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)

The effects of several polypeptides, e.g. angiotensin II, substance P, oxytocin and vasopressin, on the isolated frog gastrocnemius, chick biventer cervicis and rat hemodiaphragm preparations were studied using electrophysiological and neurochemical techniques. The effects of angiotensin II, substance P, oxytocin and vasopressin on neuromuscular transmission and muscle contraction were investigated by studying the following parameters: the directly and indirectly-elicited twitch and tetanic contractions, nerve compound action potential, uptake of 3H-methylcholine into nerve-muscle preparations, the contractures produced by depolarizing drugs, e.g. ACh or TEA. The results showed that angiotensin II (10(-10)-10(-6) M) and substance P (10(-7)-10(-6) M) enhanced neuromuscular transmission and muscle contraction by increasing the amplitudes of the indirectly-elicited twitch and tetanic contractions. Oxytocin and vasopressin (1-100 mU/ml-1) both depressed neuromuscular transmission by reducing the contractile and electrical response in the frog, chick and rat skeletal muscle. It was concluded that, like their effects on ganglionic transmission, the peptides can modify neuromuscular transmission. The mechanism by which these peptides produce their effects may be dependent on external calcium concentration. These peptides may affect both pre- and postjunctional mechanisms; prejunctionally by increasing/decreasing the release of ACh, and postjunctionally by affecting the sensitivity of the postjunctional membrane to depolarizing drugs and/or producing a contracture in the skeletal muscle.
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PMID:Actions of polypeptides at the neuromuscular junction. 241 8

The kidney is a target organ for antidiuretic hormone (ADH) and it is also the main organ involved in the clearance of this hormone. There is controversy on the mechanisms involved in the renal handling of ADH, mainly in regard to whether it is secreted or reabsorbed. Kinetic and renal clearance studies of ADH were performed in water-loaded rats and were compared with inulin (glomerular filtration marker) and tetraethylammonium (TEA, marker of organic cation secretion). The kinetics of the three molecules fitted a bicompartmental model. Distribution constants of [125I]-ADH were twofold higher than those of inulin. Elimination constant was higher for inulin than for ADH (0.049 +/- 0.001 vs. 0.020 +/- 0.003 min-1, respectively), suggesting reabsorption of the hormone. The ratios of Clearance ADH/Clearanceinulin and ClearanceTEA/Clearanceinulin were 0.14 and 4.86, respectively. In summary, data from kinetic studies and from renal clearances suggested that ADH is reabsorbed.
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PMID:Participation of the kidney in the kinetics of arginine vasopressin in the water-loaded rat. 771 46

The magnocellular neurosecretory cells of the hypothalamus (MNCs) regulate water balance by releasing vasopressin and oxytocin as a function of plasma osmolality. Release is determined largely by the rate and pattern of action potentials generated in the MNC somata. Changes in firing are mediated in part by a stretch-inactivated non-selective cation current that causes the cells to depolarize when increased osmolality leads to cell shrinkage. We have obtained evidence for a new current that may regulate MNC firing during changes in external osmolality, using whole-cell patch clamp of acutely isolated rat MNC somata. In internal and external solutions lacking K+, with high concentrations of TEA, and with Na+ as the only likely permeant cation, the current appears as a slow inward current during depolarizations and yields a large tail current upon return to the holding potential of -80 mV. Approximately 60% of the MNCs tested (79 out of 134 cells) displayed a large increase in tail current density (from 5.2+/-0.9 to 10.5+/-1.4 pA pF-1; P<0.001) following an increase in external osmolality from 295 to 325 mosmol kg-1. The current is activated by depolarization to potentials above -60 mV and does not appear to depend on changes in internal Ca2+. The current is carried by Na+ under these conditions, but is blocked by Cs+ and Ba2+ and by internal K+, which suggests that the current could be a K+ current under physiological conditions. This current could play an important role in regulating the response of MNCs to osmolality.
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PMID:A novel osmosensitive voltage gated cation current in rat supraoptic neurones. 1609 39

With a view to evaluate the role of AQP-1 and caveolin proteins in the hemostatic actions of vasopressin, hemostasis was evaluated by bleeding and clotting time respectively. Groups of mice and guinea pigs were treated with arginine vasopressin (AVP) and 1-deamino-8D-AVP (DDAVP) to evaluate their effects on the hemostasis. DDAVP and AVP were able to appreciably reduce the bleeding and clotting time after sodium thiopentone, but not effectively after TEA treatment. Animal groups were pretreated with aquaporin-1 (AQP-1) blockers or water deprived to enhance the expression of AQP-1 water channels. Another group of animals were treated with caveolin protein modulators, cholera toxin (CTX) and the effect of vasopressin analogues evaluated. The results suggest that AQP-1 water channels and caveolin proteins contribute to modulate the hemostatic mechanisms of vasopressin.
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PMID:Evaluation of vasopressin mediated effects on hemostatic mechanisms: relationship with aquaporins and caveolin proteins. 1612 12

The goal of this study was to investigate the mechanism underlaying the vasodilatory effect of paeonol, a major active element from the root bark of Chinese herbs Paeonia suffruticosa Andr. and Cynanchum paniculatum (Bunge) Kitagawa. Paeonol relaxed isolated rat aorta rings by 95.6% while the 10(-6) M forskolin-induced vasodilatation used as 100%. The EC(50) of vasodilatation by paeonol is 2.9x10(-4) M. Although paeonol exerted endothelium-independent relaxation, L-NAME treatment inhibited paeonol-induced vasodilation of endothelium intact rings, while indomethacin did not. Both L-NAME and ODQ did not affect paeonol relaxation in the rings without endothelium. In addition, paeonol markedly elevated NO generation in cultured endothelial cells. Pre-treatment of propranolol, glibenclamide, TEA and BaCl(2) did not affect paeonol relaxation of endothelium removed rings. On the other hand, pre-treated of rings (without endothelium) with paeonol markedly blocked vasoconstriction induced by AngII, PGF(2alpha), 5-HT, dopamine, vasopressin, endothelin-1 and PE. The paeonol incubation also significantly attenuated KCl-induced contraction which mainly depended on Ca(2+) influx. In Ca(2+)-free medium (containing 10(-4) M of EGTA and 60 mM of KCl), paeonol suppressed the contraction curve of CaCl(2). In addition, paeonol also inhibited contraction by PE in Ca(2+) free solution (containing 10(-4) M of EGTA) which mainly relied on intracellular Ca(2+) release. Whole-cell patch-clamp experiment showed that paeonol shifted the I-V curve and the peak value of calcium currents was significantly inhibited. In conclusion, our study suggested that voltage-dependent and receptor-operated Ca(2+) channel, as well as intracellular Ca(2+) release were all inhibited by paeonol. An intracellular Ca(2+) regulatory mechanism may be responsible to potent vasodilatory effect of paeonol.
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PMID:Vascular dilation by paeonol--a mechanism study. 2064 26