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)

In an effort to avoid the potentially dangerous side effects of vasopressin infusions, we attempted to reproduce mechanically the splanchnic hemodynamic changes induced by vasopressin without its systemic effects. Superior mesenteric arterial pressure was reduced to 50 to 70 mm Hg for 30 to 60 min in 10 normal dogs by partial balloon obstruction of the superior mesenteric artery. Balloon inflation caused a decrease in portal venous pressure (5.6 +/- 0.6 versus 2.8 +/- 0.7 mm Hg), hepatic vein wedge pressure (4.8 +/- 0.4 versus 2.3 +/- 0.5 mm Hg), and portal vein flow 424 +/- 53 versus 275 +/- 52 ml per min), and an increase in hepatic arterial blood flow (172 +/- 19 versus 217 +/- 29 ml per min). Total hepatic blood flow and oxygen delivery to the liver were unchanged. Partial balloon obstruction caused an increase in cardiac output (1950 +/- 203 versus 2317 +/- 376 ml per min) and mean arterial pressure 138 +/- 6 versus 151 +/- 7 mm Hg), whereas heart rate did not change. Partial balloon obstruction of the superior mesenteric artery caused similar changes in splanchnic hemodynamics to those of vasopressin infusions into the superior mesenteric artery, but without the potential deleterious effects of vasopressin on systemic hemodynamics.
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PMID:Portal pressure reduction induced by partial mechanical obstruction of the superior mesenteric artery in the anesthetized dog. 66 4

The effect of lowering the pressure of oxygen from 80 to 34 mm Hg was examined in anesthetized dogs that were undergoing a water diuresis. This degree of hypoxia was associated with an antidiuresis as urine osmolality (Uosm) increased from 107 to 316 mosmol/kg H(2)O (P < 0.001) and plasma arginine vasopressin increased from 0.06 to 7.5 muU/ml, (P < 0.05). However, hypoxia was not associated with significant changes in cardiac output (CO, from 4.2 to 4.7 liters/ min), mean arterial pressure (MAP, from 143 to 149 mm Hg), glomerular filtration rate (GFR, from 46 to 42 ml/min), solute excretion rate (SV, from 302 to 297 mosmol/min), or filtration fraction (from 0.26 to 0.27, NS). Hypoxia was associated with an increase in renal vascular resistance (from 0.49 to 0.58 mm Hg/ml per min, P < 0.01). The magnitude of hypoxia-induced antidiuresis was the same in innervated kidneys and denervated kidneys. To further examine the role of vasopressin in this antidiuresis, hypoxia was induced in hypophysectomized animals. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in hypophysectomized animals was the same as in intact animals. In contrast to intact animals, however, hypoxia did not induce a significant antidiuresis in hypophysectomized animals (Uosm from 72 to 82 mosmol/kg H(2)O). To delineate the afferent pathway for hypoxia-stimulated vasopressin release, hypoxia was induced in dogs with either chemo- or baroreceptor denervation. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in the denervated animals was the same as in nondenervated animals. Hypoxia resulted in an antidiuresis in chemoreceptor (Uosm from 113 to 357 mosmol/kg H(2)O, P < 0.001) but not in baroreceptor (Uosm from 116 to 138 mosmol/kg H(2)O, NS) denervated animals. To determine if hypoxia alters renal response to vasopressin, exogenous vasopressin was administered to normoxic and hypoxic groups of dogs. The antidiuretic effect of vasopressin was no different in these two groups. These results demonstrate that hypoxia induces an antidiuresis which is independent of alterations in CO, MAP, SV, filtration fraction, renal nerves, or renal response to vasopressin and occurs through baroreceptor-mediated vasopressin release. The nature of the baroreceptor stimulation remains to be elucidated.
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PMID:Mechanism of effect of hypoxia on renal water excretion. 70 76

The effect of CPB on plasma ADH levels, urine flow, and urine osmolality was studied in nine patients. All patients received morphine, 1 mg. per kilogram, and 50 per cent nitrous oxide-50 per cent oxygen for anesthesia. CPB utilized a Travenol disposable bubble oxygenator and the prime consisted of 3 L. of Ringer's lactate. Measurements were made prior to induction of anesthesia , at 30 minutes following surgical incision, and at 15, 30, and 45 minutes during CPB. There were no statistically significant changes in mean arterial BP, cardiac index, serum sodium, or serum osmolality in any period. Urine flow increased from 0.99 +/- 0.3 ml. per minute to a high of 6.13 +/- 2.0 ml. per minute at 30 minute at 30 minutes on CPB (P less than 0.02). Urine osmolality declined from a control value of 691 +/- 142 mOsm. per kilogram to a low of 425 +/- 48 mOsm. per kilogram at 45 minutes on CPB (p less than 0.05). ADH levels rose from a control value of 4.3 +/- 1.5 to 13.0 +/- 3.3 pg. per milliliter with surgical stimulatiion (p less than 0.05). During CPB the ADH levels rose to a peak of 23.7 +/- 3.6 pg. per milliliter at 30 minutes (p less than 0.01) and were declining at 45 minutes. These data suggest that the stress of CPB results in an outpouring of ADH (or vasopressin) to function as a pressor to produce an increase in peripheral resistance. The ADH concentrations far exceed those required for normal physiologic control of water excretion and the urineflow will thus vary more with the hemodynamic changes than with the ADH levels.
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PMID:Antidiuretic hormone levels during cardiopulmonary bypass. 83 Oct 6

