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)

Receptors for atrial natriuretic peptide (ANP) have been demonstrated in renal mesangial cells as well as other cell types in the glomerulus. The biochemical basis for the effects of ANP on glomerular hemodynamics remains undefined. Using cultured rat glomerular mesangial cells, we demonstrated a concentration-dependent stimulation of cGMP production in intact cells, and of guanylate cyclase in membranes. Despite the presence of a guanylate cyclase response, ANP had no inhibitory effect on basal inositol trisphosphate production nor on basal cytosolic calcium. Arginine vasopressin stimulated IP3 production, caused a rise in cytosolic calcium as measured using the calcium-sensitive fluorescent probe Indo-1, and caused mesangial cell contraction. ANP caused a slight but significant enhancement of vasopressin-stimulated IP3 production, but had no effect on the cytosolic calcium response nor on the contractile response. 8-Bromo-cGMP likewise had no effect on the generation of the calcium signal. These results indicate that the effects of ANP on glomerular hemodynamics are not mediated by an alteration in the generation of the calcium signal in mesangial cells. In contrast, addition of calcium inhibited ANP stimulated guanylate cyclase activity.
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PMID:Interaction of atrial natriuretic peptide-stimulated guanylate cyclase and vasopressin-stimulated calcium signaling pathways in the glomerular mesangial cell. 244 31

The aim of this study was to examine the hemodynamic, renal, and endocrine effects of exogenous human atrial natriuretic factor (ANF), together with its pharmacokinetics, in healthy volunteers. Ten subjects participated in this study, in which the effects of a single bolus dose of ANF and of a matched vehicle injection were compared under a 135 mmol/day sodium intake. Doses of 3, 12.5, and 25 micrograms of ANF were given to 1 subject each, and doses of 50 and 100 micrograms were given to 4 and 3 subjects, respectively. Significantly, hemodynamic changes occurred at the 100 micrograms dose, when mean blood pressure decreased by 15% and heart rate increased reciprocally. Diuresis and natriuresis tended to increase following 50 micrograms but increased significantly and in a prolonged fashion following 100 micrograms of ANF. Atrial natriuretic factor did not cause significant changes in plasma catecholamine, renin activity, and aldosterone levels at any dose, although aldosterone tended to decrease. Plasma arginine-vasopressin concentrations decreased significantly following 100 micrograms. Plasma cyclic GMP levels increased in all subjects and in a dose-dependent fashion. Plasma ANF concentrations peaked 3-5 min following the bolus injection and returned toward baseline values within 10-60 min. Although with doses of less than or equal to 50 micrograms plasma ANF levels increased up to 8 to 50-fold, compared to baseline values, the only significant change was the increase in plasma cyclic GMP levels, perhaps because the effects of ANF were successfully masked by counter-regulatory mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects and pharmacokinetics of bolus injections of atrial natriuretic factor in normal volunteers. 245 57

Studies of the molecular nature of epithelial sodium channels are in their infancy and have largely involved experiments in which the interaction between amiloride and this transport process has been examined. Because of the inherent geometric complexity of epithelial tissues, these studies have in large measure been macroscopic in nature, with the molecular details of transport being deduced. In the past five years, however, the molecular biology of these critical ion channels has been studied directly. The development of radioactive high-affinity probes, the application of patch-clamp and reconstitution techniques, the generation of specific antibodies, and the formulation of epithelial cDNA expression libraries have propelled the field of epithelial ion channels into a new era. Now, for the first time, we can rigorously address questions concerning the molecular nature of the amiloride block, the channel's selectivity to alkali metal cations, and the modulation of ion transport through this channel by other ions (such as calcium), hormones (such as vasopressin, aldosterone, and atrial natriuretic factor), or intracellular second messengers (such as cAMP or cGMP). The complexity of the epithelial sodium channel's structure may reflect the constitutive and regulatory role this protein plays in sodium homeostasis. The epithelial sodium channel is continually operating, constantly changing its activity on a second-to-second basis. Hence, its tonic functions are probably modulated by a myriad of factors, most of which are unknown. With the application of molecular techniques, a much clearer understanding of the nature and regulation of epithelial sodium channel processes in health and disease will emerge in the years to come.
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PMID:The biology of amiloride-sensitive sodium channels. 246 56

