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)

We examined the action of high (2 x 10(-8)M) and low (6 x 10(-9)M) concentrations of atrial natriuretic factor (ANF) on water and urea transport in the rat inner medullary collecting duct (IMCD) using the in vitro microperfusion technique. We measured the hydraulic conductivity (Lp x 10(-6) cm/atm per second) and both lumen-to-bath (Pu(lb] and bath-to-lumen (Pu(bl)) 14C-urea permeabilities (Pu x 10(-5) cm/s) in the absence and in the presence of vasopressin (VP). High concentrations of ANF were able to inhibit the maximum activity of (50 microU/ml) VP-stimulated Lp but physiological concentration of ANF inhibit only submaximum activity (10 microU/ml) of VP-stimulated Lp. The hydrosomotic effect of dibutyryl-cyclic 3.5 adenosine monophosphate (cAMP) (10(-4)M) was unchanged by high concentrations of ANF (2 x 10(-8)M). Also we found that high (10(-4)M) and low (10(-6)M) concentrations of exogenous cyclic 3,5-guanosine monophosphate (GMP) while unable to change the Lp in the absence of VP, decreased the maximum activity of VP-stimulated Lp significantly. We also found that ANF inhibits partially and in a reversible manner the VP-stimulated Pu(lg) but not the VP-stimulated Pu(bl). These results demonstrated that plasma concentrations of ANF observed during volume expansion (10(-10)M) are able to inhibit submaximum activity of VP-stimulated (10 microU/ml) Lp in the rat IMCD, this effect seems to occur before cAMP formation and it appears to be mediated by cGMP. ANF (6 x 10(-9)M) also reduced the VP-stimulated urea outflux.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of atrial natriuretic factor and cyclic guanosine monophosphate on water and urea transport in the inner medullary collecting duct. 196 94

The effect of 50 and 150 mg cicletanine, a new vasodilator antihypertensive, on plasma atrial natriuretic peptide (ANP), cyclic GMP and antidiuretic hormone has been investigated at rest and during standardized exercise, in a double blind cross over study in healthy subjects. Exercise significantly increased in plasma ANP, cyclic GMP and antidiuretic hormone concentrations, and cicletanine did not affect any of them either at rest or during exercise. Since the alpha-1 adrenoceptor blocker prazosine decreases, beta-adrenoceptor blockers increase and the vasodilator cicletanine does not alter the plasma ANP response to exercise, it is suggested that adrenergic receptors may be directly involved in the regulation of ANP secretion.
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PMID:Cicletanine does not affect plasma atrial natriuretic peptide concentration in healthy subjects. 196 45

The effect of a non selective and a cardio-selective beta-blocker on basal and exercise-stimulated plasma atrial natriuretic peptide concentrations in healthy volunteers has been studied. Nine healthy volunteers received single oral doses of 5 mg tertatolol, 100 mg atenolol or placebo, at one week intervals, in a double blind cross over trial. At rest plasma atrial natriuretic peptide, aldosterone, antidiuretic hormone and cyclic GMP concentrations and plasma renin activity were not modified by the treatments. During exercise plasma atrial natriuretic peptide concentrations were significantly increased by each treatment, the increment being significantly greater on beta-blockers than on placebo. The rise in atrial natriuretic peptide was 72% after placebo (from 24 to 42 pg/ml), 184% after atenolol (from 30 to 86 pg/ml), and 183% after tertatolol (from 34 to 95 pg/ml), respectively. Thus, the study has shown that in healthy subjects the plasma natriuretic peptide concentration is increased by exercise and that the increase is considerably and equally potentiated by selective and non selective beta-adrenoceptor blockade. The effect may be mainly due to a reduction in ventricular contractility with an increase in atrial pressure. The beta-blockers did not influence the resting plasma atrial natriuretic peptide levels, which suggests that in healthy subjects basal atrial natriuretic peptide secretion is not controlled via beta-receptors.
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PMID:Beta-adrenoceptor blockade potentiates exercise-induced release of atrial natriuretic peptide. 197 99

