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)

1. The magnitude of the maximum constrictor response to nerve stimulation was measured in the saphenous, ear, inferior and superior mesenteric, renal and carotid arteries in the rabbit and corresponding arteries, except the ear and carotid, in the guinea-pig. The responses varied from an average rise of 350 mm Hg in the rabbit saphenous to almost no response in the rabbit carotid. The guinea-pig arteries gave consistently smaller responses than the rabbit. The response magnitude was unrelated to wall thickness or the presence of an active uptake mechanism for noradrenaline. The response did correlate with the density of adrenergic innervation, with the wall thickness to lumen ratio and with the function of the artery and the amount of connective tissue in its wall.2. The magnitude of the maximum constrictor response to noradrenaline and six other agonist drugs, acetylcholine, histamine, 5-HT, KCl, vasopressin and angiotensin II, was compared. In all arteries noradrenaline was the most powerful agonist. The maximum responses to nerve stimulation and to noradrenaline were compared. In the rabbit saphenous and ear arteries this ratio was almost 1, but in arteries such as the rabbit renal it fell below 0.5.3. Artery wall stiffness was measured from the pressure/volume relationship during distension of a closed length of artery. In a relaxed artery two components only were present, an early easily distended phase and a late relatively undistensible phase. Noradrenaline caused a third, early, very stiff phase to appear in the pressure/volume curves. This is probably due to contracted muscle. The increase in stiffness varied from 617% in the rabbit saphenous to 152% in the rabbit carotid. In conducting arteries such as the carotid the change in stiffness was a more sensitive index of noradrenaline action than vaso-constriction.4. During the measurement of wall stiffness stress relaxation was not noticeable in relaxed arteries but was prominent in arteries contracted by noradrenaline. Stress relaxation involved both the changes in wall stiffness and the ability to constrict and was reversible even in the continuing presence of agonist drugs.5. Nerve stimulation, even in arteries where its vasoconstrictor effects were equal to those of noradrenaline, gave only slight increases in artery wall stiffness, suggesting that even in these densely innervated arteries only a small fraction of the muscle is activated by nerve stimulation.
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PMID:Constrictor and compliance responses of some arteries to nerve or drug stimulation. 433 55

The frog urinary bladder undergoes, in some conditions, a marked increase of its water permeability when incubated in hypertonic media. This increase was observed with various nonpermeant solutes. It seems to result from the shrinkage of an osmo-sensitive compartment of the tissue, probably the epithelial cells. Many similarities were found between this effect and the physiological increase in water permeability (hydrosmotic response) elicited by antidiuretic hormone (ADH): both were dependent on the physiological state of the animals, and although the response was slower after hyperosmolar than after hormonal challenge, the patterns of response were similar, and in both cases markedly dependent on bathing solution temperature. Norepinephrine and prostaglandin E(1), which in this tissue reduce the hydrosmotic action of ADH, presumably by inhibiting the adenyl cylase also reduced the effect of hyperosmolarity. Conversely this effect was potentiated by incubation in the presence of oxytocin, exogenous cyclic AMP, and theophylline, conditions in which the intracellular concentration of cyclic AMP is increased. These data demonstrate that the response to hyperosmolarity is elicited, at least partly, by mechanisms also involved in the physiological hydrosmotic response to ADH.
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PMID:The effect of hypertonic media on water permeability of frog urinary bladder. Inhibition by catecholamines and prostaglandin E 1 . 434 37

Adrenergic and cholinergic agonists and antagonists were applied microelectrophoretically to over 700 neurons in the cat supraoptic nucleus, 20 percent of which were antidromically identified as neurosecretory cells. Norepinephrine uniformly depressed all sensitive cells. Acetylcholine caused both muscarinic depression and nicotinic excitation which were antagonized by atropine and dihydro-beta-erythroidine, respectively. These results support the hypothesis that norepinephrine and acetylcholine are directly involved in controlling the release of antidiuretic hormone.
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PMID:Supraoptic neurosecretory cells: adrenergic and cholinergic sensitivity. 439 31