Transumbilical portal venous catheterization was performed in 11 patients for diagnostic selective portography. By use of a multiple-catheter technique, the effects of intravenous infusion of [8-lysine]vasopressin on portal venous mixing of tributary flows was measured by simultaneous blood sampling from the left and right portal branch, taking advantage of the oxygen saturation difference between splenic and superior mesenteric venous blood and also by infusion of 133Xe into one of the portal tributaries. Slight signs of incomplete portal mixing were observed at rest in eight of nine patients. During vasopressin infusion, the heterogeneity of oxygen saturation and xenon activity in the portal branches increased significantly. There was also a significant average shift of splenic venous blood toward the left portal branch with, in some patients, only splenic blood in this branch. Streamlining thus was a dynamic phenomenon related to the reduced and altered portal venous flow pattern. This must be considered during flow measurements, and might also have pathophysiological significance in liver diseases.
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PMID:Effect of vasopressin on the mixing of portal venous blood in awake man. 87 36

1. Acute hypoxaemia had been reported to stimulate vasopressin release in animals. 2. Hypoxaemia induced by breathing 9-3% oxygen for 15-20 min failed to produce a rise in plasma arginine vasopressin concentration in six out of eight healthy human subjects. The two subjects who developed an increase in plasma arginine vasopressin concentration had a significant rise in serum cortisol. 3. Breathing 100% nitrogen until impairment of consciousness caused no rise in plasma arginine vasopressin concentration.
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PMID:Effect of acute hypoxaemia on plasma arginine vasopressin in conscious man. 91 65

Ethanol (3%) decreases the potential difference and short-circuit current across the isolated frog skin in chloride Ringer's solution. Unidirectional fluxes of Na and Cl indicate that the drop in short-circuit current is due to an inhibition of the sodium influx. However, ethanol had no effect on the electrical parameters or sodium fluxes, when the frog skin was bathed in chloride-free solutions on both sides or the outside alone. The ethanol response is anion-dependent. In addition, chloride-free media in the inside bathing solution reduced the short-circuit current, indicating a sodium transport pathway which is dependent on chloride and confirming previous data in the literature. Other anions such as sulfate and nitrate could not substitute for chloride. The vasopressin-induced natriferic response and the ethanol effect were found to work independently of each other and different pathways of action are suggested for these agents. The intracellular sodium content of the isolated frog skin epithelium increased and potassium decreased in the presence of the Na-K adenosine triphosphatase inhibitor, ouabain, whereas ethanol or amiloride had no effect. The oxygen consumption of the isolated frog skin was unaffected by up to 10% ethanol. A general metabolic action is probably thus not mediating the response. Urea, in iso-osmotic concentrations to the ethanol, did not mimic its effect. Tritiated water fluxes (in the absence of an osmotic gradient) were reduced by 30% in the presence of 3% ethanol. It is suggested that ethanol may impede the flow of water across frog skin by a physicochemical interaction with membrane pores and the water molecules. The permeability coefficient (Ktrans) for ethanol was found to be 10 times smaller than the Ktrans for water.
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PMID:Effects of ethanol on the permeability of frog skin. 108 5

