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

1. The effect of vasopressin and insulin on active sodium transport across frog skin in the presence of internal alternariol mycotoxin was studied, using the short-circuit technique. 2. Vasopressin stimulates sodium transport across frog skin by decreasing the resistance to sodium entry into the epithelial cells, thus partially removing the inhibition on the short-circuit current due to the action of Alternariol mycotoxin. 3. Even insulin which is known to increase the short-circuit current by a different mechanism, determines a rapid reversal effect on the inhibition due to Alternariol. 4. These data confirm the different action of the two hormones on active sodium transport across frog skin, and furthermore are indicative of an inhibition of transepithelial sodium transport by Alternariol mycotoxin probably via the sodium pump.
Gen Pharmacol 1990
PMID:The effect of ADH and insulin on active sodium transport across frog skin in the presence of alternariol mycotoxin. 227 81

1. The rat hindlimb, kidney and intestine were each perfused in a nonrecirculating mode at 25 degrees C using an artificial perfusate (initial pressure 85 +/- 5 mmHg) and the effects of vasopressin and noradrenaline on oxygen uptake and perfusion pressure determined. 2. Both vasopressin (K0.5 = 0.1 nM) and noradrenaline (K0.5 = 2 nM) increased oxygen uptake as well as perfusion pressure by the perfused hindlimb; changes in oxygen uptake were closely matched by changes in pressure. The maximum increase in oxygen uptake was approx. 9 mumol/hr per g wet wt of hindlimb. 3. The perfused kidney also responded to vasopressin and noradrenaline with parallel increases in oxygen uptake and perfusion pressure for each agent. The largest increase in oxygen uptake was approx. 30 mumol/hr per g wet wt but this was not maximal. 4. Vasopressin increased oxygen uptake and pressure by the perfused intestine over the range 0.01-2 nM, but the changes in pressure only became significant at doses greater than 0.1 nM. 5. Noradrenaline inhibited oxygen uptake and increased perfusion pressure in a dose-dependent manner at pharmacological concentrations (greater than 30 nM) when shunting of perfusate may have contributed to unperfused regions. 6. A network of mesenteric blood vessels estimated to contain approx. 6% vascular tissue by weight, with the remainder white fat cells, lymphatics and connective tissue, was also perfused. 7. Vasopressin (K0.5 = 0.3 nM) and noradrenaline (K0.5 = 30 nM) each increased oxygen uptake and perfusion pressure in a dose-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)
Gen Pharmacol 1990
PMID:A comparison of vasopressin and noradrenaline on oxygen uptake by perfused rat hindlimb, kidney, intestine and mesenteric arcade suggests that it is in part due to contractile work by blood vessels. 227 98

A sensitive radioimmunoassay was developed to measure circulating levels of the neurohypophysial peptide lysine vasopressin (LVP) in the marsupial quokka (Setonix brachyurus), which is abundant on Rottnest Island off the coast of Western Australia. Animals from locations on the island where free water is completely absent were compared in midsummer with animals from sites where brackish water is available and utilized by the quokkas. In the animals from West End, where free water is absent, circulating levels of LVP averaged 89.2 +/- 19.6 pg/ml, which was significantly higher than the mean level of 35.6 +/- 15.8 pg/ml measured in individuals collected from the Lakes site with access to brackish drinking water. Rates of water and sodium turnover, measured with isotopes, were significantly greater in Lakes than West End animals, as were renal clearances of sodium, chloride, urea, and total osmolytes. Despite an obvious osmotic diuresis resulting from the ingestion of salty water, the Lakes animals were in better physical condition at the end of summer than the West End animals which lack free water, and these latter individuals showed signs of slight dehydration with elevated plasma and urinary electrolyte concentrations and osmolalities.
Gen Comp Endocrinol 1990 Jan
PMID:Effect of available surface water on levels of antidiuretic hormone (lysine vasopressin) and water and electrolyte metabolism of the Rottnest Island quokka (Setonix brachyurus). 229 26

1. The effect of noradrenaline as well as of vasopressin and angiotensin II to increase oxygen uptake and perfusion pressure by the isolated perfused rat hindlimb were completely inhibited by the vasodilators, nitroprusside (0.5 mM), nifedipine (2.5 microM) and isoprenaline (50 nM). 2. Oxygen uptake due to sciatic nerve stimulation of skeletal muscle contraction was not inhibited by 0.5 mM nitroprusside but was found to increase further that produced by a maximum dose of either noradrenaline or angiotensin II. 3. Analysis of high energy phosphates in samples of freeze-clamped hindlimb muscle showed no difference before and after vasoconstrictor addition or with muscle sampled in vivo. 4. It is concluded that norepinephrine mediated increase in oxygen uptake by the perfused rat hindlimb results from its vasoconstrictor action.
Gen Pharmacol 1990
PMID:Inhibition by vasodilators of noradrenaline and vasoconstrictor-mediated, but not skeletal muscle contraction-induced oxygen uptake in the perfused rat hindlimb; implications for non-shivering thermogenesis in muscle tissue. 229 85