The effects of the Ca2+-mobilizing hormones noradrenaline, vasopressin and angiotensin on the unidirectional influx of Ca2+ were investigated in isolated rat liver cells by measuring the initial rate of 45Ca2+ uptake. The three hormones increased Ca2+ influx, with EC50 values (concentrations giving half-maximal effect) of 0.15 microM, 0.44 nM and 0.8 nM for noradrenaline, vasopressin and angiotensin respectively. The actions of noradrenaline and angiotensin were evident within seconds after their addition to the cells, whereas the increase in Ca2+ influx initiated by vasopressin was slightly delayed (by 5-15s). The activation of Ca2+ influx was maintained as long as the receptor was occupied by the hormone. The measurement of the resting and hormone-stimulated Ca2+ influxes at different external Ca2+ concentrations revealed Michaelis-Menten-type kinetics compatible with a saturable channel model. Noradrenaline, vasopressin and angiotensin increased both Km and Vmax. of Ca2+ influx. It is proposed that the hormones increase the rate of translocation of Ca2+ through a common pool of Ca2+ channels without changing the number of available channels or their affinity for Ca2+.
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PMID:Noradrenaline, vasopressin and angiotensin increase Ca2+ influx by opening a common pool of Ca2+ channels in isolated rat liver cells. 608

The relationship between gastric blood flow and acid secretion has been studied by using a number of secretory stimulants and inhibitors and different techniques that measure gastric blood flow. Although there are conflicting data, there appears to be a consensus regarding the main aspects of this relationship. Agents that stimulate gastric acid secretion such as histamine, gastrin, cholinergic agents, and vagal stimulators also increase gastric blood flow. Other agents such as isoproterenol, epinephrine, and prostaglandins, which at low doses increase gastric blood flow, reduce gastric acid secretion at higher doses. Norepinephrine, vasopressin, and shock reduce gastric blood flow and thereby cause a decrease in secretion. Histamine H2-receptor antagonists reduce stimulated acid secretion and gastric blood flow. Histamine, gastrin, and acetylcholine have been shown to stimulate acid secretion in vitro. Therefore, these observations suggest that although blood flow is not a prerequisite for initiation of stimulated acid secretion, it can become rate-limiting at higher rates of secretion. Although the literature is replete with studies that attempt to characterize the relationship between gastric blood flow and acid secretion, conclusions have varied. Much of the difficulty has arisen because of the differences in technique used to measure gastric blood flow and the differences between anesthetized and unanesthetized animal preparations. Under some specific conditions, the different blood flow techniques give comparable results and this relationship can be defined.
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PMID:Blood flow and gastric secretion. 612 4

The effects of Pro-Leu-GlyNH2 (PLG), administered i.c.v. in doses of 3.5, 35, 350 and 3500 pmol, were studied on the alpha-MPT-induced disappearance of catecholamines in microdissected rat brain nuclei. PLG, dose-dependently, increased dopamine disappearance in the nucleus caudatus and globus pallidus, whereas a decrease in dopamine disappearance was observed in the nucleus dorsomedialis. Noradrenaline disappearance was decreased in the medial septal nucleus, anterior hypothalamic area and lateral amygdala. A tendency towards an increase in noradrenaline disappearance was observed in the nucl. supraopticus. These data show that PLG has a central site of action. The effects of PLG on dopamine disappearance are comparable to those previously found with vasopressin, while the effects of PLG on noradrenaline utilization show a striking similarity with those previously obtained with oxytocin.
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PMID:Pro-Leu-GlyNH2 affects dopamine and noradrenaline utilization in rat limbic-forebrain nuclei. 615 Jul 49

