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

In 20 patients with g hepatic cirrhosis hospitalized for upper digestive haemorrhage by rupture of oesophageal varices, the intragastric administration of norartrinal in amounts of 4-40 mg/24 h achieved definitive haemostasis in 7 cases and temporary haemostasis (with prolonged survival) in another 6 cases. The overall mortality was 80%. In three of the 7 patients in which haemorrhage was completely arrested death occurred as a result of hepatic failure. The large amounts of Norartrinal administered (up to 120 mg total dose) were well tolerated and did not have haemodynamic side-effects, or renal side-effects. The results obtained, and especially the easy method used for administration of the drug recommend this method as an alternative of the vasopressin treatment.
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PMID:[Intragastric administration of norartrinal in hemorrhage caused by rupture of esophageal varices]. 621 26

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 arterial blood flow distribution between tumour and intact renal tissue was investigated in rats with transplanted sarcomas. Changes in tissue flow were measured by the microsphere tracer technique, and the redistributing effects on blood flow of vasopressin, noradrenalin and oxytocin was recorded. Bolus injections of vasopressin gave a transient decrease of intact tissue flow, not found in tumours. At increasing doses of vasopressin and in early tumour growth phase, the flow discriminating effect tended to vanish. Constant intravenous infusion of vasopressin gave similar reduction of flow in tumour and intact tissue. Selective administration into the renal artery reduced flow in intact tissue but produced ambiguous effects in tumour tissue. Noradrenalin produced less reduction of tumour flow as compared with intact tissue flow. Oxytocin increased tumour blood flow while no flow change occurred in intact tissue. Oxytocin thus appeared to produce the most favourable redistribution of flow within tumour kidneys for the prospect of conveying cytotoxic agents selectively to the tumour.
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PMID:Effects of vasopressin, noradrenalin and oxytocin on blood flow distribution in rat kidney with neoplasm. 627 54

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

After perfusing the vascular circuit of the mesenteric artery of the rat with a Ca-free solution for 20 min, extracellular Ca was depleted, and the vasoconstrictor effect of high K solutions was abolished, while the vasopressin response was reduced by 40%, serotonin by 30% and noradrenaline and adrenaline responses by about 20%. When the Ca-free perfusion was prolonged for 2 h or more, the vascular responses to the agonists were further reduced due to depletion of cellular Ca. Successive doses of each agonist injected at 1 min intervals showed a decline of the responses, that recovered when 4 min or more were allowed to pass after the last injection. This reversible desensitization or tachyphylaxis was rapidly abolished by Ca. Noradrenaline and adrenaline showed crossed tachyphylaxis, which depressed the responses to serotonin and vasopressin. Tachyphylaxis to serotonin and vasopressin did not depress the response to the other two agonists. These findings support the conclusion that not only do noradrenaline and adrenaline share a Ca pool, but that so do serotonin and vasopressin. These two agonists each require a separate Ca pool.
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PMID:Calcium pools in the contraction of arterial smooth muscle induced by several agonists. 653 May 55

To assess in vivo functional interactions of vasopressor substances, norepinephrine and vasopressin, with renal prostaglandins and kallikrein-kinin system which are responsible for the vasodepressor mechanism in the kidney, we evaluated chronic effects of norepinephrine (1.8 mg/kg/day ip) and vasopressin (7.2 U/kg/day ip) on urinary prostaglandin E excretion and urinary kallikrein excretion in conscious rats. Both norepinephrine and vasopressin induced a sustained increase in systolic blood pressure. Norepinephrine induced slight but significant increases in urinary prostaglandin E excretion and urinary kallikrein excretion which were sustained for up to 6 days. Vasopressin induced a marked increase in urinary prostaglandin E excretion which was sustained for up to 6 days, whereas it induced a sustained decrease in urinary kallikrein excretion. Circulating angiotensin II levels was not changed by norepinephrine, but was decreased by vasopressin. These results indicate that renal prostaglandin E may not correlate with renal kallikrein-kinin and renin-angiotensin system in the responses to norepinephrine and vasopressin, and that vasopressin may be a more potent stimulator of the synthesis or release of renal prostaglandin E.
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PMID:Chronic effects of norepinephrine and vasopressin on urinary prostaglandin E and kallikrein excretions in conscious rats. 656 34

The effects of local intra-arterial infusions of serotonin (5 or 25 micrograms base/min) or norepinephrine (1 or 5 micrograms base/min) on cutaneous (skin) and skeletal muscle vasculatures were investigated in canine forelimbs perfused at constant flow in dogs anesthetized with pentobarbital. Norepinephrine produced dose-related constriction of the skin and skeletal muscle vasculatures. In the cutaneous vascular circuit, norepinephrine produced large artery, small vessel, and large vein constriction. The increase in cutaneous vascular resistance was primarily due to an increase in small vessel resistance. Serotonin did not increase skeletal muscle vascular resistance but produced marked cutaneous vasoconstriction subsequent to large artery and large vein constriction. The small vessels, if anything, tended to dilate. The skin and skeletal muscle vascular responses to serotonin and norepinephrine were similar in innervated and acutely denervated forelimbs. Phentolamine pretreatment completely blocked all vascular actions of norepinephrine, and largely inhibited the cutaneous vasoconstriction produced by the infusion of the low dose of serotonin. However, the cutaneous large artery and large vein constriction produced by the infusion of the high dose of serotonin was not affected by phentolamine pretreatment. Cyproheptadine pretreatment blocked or largely inhibited the cutaneous vasoconstriction produced by serotonin only in doses which also inhibited norepinephrine and vasopressin cutaneous vasoconstriction. Pretreatment with methysergide blocked or largely inhibited the cutaneous large artery and large vein constriction produced by infusions of serotonin. Norepinephrine and vasopressin produced significant vasoconstriction in the presence of methysergide. These data suggest that the cutaneous large artery and large vein constriction produced by serotonin is not due to the activation of postjunctional alpha-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that serotonin receptors mediate the cutaneous vasoconstriction produced by 5-hydroxytryptamine in canine forelimbs. 662 7

Light and electron microscopy were used to study the effects of a lithium-supplemented diet on renal structure in the rat. At the end of a 7-week experimental period serum lithium levels were 1.14 +/- 0.20 mM. Lesions consisting of groups of dilated tubules were found in the immediate vicinity of the interlobular arteries in all experimental animals. These tubules were identified as the connecting tubule or the initial portion of the collecting tubule. The epithelium of these tubules was generally flattened but was punctuated by markedly swollen epithelial cells. PAS-positive deposits found in both types of cells were identified as glycogen. Electron microscopy revealed considerable lithium-induced damage in the swollen cells including increased numbers of mitochondria, many of which were swollen or otherwise damaged, dilated cisternae of endoplasmic reticulum and vacuolization of the apical cytoplasm. The flattened cells of these tubules were similar to the dark or intercalated cells of normal collecting tubules. Some detachment of epithelial cells from their basement membrane was evident in these tubules. Damage was less severe in distal convoluted tubules. Lithium-induced changes were not observed in glomeruli, proximal tubules or ascending thick limbs of Henle. In medullary collecting tubules damage was less severe than in cortical collecting tubules, but detachment of epithelial cells was a common finding. The interstitial tissue of the papilla exhibited histochemical and ultrastructural changes consistent with lithium blockade of the action of antidiuretic hormone. The ultrastructural damage to cortical tubules is similar to that found in patients receiving therapeutic lithium for long periods of time. The anatomic sites of lithium-induced pathology correspond to the location of lithium-induced pathophysiology.
Nephron 1983
PMID:Effects of lithium on the structure of the rat kidney. 686 74


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