The effect of 1-deamino-8-D-arginine-vasopressin, dDAVP, the synthetic analogue of vasopressin, upon the active sodium transport across the frog skin was studied using standard microelectrode technique and compared with the effect of synthetic arginine-vasopressin, AVP. dDAVP applied to the basolateral side of the epithelium stimulated the active sodium transport as reflected by the increase of short-circuit current, Isc, and transepithelial electrical potential difference, Voc. Potential difference across both the apical, Vo, and the basolateral, Vi, cell membranes decreased. The driving force of transepithelial sodium transport, ENa, did not change. The transepithelial electrical resistance, Rt, ohmic resistance of the active sodium transport, RNa, and apical cell membrane resistance, Ro, rapidly decreased, while the resistance of the basolateral cell membrane, Ri, and the resistance of the shunt pathway, Rs, remained unchanged. It is concluded that dDAVP primarily increases sodium permeability of the apical cell membrane which subsequently stimulates sodium pump activity. This action is similar to that of AVP.
Gen Physiol Biophys 1990 Feb
PMID:Comparison of the effects of dDAVP and AVP on the sodium transport in the frog skin. 231 15

The regulation of transepithelial water permeability in toad urinary bladder is believed to involve a cycling of endocytic vesicles containing water transporters between an intracellular compartment and the cell luminal membrane. Endocytic vesicles arising from luminal membrane were labeled selectively in the intact toad bladder with the impermeant fluid-phase markers 6-carboxyfluorescein (6CF) or fluorescein-dextran. A microsomal preparation containing labeled endocytic vesicles was prepared by cell scraping, homogenization, and differential centrifugation. Osmotic water permeability was measured by a stopped-flow fluorescence technique in which microsomes containing 50 mM mannitol, 5 mM K phosphate, pH 8.5 were subject to a 60-mM inwardly directed gradient of sucrose; the time course of endosome volume, representing osmotic water transport, was inferred from the time course of fluorescence self-quenching. Endocytic vesicles were prepared from toad bladders with hypoosmotic lumen solution treated with (group A) or without (group B) serosal vasopressin at 23 degrees C, and bladders in which endocytosis was inhibited by treatment with vasopressin at 0-2 degrees C (group C), or with vasopressin plus sodium azide at 23 degrees C (group D). Stopped-flow results in all four groups showed a slow rate of 6CF fluorescence decrease (time constants 1.0-1.7 s for exponential fit) indicating a component of nonendocytic 6CF entrapment into sealed vesicles. However, in vesicles from group A only, there was a very rapid 6CF fluorescence decrease (time constant 9.6 +/- 0.2 ms, SEM, 18 separate preparations) with an osmotic water permeability coefficient (Pf) of greater than 0.1 cm/s (18 degrees C) and activation energy of 3.9 +/- 0.8 kcal/mol (16 kJ/mol). Pf was inhibited reversibly by greater than 60% by 1 mM HgCl2. The rapid fluorescence decrease was absent in vesicles in groups B, C, and D. These results demonstrate the presence of functional water transporters in vasopressin-induced endocytic vesicles from toad bladder, supporting the hypothesis that water channels are cycled to and from the luminal membrane and providing a functional marker for the vasopressin-sensitive water channel. The calculated Pf in the vasopressin-induced endocytic vesicles is the highest Pf reported for any biological or artificial membrane.
J Gen Physiol 1989 Dec
PMID:Very high water permeability in vasopressin-induced endocytic vesicles from toad urinary bladder. 251 41

We describe the effects of arginine-vasopressin (AVP) and five related peptides on the contractile vacuole, the osmoregulatory organelle of the fresh water Amoeba proteus. Arginine-vasopressin, lysine-vasopressin, and SKF 101926, a synthetic antagonist of vasopressin, cause a significant increase in the rate of output of the contractile vacuole. Deamino-vasopressin (dAVP), oxytocin, and arginine-vasotocin have no such activity, although dAVP interferes with the action of AVP when present in equimolar concentration. Relatively high concentrations are required and the effect of active peptides is readily reversible. When the normal, hypotonic medium (a synthetic pond water) is replaced by isotonic sucrose, the action of AVP on the vacuole is abolished. Thus vasopressin is believed to act by increasing permeability of the Amoeba plasma membrane to water.
Gen Comp Endocrinol 1989 Oct
PMID:The effects of vasopressin and related peptides on osmoregulation in Amoeba proteus. 259 42