Effect of atrial natriuretic peptide (ANP) on cytosolic free calcium [( Ca2+]i) was studied in monolayers of cultured vascular smooth muscle (VSM) cells loaded with a fluorescent calcium indicator, fura-2. Vasoconstrictive hormones, angiotensin II (AII) and Arg8-vasopressin (AVP) induced initial rapid rises in [Ca2+]i, followed by sustained elevation of [Ca2+]i. ANP (Atriopeptin III 10(-8) M) decreased both the resting level and the sustained elevation of [Ca2+] i induced by AII and AVP. ANP also decreased the rise in [Ca2+]i induced by high potassium (K+) depolarization. AVP-induced initial rapid rise in [Ca2+]i was not inhibited by ANP in the presence or absence of the phosphodiesterase inhibitor, isobutylmethylxanthine 0.1 mM, which has been shown to fully enhance ANP-induced cyclic GMP accumulation. On the other hand, a calcium antagonist, nicardipine, inhibited the high K+-induced rise in [Ca2+]i, whereas it had no effect on not only initial but also sustained rises in [Ca2+]i induced by AVP or AII. These results suggest that ANP has an ability to decrease [Ca2+]i not through inhibition of voltage-sensitive calcium channels, and that neither ANP nor ANP-induced cyclic GMP may affect initial hormone-induced rise in [Ca2+]i. In conclusion, an ability to decrease [Ca2+]i is implicated in ANP-induced relaxation of VSM.
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PMID:The effect of atrial natriuretic peptide on cytosolic free calcium in cultured vascular smooth muscle cells. 247 68

Prolonged exposure of A-10 cells to Arginine Vasopressin (AVP) resulted in the following responses: (a) loss of vasopressin receptors from the cell surface (30-40%), (b) increased basal levels of inositol and inositol monophosphate, (c) decreased inositol di- and trisphosphate production and decreased intracellular calcium release in response to a second challenge with AVP, (d) attenuation of AVP-mediated inhibition of isoproterenol-stimulated cAMP and ANF-stimulated cGMP accumulation and (e) attenuation of thrombin and ATP-mediated increase in inositol di- and trisphosphate accumulation and intracellular calcium release. All the above responses depended on the time of exposure of the cells to AVP with the responses being attenuated as early as 5-10 min of exposure to AVP. The desensitization also depended on the concentration of AVP used with 50% of maximal desensitization for each response being observed at 5 nM of AVP. This concentration of AVP corresponded well with the Kd of vasopressin for binding to these sites. Desensitization of protein kinase C (PKC) by prolonged exposure of the cells to PDBu or addition of the PKC inhibitor staurosporine during pretreatment with AVP did not prevent AVP-mediated desensitization, suggesting that PKC may not be involved in AVP-mediated desensitization in smooth muscle cells. It is concluded that AVP induced both homologous and heterologous desensitization of phosphatidylinositol turnover and calcium release in smooth muscle cells. The desensitization processes did not appear to be mediated by protein kinase C. The possibility that the locus of the heterologous desensitization may be at the level of substrates such as PI, PIP and PIP2 is discussed.
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PMID:Homologous and heterologous desensitization mediated by vasopressin in smooth muscle cells. 253 42

Primary rat aortic cells, when treated with arginine vasopressin or depolarizing concentrations of K+, responded to atriopeptin II and 8-bromo-cGMP (8-Br-cGMP) with decreases in intracellular Ca2+ levels. The effects of atriopeptin and 8-Br-cGMP were diminished in cells which had been passaged many times. Low levels of cGMP-dependent protein kinase were present in soluble extracts prepared from the unresponsive cells in later passage compared with extracts from responsive cells. Unresponsive cells, when induced to incorporate cGMP-dependent protein kinase into the cytoplasm using the osmotic lysis procedure of Okada and Rechsteiner (Okada, C. Y., and Rechsteiner, M. (1982) Cell 29, 33-41), responded to atriopeptin and 8-Br-cGMP with reductions in peak Ca2+ levels in response to vasopressin and depolarizing concentrations of K+. Cells which were furnished with affinity-purified antibody to the cGMP-dependent protein kinase after the introduction of the kinase remained unresponsive to the effects of atriopeptin. In addition, antibody furnished to responsive primary cultured cells inhibited the effects of atriopeptin and 8-Br-cGMP on Ca2+ levels. These data suggest that repetitively passaged cultured rat aortic smooth muscle cells lose their responsiveness to cGMP concurrently with the loss of cGMP-dependent protein kinase. Restoration of kinase to the cells results in the restoration of responsiveness to cGMP. Thus cGMP-dependent protein kinase appears to be the mediator of the reduction in Ca2+ levels upon elevation of intracellular cGMP.
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PMID:Regulation of intracellular Ca2+ levels in cultured vascular smooth muscle cells. Reduction of Ca2+ by atriopeptin and 8-bromo-cyclic GMP is mediated by cyclic GMP-dependent protein kinase. 253 16