The present study was conducted to measure norepinephrine release during sympathetic nerve stimulation and to evaluate vascular reactivity in the isolated perfused mesenteric vasculature of normotensive and Doca-salt hypertensive rats. Significantly greater vasoconstrictor responses to periarterial nerve stimulation, norepinephrine, and vasopressin, but not to barium chloride, were observed in the mesenteric vasculature of the hypertensive rats in comparison with the control normotensive group. Norepinephrine release, measured as total tritium overflow, during periarterial nerve stimulation at 4 Hz for 2 min, was identical in both normotensive and hypertensive animals. Phentolamine (5.3 micro M) significantly increased tritium overflow, but to the same extent in the normotensive and the hypertensive mesenteric vasculature, suggesting that the negative feedback presynaptic alpha-adrenoceptor mechanism, which has been proposed to modulate transmitter release, was unaltered in this form of hypertension. These results indicate that hyperresponsiveness of the mesenteric vasculature to periarterial nerve stimulation in the hypertensive rats is due to increased sensitivity of the vascular alpha-adrenoceptor and not facilitation of the transmitter release. The increased vascular reactivity to norepinephrine and vasopressin may be involved in the maintenance of Doca-salt hypertension.
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PMID:Sympathetic nerve function and vascular reactivity in Doca-salt hypertensive rats. 625 76

The pressor response to lysine vasopressin was tested in groups of male Wistar, Brattleboro, Wistar-Kyoto, and spontaneously hypertensive rats. Moreover, the influence of sodium intake, angiotensin II, saralasin, captopril, norepinephrine, and isoproterenol on vasopressin pressor responses was evaluated. The right iliac artery and one or both femoral veins of the animals were catheterized under light ether anesthesia. The experiments were carried out following a 2-h stabilization period with the rats awake and semirestrained. Pressor responsiveness was evaluated acutely on the basis of dose-response curves (0.5-4 mU). In the Wistar rats, angiotensin II (10 and 30 ng/min) and isoproterenol (10 ng/min) markedly decreased the response to vasopressin, whereas variations in sodium intake and blood pressure per se did not seem to exert any influence. Norepinephrine (250 ng/min) slightly enhanced the pressor responsiveness to the smaller doses of lysine-vasopressin. Brattleboro rats with congenital diabetes insipidus were less sensitive to vasopressin than the other animals, and neither angiotensin II nor isoproterenol induced any change. In conclusion, the pressor responsiveness to vasopressin can vary considerably depending on several factors. These must be taken into account when evaluating the possible pressor role of vasopressin in experimental and clinical settings.
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PMID:Pressor responses of rats to vasopressin: effect of sodium, angiotensin, and catecholamines. 633 8

Norepinephrine (NE) 10(-6) M or vasopressin (VP) 12.5 microU/ml were injected into the isolated carotid sinus of anesthetized rabbits. The sinus was exposed either to the arterial pressure or to a pressure controlled reservoir. Multifiber and single fiber recordings were made. Both NE and VP increased baroreceptor activity at all sinus pressures but decreased activity in a few fibers. The results are consistent with the drugs having their effects on smooth muscle fibers in the adventitia.
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PMID:Effect of norepinephrine and vasopressin on carotid sinus baroreceptor activity in the anesthetized rabbit. 646 86

The effects of various agents which have been implicated in the regulation of vasopressin release, on the supraoptic neuroendocrine cells were studied intracellularly. L-glutamate (10(-4)M) and gamma-aminobutyric acid (10(-6) M) had potent excitatory and inhibitory actions, respectively. Acetylcholine (10(-6) M) depolarized the membrane and increased the membrane input resistance. Norepinephrine (10(-5) M) produced either excitatory or inhibitory action on the spontaneous firing rate depending on the cell impaled. Morphine (10(-8)-10(-6) M) strongly depressed the spontaneous firing rate whereas it has no noticeable effect on the membrane potential and input resistance. Angiotensin II (10(-5) M) had no effect on any of the cells tested.
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PMID:Pharmacological characterization of the magnocellular neuroendocrine cells of the guinea pig supraoptic nucleus in vitro. 652 56


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