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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using dispersed cultures of fetal rat hypothalami, we studied the effects of forskolin and the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), activators of protein kinase A and C, respectively, upon vasopressin (VP) secretion, VP mRNA expression and VP mRNA poly(A) tail length. Forskolin stimulated the VP mRNA content and peptide secretion 2.6-fold and induced an increase in the poly(A) tail length of approximately 90 nucleotides. TPA induced an increase in VP mRNA size and stimulated 1.9-fold the secretion of VP without an increase in VP mRNA content. Depolarization with potassium induced an increase in the VP peptide secreted of 2.2-fold, with no effect on the VP mRNA content or size. Increased osmolality had no effect on either VP peptide or VP mRNA. We conclude that VP expression in cultured fetal rat hypothalamic cells is regulated via both protein kinase A and protein kinase C pathways.
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PMID:Regulated expression of vasopressin gene by cAMP and phorbol ester in primary rat fetal hypothalamic cultures. 135 50

Methods of blocker-induced noise analysis were used to investigate the way in which forskolin and vasopressin stimulate Na transport at apical membranes of short-circuited frog skin transporting Na at spontaneous rates of transport. Experiments were done under conditions where the apical Ringer solution contained either 100 mM Na or a reduced Na concentration of 5 or 10 mM Na and buffered with either HCO3 or HEPES. Reduction of apical solution Na concentration caused a large autoregulatory increase of Na channel density (NT) similar in magnitude to that observed previously in response to blocker (amiloride) inhibition of apical membrane Na entry. Forskolin at 2.5 microM caused maximal and reversible large increases of NT, which were larger than could be elicited by 30 mU/ml vasopressin. In both the absence and presence of the autoregulatory increase of NT (caused by reduction of apical Na concentration), forskolin caused large increases of NT. Although the fractional increases of NT in response to forskolin were roughly similar, the absolute increases of NT were considerably larger in those tissues studied at reduced Na concentration and where baseline values of NT were markedly elevated by reduction of apical Na concentration. Because the effects on NT were additive, it is likely that the cAMP-dependent and autoregulatory mechanism that lead to changes of NT are distinct. We speculate that autoregulation of NT may involve change of the size of a cytosolic pool of Na-containing vesicles that are in dynamic balance with the apical membranes. cAMP-dependent regulation of NT may involve change of the dynamic balance between vesicles and the apical membranes of these epithelial cells. Alternative hypotheses cannot at present be ruled out, but will require incorporation of the idea that regulation of NT can occur both by hormonal and nonhormonal (autoregulatory) mechanisms of action.
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PMID:Activation of epithelial Na channels by hormonal and autoregulatory mechanisms of action. 166 57

Urinary osmotic concentration capacity during renal ontogeny is subject to changes of medullary cytoarchitecture and of segmental epithelial transport characteristics. Osmotic equilibrium between interstitial and tubular fluid of the terminal nephron segment in response to vasopressin is an absolute essential of maximal urinary osmotic concentration. The regulation of osmotic water permeability (Pf) in this terminal epithelial segment during ontogenetic differentiation has not been documented. The inner medullary collecting duct (IMCD), the terminal 40% of total segmental length, was dissected at two stages of postnatal ontogenetic differentiation from immature (days 7-15) and from mature (days 33-37) rat kidneys and perfused in vitro. Pf (micron/s) was measured (bath hyperosmotic) in the absence and presence of arginine vasopressin (AVP, 230 pM). Basal Pf was 32.3 +/- 4.03 (n = 26) in the immature IMCD (IMCDi) and 111.5 +/- 20.6 (n = 15) in the mature segment (IMCDm). AVP increased Pf in IMCDi from 46.4 +/- 10.5 to 102 +/- 25.7 micron/s, whereas in IMCDm the AVP-dependent change of Pf was from 104.2 +/- 41.2 to 693 +/- 176 micron/s. AVP (2,300 pM) did not further increase Pf in IMCDi. Forskolin (50 microM) changed Pf in IMCDi from 34.9 +/- 6.3 to 104.1 +/- 16 micron/s; the corresponding change in IMCDm was from 150 +/- 32 to 985.8 +/- 133 micron/s. An analogue of adenosine 3',5'-cyclic monophosphate (cAMP; 10(-3) M) increased Pf in IMCDi from 35.5 +/- 11.4 to 138.5 +/- 32.6 and in IMCDm from 79.6 +/- 32.3 to 702.2 +/- 283 micron/s.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of osmotic water permeability during differentiation of inner medullary collecting duct. 203 57

