 32

The aims of the present study were to determine whether natriuretic peptide receptors coupled to guanylate cyclase are present in the neural lobe (NL) of the pituitary and eventually localized on pituicytes and/or on nerve fibers and whether cyclic GMP may be involved in the regulation of vasopressin secretion. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) enhanced cyclic GMP content of NLs in a dose-related fashion, with ED(50) values of about 5 x 10(-8)M, while CNP failed to significantly elevate guanylate cyclase activity. ANP stimulated cyclic GMP accumulation in NLs lacking functional nerve fibers, while it was without significant effect on isolated nerve terminals. In the brain, ANP-enhanced cyclic GMP production was similarly expressed in glial and not in neuronal cultures, although intracellular guanylate cyclase activity (stimulated by sodium nitroprusside) was present in both cell types. Finally, the cell permeant S-bromoguanosine 3':5'-monophosphate GMP failed to change either basal or isoproterenol-stimulated vasopressin secretion from incubated NLs. We conclude that in the NL, as well as in brain tissue cultures, the guanylate cyclase-NP receptor complex (most probably the ANP-A subtype) is localized on pituicytes/filial cells rather than on nerve fibers/cells and that cyclic GMP may not be directly involved in the regulation of vasopressin output from the NL.
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PMID:Evidence for the presence of guanylate cyclase-coupled receptors for atrial natriuretic peptide on pituicytes of the neurohypophysis. 1991 20

Atrial (ANP), brain (BNP), and C-type (CNP) natriuretic peptides act by binding to three main subtypes of receptors, named NPR-A, -B, and -C. NPR-A and NPR-B are coupled with guanylate cyclase. Not only NPR-C is involved in removing natriuretic peptides from the circulation but it also acts through inhibition of adenylyl cyclase. NPR-A binds ANP and BNP; NPR-B preferentially binds CNP; and NPR-C binds all natriuretic peptides with similar affinities. All natriuretic peptides and their receptors are widely present in the hypothalamus, pituitary, adrenal cortex, and medulla. In the hypothalamus, they reduce norepinephrine release, inhibit oxytocin, vasopressin, corticotropin-releasing factor, and luteinizing hormone-releasing hormone release. In the hypophysis, natriuretic peptides inhibit basal and induced ACTH release. Conversely, the effects of natriuretic peptides on secretion of growth, luteinizing, and follicle-stimulating hormones are not clear. Natriuretic peptides are known to inhibit basal and stimulated aldosterone secretion, through an increase of intracellular cGMP, and to inhibit the growth of zona glomerulosa. Inhibition or stimulation of glucocorticoid secretion by adrenocortical cells has been reported on the basis of the species involved, and an indirect effect mediated by adrenalmedullary cells has been hypothesized. In the adrenal medulla, natriuretic peptides inhibit catecholamine release and increase catecholamine uptake. It appears that natriuretic peptides may play a role in the pathophysiology of adrenocortical neoplasias and pheochromocytomas.
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PMID:Natriuretic peptides in the regulation of the hypothalamic-pituitary-adrenal axis. 2079 80

Natriuretic peptides are a group of hormones including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C type (CNP), urodilatin and guanilyn. ANP (half-life: 2-4 min), is secreted by the atrium, BNP (half-life: 20 min) by the ventricle, CNP by the vascular endothelium, urodilatin by the kidney and guanylin by the intestine. These natriuretic peptides prevent water and salt retention through renal action, vasodilatation and hormonal inhibition of aldosterone, vasopressin and cortisol. These peptides also have a recently demonstrated metabolic effect through an increase of lipolysis, thermogenesis, beta cell proliferation and muscular sensitivity to insulin. Blood levels of these natriuretic peptides depend on "active NPR-A receptors/clearance NPR-C receptors", the last ones being abundant on adipocytes. Therefore, natriuretic peptides act as adipose tissue regulator and constitute a link between blood pressure and metabolic syndrome. They are used as markers and treatment of cardiac failure. Other applications are on going. BNP and NT-proBNP (inactive portion de la pro-hormone) are used as markers of cardiac failure since they have a longer half-life than ANP. BNP decrease is quicker and more important than that one of NT-ProBNP in case of improvement of cardiac failure. Chronic renal insufficiency and beta-blockers increase BNP levels. BNP measurement is useless under treatment with neprilysine inhibitors such as sacubitril, one of the neutral endopeptidases involved in catabolism of natriuretic peptides. The association sacubitril/valsartan is a new treatment of chronic cardiac failure, acting through the decrease of ANP catabolism.
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PMID:[Atrial natriuretic hormones and metabolic syndrome: recent advances]. 2949 76