Isolated rat hepatocytes in primary monolayer culture were maintained for 18-24 h in the presence of 10% (v/v) serum and [3H]inositol. Vasopressin (100 nM) stimulated the production of inositol mono-, bis- and tris-phosphates (IP1, IP2, and IP3). Prior exposure of hepatocytes to 8-bromo cyclic AMP (8Br-cAMP; 100 microM), but not 8-bromo cyclic GMP, enhanced the vasopressin-mediated stimulation of inositol phosphate accumulation, but had no significant effect on their formation in the absence of vasopressin. The effect of the cyclic AMP analogue was mimicked by glucagon (10 nM), and was seen whether cyclic AMP or glucagon was added 5 min or 12 h before the addition of vasopressin. An 8 h incubation with dexamethasone (100 nM) enhanced the accumulation of IP3, but not that of IP2 or IP1, in the presence of 8Br-cAMP and vasopressin. Cycloheximide or actinomycin D had little effect on the vasopressin stimulation of inositol phosphate accumulation, after an 8 h incubation in the presence or absence of 8Br-cAMP.
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PMID:Exposure of cultured hepatocytes to cyclic AMP enhances the vasopressin-mediated stimulation of inositol phosphate production. 253 87

The molecular mechanisms which regulate expression of vasopressin (AVP)- and oxytocin (OT)-encoding genes are unknown. We have investigated the regulatory role of one class of second messenger, the cyclic nucleotides, by examining levels of both adenosine 3',5'-monophosphate (cAMP) and guanosine 3',5'-monophosphate (cGMP) in hypothalamic nuclei of rats during osmotic stimulation. In vivo studies, in which rats were given 2% saline to drink for different periods (salt loading), demonstrated elevated levels of cAMP in the supraoptic nucleus (SON) after 2 days. Raised levels were also evident at 3 and 7 days. A similar (less marked) pattern was observed in the paraventricular nucleus (PVN) but not in the suprachiasmatic nucleus (SCN). cGMP was present at much lower levels than cAMP and did not exhibit parallel dynamics during salt loading; however, significant changes in cGMP levels were found in the SON and PVN. In vitro studies, in which explant cultures of punched hypothalamic nuclei were challenged with hypertonic media, demonstrated that increasing medium osmolality from 290 to 310 mOsm/kg doubled the level of cAMP in the SON but did not change levels in the PVN or SCN. A greater stimulus, 325 mOsm/kg, caused a 4-fold increase in SON cAMP, and small cAMP responses in the PVN and SCN. Marked cGMP responses were also observed in the SON following stimulation at 310 and 325 mOsm/kg, smaller responses being found in the PVN and SCN. These results are consistent with previous demonstrations of SON neuron osmosensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclic nucleotide dynamics in the rat hypothalamus during osmotic stimulation: in vivo and in vitro studies. 254 82

Many vasoactive agents have been shown to bind to specific receptors on endothelial cells. Among these is atrial natriuretic factor (ANF). Binding of ANF to endothelial cells has been demonstrated to induce elevation of intracellular guanosine 3',5'-cyclic monophosphate (cGMP). Other vasoactive agents have been shown to cause elevation of intracellular adenosine 3',5'-cyclic monophosphate (cAMP), Ca, and diacylglycerol. However, the endothelial cell response that occurs subsequent to elevation of cGMP or other second messengers is not well understood. Recently, endothelial cells have been shown to possess a Na-K-Cl cotransport system that is stimulated by vasopressin and bradykinin and inhibited by isoproterenol. Thus it is possible that modulation of Na-K-Cl cotransport may play a role in the endothelial cell response to second messengers that are elevated by ANF and other vasoactive agents. This possibility was examined in the present study by evaluating the effects of a variety of vasoactive agents and their second messengers on endothelial cell Na-K-Cl cotransport. Cotransport was assessed as bumetanide-sensitive K influx in cultured bovine aortic endothelial cells. A number of agents were found to reduce Na-K-Cl cotransport, including ANF, acetylcholine, histamine, and norepinephrine. Cotransport was found to be stimulated by angiotensin II, as well as vasopressin and bradykinin. Na-K-Cl cotransport was also inhibited by elevation of intracellular cGMP or cAMP or by treatment of the cells with phorbol ester to activate protein kinase C. However, A23187-induced elevation of intracellular Ca caused stimulation of Na-K-Cl cotransport.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of Na-K-Cl cotransport in endothelial cells by atrial natriuretic factor. 254 34

Lipid methylation has been studied in homogenized dog kidney cortical tubules. At pH 9, using S-adenosyl-L-methionine as methyl donor, most of the methyl groups appeared incorporated into phosphatidylcholine, the activity showing an apparent Km of 16 microM. This enzymatic activity was unchanged by the presence of the divalent cations Ca2+ or Mg2+, cAMP or cGMP. In addition, lipid methylation was also unchanged after treatment of intact tubules with angiotensin II, parathyroid hormone or vasopressin. An increased phosphatidylcholine synthesis was observed in the remnant kidney cortical tubules after uninephrectomy through an activation of phosphocholine transferase without detectable modification of lipid methylation. These findings suggest that lipid methylation is not regulated by these biochemical or functional stimuli tested in canine renal cortical tubules.
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PMID:Lipid methylation, hormone action and compensatory hypertrophy in renal cortical tubules. 254 7


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