The recent isolation of vasopressin (VP) from the rat and human pancreas led us to investigate the effects of VP on insulin secretion. In the SV 40-transformed hamster beta cell line (HIT), 0.1-1.0 nM VP caused rapid stimulation of insulin secretion. Slight but significant inhibition of insulin secretion was observed in the presence of 10 pM VP. These effects of VP on insulin secretion were paralleled by dose-dependent changes in inositol phosphate (IP) production, indicating mediation by V1-type VP receptors. VP stimulated IP3 production at 30 sec and production of IP1 by 60 sec. VP (0.1 nM to 1 microM) failed to stimulate the release or cellular content of cAMP, whereas forskolin was an effective stimulus. Forskolin and VP together caused at least additive stimulation of insulin secretion. Taken together, these observations indicate that VP is not acting via V2-mediated pathways. However, VP-induced stimulation of insulin and IP production were only slightly inhibited by a V1a pressor antagonist in 100- or 1,000-fold excess, indicating that VP effects are not mediated by V1a receptors. The V1 receptor involved may represent a V1b or a novel type of VP receptor. These observations suggest a potential physiological role of VP in regulating insulin secretion.
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PMID:Effects of vasopressin on insulin secretion and inositol phosphate production in a hamster beta cell line (HIT). 215 17

Addition of vasopressin to hypothalamo-neurohypophysial explants in vitro increased cyclic AMP accumulation whereas exogenous oxytocin decreased cyclic AMP. An opposite response pattern was observed in the neural lobe of the pituitary where vasopressin decreased and oxytocin increased cyclic AMP accumulation. Forskolin elicited a 3-fold greater increase in cyclic AMP in the neural lobe than in the supraoptic nucleus and enhanced the sensitivity of the tissues to both vasopressin and oxytocin. The ability of both vasopressin and oxytocin to modulate local cyclic AMP metabolism suggests the possibility of internal feedback within the hypothalamo-neurohypophysial system.
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PMID:Vasopressin and oxytocin regulation of cyclic AMP accumulation in rat hypothalamo-neurohypophysial explants in vitro. 216 30

HRA-19a1.1. cells, derived from a primary human rectal adenocarcinoma, form polarised monolayers when grown on tissue-culture plastic. HRA-19 monolayers have a heterogeneous morphology even after 150 passages in vitro or single cell cloning. The morphological changes observed in HRA-19 monolayers were postulated to be the result of vectorial fluid transport leading to accumulation of fluid between cells. To test this hypothesis, a variety of agents that control ion transport in colorectal epithelium were tested for their effect on HRA-19 morphology. Forskolin, cholera toxin and prostaglandin E2 all markedly changed HRA-19 monolayer morphology, with the rapid disappearance of intercellular spaces. These agents all stimulate Cl- secretion in colorectal epithelium, i.e. transport from basolateral to apical surface, and therefore would be expected to reduce fluid accumulation at the basolateral side of the cell. Conversely, vasopressin, which stimulates absorption of Na+ and water across colorectal epithelium, leads to a small increase in intercellular spaces in the monolayer. In collagen gel cultures, addition of cholera toxin, forskolin or prostaglandin E2 resulted in a large increase in colony size. In such treated cultures, the colonies were 'bubble-like', often composed of a single rim of flattened cells, which appeared to encompass a fluid-filled space. Similar morphological changes were observed when HRA-19 cells were co-cultured with 3T3 cells. This effect was probably due, at least in part, to prostaglandin production by the 3T3 cells, as the effect could be markedly reduced by the addition of indomethacin to these cultures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Control of fluid transport in human rectal adenocarcinoma cells (HRA-19) in monolayer and collagen gel cultures. 219 Sep 94