1. Effects of atrial natriuretic peptide (ANP) on tension development, particulate guanylate cyclase activity and guanosine 3':5'-cyclic monophosphate (cyclic GMP) concentrations of uteri from oestrogen-treated, progesterone-treated, ovariectomized and pregnant rats were determined in vitro. 2. ANP inhibited the tension development by myometrial tissues from oestrogen-treated virgin rats and the sterile horn of 10 to 14 day pregnant rats but not of the uterus from pregnant and progesterone-treated rats. 3. Inhibition of cyclo-oxygenase and lipoxygenase activities did not restore the tocolytic activity of ANP on gravid uterus. ANP exerted a tocolytic effect on nongravid uterus submaximally stimulated by prostaglandin F2 alpha (PGF2 alpha), oxytocin, vasopressin, angiotensin II or 5-hydroxytryptamine (5-HT). 4. Ovariectomy decreased the tocolytic effects of ANP, which could be restored by oestrogen treatment. 5. The refractoriness to the tocolytic effect of ANP in pregnant rats was not accompanied by a decrease in its relaxant effects on isolated aortic strips. 6. Tocolytic effects of isoprenaline, isobutylmethyl xanthine and hydroxylamine were not influenced by pregnancy or progesterone treatment. Up to a concentration of 3 mM, sodium nitroprusside did not affect myometrial tension development. 7. Pregnancy and progesterone treatment markedly inhibited ANP-induced increases in myometrial particulate guanylate cyclase activity and cyclic GMP concentrations but did not influence the effects of ANP on aortic cyclic GMP concentrations. 8. It is concluded that exposure of the myometrium to circulating and placentally-produced progesterone is responsible for the pregnancy-induced decrease in the effects of ANP on myometrial particulate guanylate cyclase activity and cyclic GMP concentrations and in turn on myometrial tension development.
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PMID:Refractoriness of the gravid rat uterus to tocolytic and biochemical effects of atrial natriuretic peptide. 197 61

Recently, it was shown that in LLC-PK1 kidney epithelial cells hormones such as vasopressin or oxytocin increase cyclic GMP in a receptor-mediated and L-arginine-dependent manner. In the present study, the possible existence of cross-tolerance to vasopressin and oxytocin was investigated in nitrate-tolerant LLC-PK1 cells. Pretreatment with 1 mM glyceryl trinitrate for 3 h decreased cyclic GMP stimulation by 1 microM vasopressin and 1 microM oxytocin by 49% and 54%, respectively. Under the same conditions, cyclic GMP stimulation at 1 microM sodium nitroprusside was diminished by 56% whereas the cyclic GMP response to 100 microM glyceryl trinitrate was virtually abolished. Our results demonstrate that a substantial degree of cross-tolerance to L-arginine-dependent guanylate cyclase activators occurs in nitrate-pretreated nonvascular cells which may be due to glyceryl trinitrate-induced desensitization of soluble guanylate cyclase.
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PMID:Cross-tolerance to L-arginine-dependent guanylate cyclase activators in nitrate-tolerant LLC-PK1 kidney epithelial cells. 197 70

To investigate whether altered renal medullary prostaglandin (PG) synthesis is involved in the development of hypertension in spontaneously hypertensive rats (SHR), we compared the hormonal responsiveness of cultured renal papillary collecting tubule (RPCT) cells from SHR and Wistar-Kyoto rats (WKY) as control. Basal levels of PGE2 and cAMP were lower in 4-weeks-old SHR than in WKY, while PGE2 synthesis after stimulation with arachidonate, A23187 or bradykinin and the level of cAMP responded to vasopressin or exogenous PGE2 were similar in both strains. There was no difference in basal nor stimulated levels of cGMP between both strains. In 16-week-old rats, basal levels of cAMP, cGMP and PGE2 were significantly lower than in 4-week-old rats, but no differences were recognized between both 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:[Responsiveness of cultured papillary collecting tubules to vasoactive hormones: comparison between spontaneously hypertensive rats and Wistar-Kyoto rats]. 206 16

ANP stimulates a profound natriuresis and diuresis by a series of concerted actions along the nephron, including stimulation of glomerular filtration and inhibition of net salt and water reabsorption in the cortical and inner medullary collecting ducts. Several actions of ANP contribute to its natriuretic and diuretic effects in the collecting duct. These include reductions in aldosterone secretion, increases in hydrostatic pressures opposing Na+ reabsorption, possible stimulation of medullary washout, and direct inhibition of salt and water transport. In both CCD and IMCD, ANP antagonizes the hydroosmotic actions of vasopressin, which leads to diuresis. The mechanisms by which ANP inhibits response to vasopressin remain unclear, although in IMCD, cGMP can duplicate the response to ANP. In CCD, ANP can inhibit Na+ reabsorption via cGMP; the transport pathway regulated by ANP is unknown. In IMCD, ANP acting via cGMP inhibits a conductive Na+ or cation channel, which appears to be on the luminal membrane.
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PMID:Renal actions of atrial natriuretic peptide: regulation of collecting duct sodium and water transport. 213 59