Neurophysiological, neurochemical and behavioral studies of the effects of ethanol on the nervous system have so far failed to identify specific, direct, primary mechnisms of action that may account for the typical pattern of alcohol intoxication in vivo. Electroencephalogram and evoked response studies indicate biphasic effects in the intact subject, which may correlate better with the level of arousal than with a specific drug action. Effects on spinal reflexes are also biphasic, probably representing the net result of direct influence on resting membrane potential, primary afferent depolarization, and neurotransmitter release. With the exception of its inhibitory effect on release of oxytocin, vasopressin and possibly other hypothalamic peptides, ethanol does not appear notably different in its spectrum of effects from a wide range of other hypnotics, anesthetics and minor tranquilizers. Interpretation of the findings is complicated by the fact that functional alteration of any given neuronal system by ethanol in vivo may reflect a) direct local action of ethanol on the cells under study, b) change in the input to those cells because of an action elsewhere in the nervous system, c) effects of ethanol metabolites, or d) indirect consequences of decreased blood flow, oxygen or metabolite supply, hormonal action, or hypothermia, due to disturbances of homeostasis in the whole body as a result of deep intoxication. To date, attempts to circmvent b, c and d by the study of brain tissue in vitro have shown consistent effects of ethanol only at concentrations well above those that are meaningful in vivo. Relatively specific patterns of action of different drugs in vivo may prove to be largely dependent on their customary rates and routes of administration, and on summation of minor differences in the dose-response curves with different types of neuron, even though the basic types of molecular action may be essentially similar.
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PMID:Direct effects of ethanol on the nervous system. 109 39

A comparison study of several vasoconstrictor and vasodilator agents was conducted measuring changes in intestinal blood flow and oxygen consumption during 10-min periods of intra-arterial infusion. Blood flow was measured in a branch of the superior mesenteric artery of anesthetized dogs with an electromagnetic blood flow meter, and the arteriovenous oxygen content difference across the gut segment was determined photometrically. Vasopressin (4 x 10(-3) and 7x 10(-4) U/kg-min) diminished blood flow 60 and 28% and reduced oxygen consumption 54 and 22%, respectively (all P less than 0.001). In a dose which did not lower blood flow, vasopressin still caused a decline in oxygen consumption (P less than 0.01). Epinephrine (5 x 10(-2) mug/kg-min) decreased blood flow 19% (P less than 0.001) but did not reduce oxygen consumption. After beta-adrenergic blockade, however, the same dose of epinephrine decreased blood flow 41% and oxygen consumption 33% (both P less than 0.001). Responses to angiotension II, calcium chloride, and prostaglandin F2alpha resembled effects of vasopressin rather than those of epinephrine, namely decreased blood flow and decreased oxygen consumption. The vasodilator agents, prostaglandin E1, is isoproterenol, and histamine, increased (P less than 0.001) both blood flow (130, 80, and 98%, respectively) and oxygen consumption (98, 64, and 70%, respectively). Vasopressin, angiotensin II, calcium chloride, and prostaglandin F2alpha appear to contract arteriolar and precapillary sphincteric smooth muscle indiscriminately to evoke both intestinal ischemia and hypoxia. Epinephrine is the exceptional constrictor in this case, producing diminished blood flow without a reduction in oxygen uptake.
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PMID:Effect of vasoactive agents on intestinal oxygen consumption and blood flow in dogs. 115 Aug 81

Continuous i.v. infusions of histamine (5 mug/kg - min), vasopressin (10 mU/kg -min), or angiotensin II (0.5 mug/kg - min) were given to fasting cats. Hepatic arterial flow was decreased 30% by histamine, increased 30% by vasopressin, and not significantly affected by angiotensin, whereas portal venous flow was increased 25% by histamine, decreased 40% by vasopressin, and not significantly affected by angiotensin. The hepatic arterial conductance was decreased about 25% by histamine and angiotensin, and not significantly affected by vasopressin. The gastrointestinal conductance was decreased about 40% by vasopressin and angiotensin, and increased 25% by histamine. The conductance in the intrahepatic low pressure vessels was not affected by histamine and vasopressin, but decreased 25% during the infusion of angiotensin. These hemodynamic effects, however, were not accompanied by changes in the liver function or hepatic metabolism as judged from the splanchnic elimination of ethanol, the hepatic uptake and excretion of ICG, the hepatic oxygen consumption, and lactate and ketone production. This indicates that the functional capacity of the liver and thereby the number of sinusoids perfused is not markedly influenced by these drugs. Vasopressin caused a decrease in the oxygen consumption and an increase in the lactate production in the prehepatic splanchnic area, which may be due to a redistribution of the gastrointestinal blood flow.
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PMID:Effects of histamine, vasopressin, and angiotensin II on hepatosplanchnic hemodynamics, liver function, and hepatic metabolism in cats. 118 38

The effects of repeated intravenous constant infusion of lysine-8-vasopressin (LVP) in a series of 12 conscious patients with portal venous catheters were studied. The portal venous pressure fell, the arterio-portal venous oxygen difference and the systolic and diastolic blood pressures rose and the heart rate decreased. Although no signs of tachyphylaxis were seen in portal venous pressure, systolic blood pressure or heart rate, they were observed both in the arterio-portal venous oxygen difference, indicating a tachyphylactic reaction in the effects on splanchnic blood flow, and in the diastolic blood pressure.
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PMID:Vasopressin tachyphylaxis. A study in conscious man. 126 40


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