Forskolin, a natural diterpene activating the adenyl cyclase in a receptor-independent manner, increases symmetrically both transepithelial fluxes of urea and erithrytol through the frog skin. The effect is dose-dependent, being 5 X 10(-6) M the dose necessary to obtain the maximal action. Forskolin-induced permeabilization is inversely proportional to the molecular weight of water soluble molecules (urea greater than erythritol greater than mannitol); also the permeability of a mainly lipid soluble molecule, i.e. antipyrine, is slightly increased by the diterpene. The permeability pattern is more similar to that induced by isoprenaline as compared to that elicited by vasopressin. Differently from what occurs in other tissues, small doses of forskolin (10(-8) M) are unable to potentiate the actions of vasopressin and isoprenaline on urea permeability across the frog skin. Moreover, the maximal action of forskolin is not additive with the maximal ones of isoprenaline and vasopressin.
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PMID:Action of forskolin on non-electrolyte permeability across the frog skin as compared to that of vasopressin and isoprenaline. 244 77

Electrically stimulated release of vasopressin from isolated rat neurohypophysis was measured in the presence and absence of forskolin. Forskolin inhibited the release of vasopressin evoked by continuous stimulation at constant frequency, and enhanced the release evoked by trains of pulses separated by silent intervals. It is suggested that this biphasic effect of forskolin is consistent with an involvement of cyclic adenosine monophosphate (cAMP) in the regulation of cytosolic Ca2+ in the neurosecretory terminals. These results may partly explain some of the discrepant effects of increasing tissue cAMP observed between those studies using electrical pulses, and those using high K+, for stimulation of vasopressin release.
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PMID:Facilitation by forskolin of electrically evoked vasopressin release in vitro requires bursting pattern of stimulation. 254 2

The effects of forskolin, an activator of adenylate cyclase, on the release of vasopressin from isolated rat neurointermediate lobes during a 10 min period of potassium stimulation were investigated. Forskolin was added 5 min after the onset of potassium stimulation. A concentration-dependent reduction in the amount of hormone released during the remaining 5 min period of stimulation was observed. The results suggest that an increase in cyclic AMP following depolarisation inhibits hormone release. This contrasts with several other reports showing that an increase in cyclic AMP prior to stimulation enhances release. We therefore propose that cyclic AMP plays a dual role in stimulus-secretion coupling in the neurohypophysis.
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PMID:Forskolin inhibits potassium-evoked release of vasopressin from rat neurohypophyses. 298 89

The molecular mechanism of desensitization of antidiuretic hormone receptors is not well understood. Preincubation of LLC-PK1 cells with lysine vasopressin (LVP) (10(-6) M, 5 h) decreased subsequent LVP-stimulated cAMP accumulation in cells by 83% and reduced the Vmax of LVP-stimulated adenylate cyclase by 81%. Such preincubation also reduced by 90% the binding of [3H]LVP to both intact cells and isolated plasma membranes, suggesting a loss of vasopressin receptors. Both the reduction in cAMP response and the apparent loss of receptors showed similar dose and time dependence. Monensin (33 microM) did not alter [3H]LVP binding or stimulation of cAMP by LVP, nor did it prevent desensitization. However, membranes prepared from cells preincubated with LVP in the presence of monensin did not show a decrease in [3H]LVP binding. Forskolin preincubation, at 0.1, 1, 10 and 100 microM, did not alter [3H]LVP binding or accumulation of cellular cAMP by LVP, nor did it induce desensitization to LVP. Cells desensitized with varying LVP concentrations in the presence of 10 microM forskolin displayed the same loss of [3H]LVP binding and LVP responsiveness as observed in the absence of forskolin. LVP-desensitized cells, upon removal from LVP-containing medium, recovered cAMP responsiveness to LVP and specific binding of [3H]LVP at the same rate, achieving control levels after 50 h. Recovery was prevented by cycloheximide (25 micrograms/ml). These findings are consistent with a desensitization process involving LVP-mediated receptor internalization, and a recovery process requiring protein synthesis.
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PMID:Desensitization of LLC-PK1 cells by vasopressin results in receptor down-regulation. 298 32


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