In order to clarify the mechanism(s) by which cyclic GMP inhibits the generation of inositol phosphates in rat aorta segments and cultured bovine aortic smooth muscle cells, we studied phosphoinositide hydrolysis and GTPase activity in homogenates and membrane preparations of cultured bovine aortic smooth muscle cells. Pretreatment of homogenate preparations with cyclic GMP plus ATP did not inhibit [8-arginine, 3H] vasopressin (AVP) binding, but resulted in a total suppression of the AVP-induced GTPase activation. The pretreatment with cyclic GMP and ATP also inhibited the formation of inositol phosphates induced by AVP in the presence of low concentrations of guanosine 5'-(gamma-thio)triphosphate (GTP gamma S), or by high concentrations of GTP gamma S alone. However, the formation of inositol phosphates by high concentrations of Ca2+ alone was not blocked. These results suggest that the ability of cyclic GMP to inhibit phosphoinositide hydrolysis results from an inhibition of a guanine nucleotide regulatory protein activation, and the interaction between guanine nucleotide regulatory protein and phospholipase C. While the precise site of this inhibition is not presently known, the inhibition by cyclic GMP is dependent upon the addition of ATP and probably entails a phosphorylation event since adenylylimidodiphosphate can not substitute for the ATP requirement.
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PMID:Mechanism of cyclic GMP inhibition of inositol phosphate formation in rat aorta segments and cultured bovine aortic smooth muscle cells. 215 23

The major action of forskolin, the diterpine activator of adenylate cyclase, in primary (unpassaged) rat aortic smooth muscle cells is to reduce vasopressin-stimulated Ca2+ concentrations. In repetitively passaged cells, however, forskolin by itself increased Ca2+ levels by apparently stimulating Ca2+ uptake into the cell and had much smaller effects on inhibiting vasopressin-stimulated Ca2+ elevations. Both primary and passaged smooth muscle cells contained adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase. Guanosine 3',5'-cyclic monophosphate (cGMP)-dependent protein kinase was greatly reduced or absent in passaged smooth muscle cells. The introduction of purified cGMP-dependent protein kinase into the cytoplasm of passaged cells prevented forskolin from elevating intracellular Ca2+ and restored the capacity of forskolin to reduce vasopressin-stimulated Ca2+ mobilization. Similar effects were observed for isoproterenol in passaged smooth muscle cells. When introduced into cells, the active catalytic subunit of the cAMP-dependent protein kinase did not lead to reductions in Ca2+ levels. These results suggest that cAMP elevations lead to profound changes in Ca2+ metabolism through activation of both cAMP- and cGMP-dependent protein kinases. Activation of cGMP-dependent protein kinase by cAMP leads to the reduction in intracellular Ca2+, whereas activation of cAMP-dependent protein kinase may only mediate the uptake of Ca2+ from extracellular sources.
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PMID:cGMP-dependent protein kinase mediates the reduction of Ca2+ by cAMP in vascular smooth muscle cells. 215 36

Hypotension related to the intraoperative use of desmopressin acetate to improve platelet function following cardiopulmonary bypass has recently been reported. To investigate the direct vascular actions of this drug as a potential mechanism of its induced hypotension, cumulative, dose-dependent (3.7 X 10(-10) to 1.2 X 10(-7) M) effects of desmopressin were studied in isolated phenylephrine precontracted rings of rat and rabbit thoracic aorta and rabbit pulmonary artery. Desmopressin was a potent vasodilator of all vessel types studied with significant (P less than 0.05) vasodilation beginning at 7.5 X 10(-9) M. Vascular relaxation of all vessels was greater when the vascular endothelium was intact (P less than 0.05). Indomethacin potentiated (P less than 0.05) vascular relaxation in rat and rabbit aortic rings and partially inhibited (P less than 0.05) relaxation in rabbit pulmonary artery rings. Selective antagonists of vasopressin V1 (d(CH2)5-Tyr(Me)AVP, 1 X 10(-6) M) and V2 (d(CH2)5[D-Ile2,Ala-NH2(9)] AVP, 1 X 10(-6) M) receptors and of histamine H1 (diphenhydramine, 1 X 10(-5) M) and H2 (cimetidine 1 X 10(-5) M) receptors had no effect on desmopressin-induced relaxation of rat aortic rings. Chlorobutanol, the diluent in which desmopressin is supplied, was devoid of vascular effects. To study the effects of desmopressin on vascular cyclic GMP and cyclic AMP concentrations, a cultured bovine aortic smooth muscle--rat vascular smooth muscle coculture model was employed. Desmopressin (1 X 10(-7) and 1 X 10(-8) M) did not significantly alter control values of either cyclic nucleotide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Desmopressin is a potent vasorelaxant of aorta and pulmonary artery isolated from rabbit and rat. 216 Feb 8


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