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)

Renal papillary collecting tubule (RPCT) hormone responsiveness was compared between cultured RPCT cells from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Unstimulated cells from 4-week-old SHR produced less prostaglandin E2 (PGE2) and cyclic (c)AMP than comparable cells from WKY, while cells from both stains synthesized similar amounts of PGE2 after stimulation with arachidonate, A23187 or bradykinin and similar amounts of cAMP after stimulation with vasopressin or PGE2. There was no difference in basal or stimulated levels of cyclic (c)GMP between the strains. In RPCT cells from 16-week-old rats, basal levels of cAMP, cGMP and PGE2 were significantly lower than those from 4-week-old rats, but they did not differ between the strains. These results suggest that RPCT cells of SHR and WKY at the post-weaning period may differ in the metabolism of PGE2 and cAMP. This difference may be attributed to the possible defect in arachidonate availability in SHR.
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PMID:Papillary collecting tubule responsiveness to vasoactive hormones in spontaneously hypertensive rats. 285 55

In the present study, we examined the effects of guanine nucleotides on vasopressin-induced osmotic water flow and sodium transport in the 14-h preincubated frog bladder. We also examined the effects of the adenylate cyclase-cyclic AMP and cyclic AMP-dependent protein kinase system in the bladder's epithelial cells. Gpp(NH)p significantly enhanced vasopressin-induced water flow while it did not affect cyclic AMP-induced water flow. However, Gpp(NH)p did not enhance the vasopressin-induced increment of sodium transport across the frog bladder. The adenylate cyclase activity of the crude homogenate was enhanced by vasopressin, Gpp(NH)p and NaF. The effects of Gpp(NH)p and vasopressin, at their maximum doses, on the enzyme activities were additive, while other combinations were not. Specific Gpp(NH)p binding sites were found in the pellet fraction after 2,400 X g centrifugation. No direct effect on the protein kinase activity was observed in the presence of 10(-6) M nucleotides, such as GTP, GDP, GMP, CTP, UTP, ITP and Gpp(NH)p. Cyclic AMP stimulated the phosphorylation of discrete protein bands, however, Gpp(NH)p did not influence cyclic AMP-dependent protein phosphorylation of crude homogenate of the bladder's epithelial cells. These results suggest the guanine nucleotides stimulate the vasopressin-induced osmotic water flow in frog bladder by enhancing the vasopressin-mediated adenylate cyclase activity, so that accumulated cyclic AMP might activate cyclic AMP-dependent protein kinase.
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PMID:Effects of guanine nucleotides on vasopressin-induced water flow and sodium transport of the frog bladder. 660 7

The roles of heterotrimeric GTP-binding regulatory proteins (G-proteins) and inositol polyphosphates in the mechanism by which vasopressin stimulates Ca2+ inflow in hepatocytes were investigated by using single cells loaded with fura2 by microinjection. Vasopressin-stimulated Ca2+ inflow was mimicked by microinjection of guanosine 5'-[gamma-thio]triphosphate (GTP[S]) or guanosine 5'-[beta gamma-imido]triphosphate to the cells, but not adenosine 5'-[gamma-thio]triphosphate (ATP[S]) or guanosine 5'-[beta-thio]diphosphate (GDP[S]). Extracellular Gd3+ (5 microM) inhibited both vasopressin- and GTP[S]-stimulated Ca2+ inflow. GDP[S], but not GMP, administered to hepatocytes by microinjection, completely inhibited vasopressin-stimulated Ca2+ inflow and partially inhibited vasopressin-induced release of Ca2+ from intracellular stores. The microinjection of pertussis toxin had no effect either on the release of Ca2+ from intracellular stores or on Ca2+ inflow induced by vasopressin, but completely inhibited changes in these processes induced by epidermal growth factor (EGF). Hepatocytes isolated from rats treated with pertussis toxin for 24 h exhibited no vasopressin- or GTP[S]-stimulated Ca2+ inflow, whereas the vasopressin-stimulated release of Ca2+ from intracellular stores was similar to that observed for control cells. Heparin or ATP[S] inhibited, or delayed the onset of, both vasopressin-induced release of Ca2+ from intracellular stores and vasopressin-stimulated Ca2+ inflow. Vasopressin-induced oscillations in intracellular [Ca2+] were observed in some heparin-treated cells. It is concluded that the stimulation by vasopressin of Ca2+ inflow to hepatocytes requires inositol 1,4,5-trisphosphate (InsP3) and, by implication, the pertussis-toxin-insensitive G-protein required for the activation of phospholipase C beta [Taylor, Chae, Rhee and Exton (1991) Nature (London) 350, 516-518], and another G-protein which is slowly ADP-ribosylated by pertussis toxin and acts between InsP3 and the putative plasma-membrane Ca2+ channel. EGF-stimulated Ca2+ inflow involves at least one G-protein which is rapidly ADP-ribosylated and is most likely required for InsP3 formation.
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PMID:A slowly ADP-ribosylated pertussis-toxin-sensitive GTP-binding regulatory protein is required for vasopressin-stimulated Ca2+ inflow in hepatocytes. 817