The standard microelectrode technique was used to electrophysiologically characterize the effect of insulin on both apical and basolateral cell membranes of the frog skin, a model Na-transporting epithelium. Insulin applied to the basolateral side of the epithelium stimulated the sodium transport as shown by both increased short-circuit current, Isc, (P less than 0.02) and transepithelial potential difference, Voc, (P less than 0.002). Potential difference across the apical cell membrane, Vo, decreased (P less than 0.002) as did the apical cell membrane resistance, Ro, (P less than 0.05). The driving force of sodium ions, ENa, increased after insulin (P less than 0.005). These findings confirm that insulin acts both to increase the apical cell membrane permeability for ions and to stimulate the sodium pump in the basolateral membrane. The effects of insulin were compared with those of a vasopressin analog (dDAVP), known to stimulate transepithelial sodium transport by increasing the permeability of the apical cell membrane for sodium ions. dDAVP applied at the height of insulin effect further stimulated transepithelial transport, but insulin applied at the height of dDAVP action did not. It is concluded that the direct stimulation of the sodium pump by insulin may not represent a decisive component in the stimulation of transepithelial transport across the frog skin. A more potent stimulus for sodium transport is obviously the increased permeability of the apical membrane for ions.
Gen Physiol Biophys 1989 Jun
PMID:Microelectrode study of insulin effect on apical and basolateral cell membrane of frog skin: comparison with the effect of 1-deamino-8-D-arginine-vasopressin (dDAVP). 267 Jun 63

1. The inhibitory actions of amiodarone on the isolated rabbit heart and aorta have been studied. 2. Amiodarone inhibited vasopressin- and ergonovine-induced coronary spasm, starting from a concentration of 10(-7) M which did not affect myocardial contractility to 10(-4) M, which decreased myocardial contractility. 3. Sinus node activity was largely unaffected even when the highest dose of 10(-4) M was used. 4. Amiodarone did not modify the smooth muscle contraction in rabbit aorta strips precontracted with noradrenaline or potassium. 5. Comparison with other inhibitors of the cardiovascular system (alpha- and beta-blockers, nitrates, calcium entry blockers) points out a peculiar pharmacological profile of amiodarone and indicates some doubts about its presumed anti-adrenergic properties.
Gen Pharmacol 1989
PMID:Inhibitory actions of amiodarone on the isolated rabbit heart and aorta. 274 97

Interactions between the different signaling roles of myo-inositol 1,4,5-trisphosphate and 1,2-diacylglycerol, the products of agonist-stimulated phosphatidylinositol 4,5-bisphosphate breakdown, are assessed in isolated rat hepatocytes. Measurements of the kinetics of accumulation of individual [3H]inositol phosphates after the addition of different Ca2+-mobilizing agonists in general support the role of inositol 1,4,5-trisphosphate as the second messenger responsible for release of sequestered intracellular Ca2+. Various agonists, when added at maximal concentrations, however, produce qualitatively and quantitatively different responses, which reflect varying abilities of the agonists to activate phospholipase C. Qualitative differences are revealed by a pronounced biphasic pattern to the Ins(1,4,5)P3 accumulation after vasopressin and phenylephrine stimulation, which is indicative of negative feedback. It is suggested that this effect is mediated by a partial diacylglycerol activation of protein kinase C, which in vitro causes an activation of inositol phosphate 5-phosphatase and hence promotes removal of Ins(1,4,5)P3 to Ins(1,4)P2. An alternative mechanism proposed by Biden and Wollheim (1986) of a secondary Ca2+ activation of Ins(1,4,5)P3 3-kinase is considered less likely as a general mechanism, since highly purified kinase prepared from rat brain shows only an inhibition by Ca2+. Glucagon, 8-Br-cAMP, and EGF induce small increases of Ins(1,4,5)P3 in hepatocytes, together with slower and smaller increases of cytosolic free Ca2+ than those produced by vasopressin or phenylephrine, with Ca2+ being mobilized from the same intracellular pools with each of the agonists. The Ca2+-mobilizing effect of glucagon, therefore, may be entirely due to a cAMP-dependent process, although a direct receptor-mediated activation of phospholipase C, as suggested by Wakelam et al. (1986), remains a possibility. The EGF receptor appears to be coupled to phospholipase C, presumably via a G-protein. It is speculated that the mechanism by which cAMP increases Ins(1,4,5)P3 levels in hepatocytes could either be by phosphorylation and inhibition of inositol phosphate 5-phosphatase or by phosphorylation and facilitation of the coupling between the G-protein and phospholipase C. When protein kinase C is maximally activated by pretreatment of hepatocytes with PMA, the stimulatory effects of phenylephrine, glucagon, 8-Br-cAMP, and EGF on the accumulation of inositol phosphates and increase of cytosolic free Ca2+ are largely inhibited.(ABSTRACT TRUNCATED AT 400 WORDS)
Soc Gen Physiol Ser 1987
PMID:Mechanisms involved in receptor-mediated changes of intracellular Ca2+ in liver. 285 Jun 13


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