We measured volume regulating and stress hormones (AVP, aldosterone, ANP, c-GMP, angiotensin II, PRA, epinephrine, norepinephrine, ACTH, cortisol) in venous blood twice during a lower body negative pressure (LBNP) maneuver in one cosmonaut (31 years, 75 kg, 180 cm) preflight (supine), inflight (6th d in orbit), and on the 4th d (supine) after a 10-d flight. Antecubital blood was taken at the beginning (3 min: "a") and after ceasing (2 min: "b") 40 min LBNP (-15/-30/-35 mm Hg for 15/15/10 min). At the beginning of LBNP, no big changes of resting hormone levels are to be expected. Comparison of "a" values: Inflight, there was a 4-5-fold increase in vasopressin and epinephrine, a slight increase in aldosterone, ANP, norepinephrine, cortisol and ACTH, and a decrease in PRA levels. Postflight, vasopressin was almost as much increased as inflight, and aldosterone and ANP levels were higher than pre- or inflight. PRA, epinephrine, norepinephrine, and cortisol were moderately increased, whereas ACTH and angiotensin II were diminished. Comparison of "b" to "a" values (2 min after LBNP to 3 min intra-LBNP): Preflight, ANP, PRA, and epinephrine rose more than 100%. The inflight response was higher for aldosterone but lower for all other volume active hormones. Postflight, the increase in PRA was pronounced, whereas little change occurred in other hormones. Cortisol and ACTH fell similarly during LBNP under all conditions. In summary, the data provide evidence that not only the endocrine status but also the neuroendocrine responsiveness to stimulation; i.e., the hormone response during cardiovascular load, are altered by the stay in microgravity and readaptation to normal conditions.
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PMID:Hormonal changes with lower body negative pressure on the 6th day in microgravity in one cosmonaut. 828 31

Arginine vasopressin (AVP) receptors are expressed early in the developing spinal cord. To characterize AVP-induced conductances in lower thoracic sympathetic preganglionic (SPN) and other lateral horn neurons, we used patch-clamp recording techniques in neonatal (11-21 days) rat spinal cord slices. Most (90%) of 273 neurons, including all 68 SPNs, responded to AVP with membrane depolarization and/or a V1 receptor-mediated, dose-dependent (0.01-1.0 microM) and tetrodotoxin (TTX)-resistant inward current. A role for G-proteins was indicated by persistence of this inward current after intracellular dialysis with GTP-gamma-S or GMP-PNP, its marked reduction with GDP-beta-S, and significant reduction, but not abolition, after preincubation with pertussis toxin or in the presence of N-ethylmaleimide. Analysis of individual current-voltage (I-V) relationships in 57 cells indicated the presence of two different membrane conductances. In 21 cells, net AVP-induced currents reversed around -103 mV, reflecting reduction in one or more barium-sensitive potassium conductances; in 12 cells, net AVP-induced current reversed around -40 mV and was not significantly sensitive to several potassium channel blockers including barium, tetraethylammonium chloride (TEA), 4-aminopyridine (4AP), cesium, or glibenclamide, suggesting increase in a nonselective cationic conductance that was separate from Ih; in 24 cells where I-V lines shifted in parallel, AVP-induced inward currents were significantly greater and probably involved both conductances. These data indicate that SPNs and a majority of unidentified neonatal lateral horn neurons possess functional G-protein-coupled V1-type vasopressin receptors. The wide distribution of AVP receptors in neonatal spinal lateral column cells suggests a role that may extend beyond involvement in regulation of autonomic nervous system function.
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PMID:Vasopressin-induced currents in rat neonatal spinal lateral horn neurons are G-protein mediated and involve two conductances. 977 48

ATP stimulates vasopressin (VP) release from explants of the hypothalamo-neurohypophyseal system (HNS), but the response is not sustained for the duration of exposure to ATP. Since adenosine, a metabolite of ATP, inhibits VP release from neurohypophysial terminals and adenosine receptors (AR) are expressed in supraoptic nucleus (SON) neurons, we postulated that conversion of ATP to adenosine contributed to termination of ATP-stimulated VP release from HNS explants. This was tested using a non-selective AR antagonist, 5-amino-9-chloro-2-(2-furyl)-1, 2, 4-triazolo [1, 5-c] quinazoline (CGS-15943). CGS-15943 did not affect basal VP release and did not alter the initial response to ATP. A selective A1R antagonist, 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX), increased basal VP release at 1 microM, without altering the response to ATP. However, at a higher concentration of DPCPX (10 microM), VP release was enhanced by ATP for an extended period of time. Inhibition of the enzymatic conversion of ATP to adenosine using a combination of a potent ecto-5'-nucleotidase inhibitor, alpha,beta-methylene adenosine 5'-diphosphate (AMP-CP), and a competitive substrate for ecto-5'-nucleotidase (guanosine monophosphate, GMP) did not affect basal VP release. Enzymatic inhibition did slightly prolong the response to ATP, but it was not sustained for the duration of exposure to ATP. We conclude that an endogenous inhibitory influence of adenosine decreases basal VP release from HNS explants and that conversion of exogenously applied ATP to adenosine contributes to termination of ATP-induced stimulation of VP release, but additional mechanisms such as receptor desensitization also limit the response to extended exposure to ATP.
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PMID:Does conversion of ATP to adenosine terminate ATP-stimulated vasopressin release from hypothalamo-neurohypophyseal explants? 1589 96

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