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)

Vasopressin has been found to impair hepatic function in patients with cirrhosis. The aim of this study was to investigate whether oxygen inhalation could improve hepatic function during vasopressin infusion. Vasopressin (0.3 iu/min) was infused into eight patients with cirrhosis for 50 min. During the first 30 min they were ventilated by room air and for the following 20 min by oxygen (approximate 50% of FiO2). The extra oxygen inhalation caused a typical increase in arterial (+7%, P less than 0.01), portal venous (+8%, P less than 0.05), and hepatic venous (+9%, P less than 0.01) oxygen content. No effect was noted in arterio-hepatic venous and portal venous-hepatic venous oxygen content difference in comparison with the values after vasopressin alone. The hepatic perfusion remained unchanged. These results suggest that the extra oxygen did not increase hepatic oxygen uptake. Similarly, intrinsic clearance of indocyanine green did not improve. It is concluded that oxygen supplement in this setting has no hepatic benefit in patients with cirrhosis.
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PMID:Lack of hepatic benefit by oxygen inhalation during vasopressin infusion in patients with cirrhosis. 161 Oct 13

Renal cortical thick ascending limbs of Henle's loop (CAL) and distal convoluted tubules (DCT) represent sites at which much of the final regulation of urinary ionic composition, particularly that of calcium, is accomplished in both humans and in rodents. We sought in the present work to develop an efficient means for isolating parathyroid hormone (PTH)-sensitive cells from these nephron segments and to grow them in primary culture. [CAL+DCT] cells were isolated from mouse kidney using an antiserum against the Tamm-Horsfall glycoprotein which, in the renal cortex, is produced exclusively by these cells. A second antibody conjugated to coated ferrous particles permitted magnetic separation of [CAL+DCT] cells from Tamm-Horsfall negative renal cortical cells. Approximately 3 X 10(6) cells per kidney with a trypan blue exclusion greater than 94% were isolated by these procedures. Experiments were performed to characterize the cells after 7 to 10 days in primary culture. PTH and isoproterenol, but neither calcitonin nor vasopressin, stimulated cyclic AMP (cAMP) formation in [CAL+DCT] cells, consistent with the pattern of hormone-activated cAMP synthesis found in freshly isolated CAL and DCT segments. Alkaline phosphatase, an enzyme present dominantly in proximal tubule brush border membranes, was virtually absent from [CAL+DCT] cells but was present in Tamm-Horsfall negative cells. Similarly, Na-glucose cotransport was absent in [CAL+DCT] cells but present in Tamm-Horsfall negative renal cortical cells. Finally, transport-related oxygen consumption in [CAL+DCT] cells was blocked by bumetanide and by chlorothiazide, diuretics that inhibit sodium transport in CAL and DCT nephron segments. These results demonstrate that PTH-sensitive [CAL+DCT] cells can be isolated in relatively high yield and viability and grown in cell culture. Primary cultures of these cells exhibit a phenotype appropriate to their site of origin in the nephron.
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PMID:Immunomagnetic separation, primary culture, and characterization of cortical thick ascending limb plus distal convoluted tubule cells from mouse kidney. 164 64

1. Arginine vasopressin reduces whole-body oxygen consumption in conscious dogs. To determine whether this decrease could result from limited oxygen delivery, studies were performed in two groups of chronically instrumented dogs. 2. In the first group (n = 7), vasopressin was infused at a rate of 18.5 pmol min-1 kg-1 while the animals were breathing 10% oxygen. Hypoxaemia alone (arterial partial pressure of oxygen 4.67 kPa) decreased whole-body oxygen delivery by 30%. The fall in whole-body oxygen consumption induced by vasopressin during hypoxaemia was not different from that measured under normoxic conditions, even though whole-body oxygen delivery was more reduced. 3. In a second group of seven dogs, hindquarter blood flow (electromagnetic flowmeter on lower abdominal aorta) and oxygen consumption (blood flow multiplied by arteriovenous oxygen difference) were measured as infusions of vasopressin were given either systemically or into the lower abdominal aorta. Systemic vasopressin infusions at 0.92, 4.6 and 18.5 pmol min-1 kg-1 reduced hindquarter blood flow, oxygen delivery and oxygen consumption, but the decreases in blood flow and oxygen delivery were dose-related whereas that in oxygen consumption was not. Intra-arterial infusions of vasopressin that increased venous concentrations as much as or more than systemic infusion of 0.92 pmol of vasopressin min-1 kg-1 had no effect on oxygen consumption, even though the higher intra-arterial rate reduced blood flow and oxygen delivery as much as the systemic infusion. Thus systemic but not locally administered vasopressin reduced hindquarter oxygen consumption.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduced oxygen consumption induced by vasopressin in dogs depends on systemic administration. 166 81

There is no doubt that under normal conditions powerful local metabolic regulation adjusts coronary blood flow to myocardial oxygen consumption. However, despite substantial experimental efforts the responsible mediators are still largely unknown. Adenosine, a purported mediator of local metabolic control of coronary blood flow, is probably only involved in transient flow adaptations but not in steady state coronary autoregulation. Even below the autoregulatory range a substantial vasodilator reserve persists, and recruitment of such a vasodilator results in improved regional myocardial blood flow and attenuated regional ischaemic dysfunction. Beta-adrenergic coronary dilation is of minor functional importance. Alpha-adrenergic coronary constriction acts to attenuate increases in coronary blood flow during sympathetic activation under normal conditions, so that myocardial oxygen extraction increases to match the increased oxygen consumption. Alpha-adrenergic coronary constriction remains operative in ischaemic myocardium, thus precipitating or contributing to acute myocardial ischaemia during sympathetic activation and exercise in experimental animals, as well as in patients with stable angina. The vagal transmitter acetylcholine-upon exogenous intracoronary infusion-induces critical constriction of epicardial coronary arteries with endothelial dysfunction and atherosclerosis. However, a vagal initiation of coronary spasm or myocardial ischaemia has not been documented so far. Similarly, peptide hormones/transmitters such as NPY, vasopressin and angiotensin can induce myocardial ischaemia upon exogenous administration. Their pathophysiological role in myocardial ischaemia, however, remains to be established.
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PMID:Control of coronary vasomotor tone in ischaemic myocardium by local metabolism and neurohumoral mechanisms. 166 59

Experiments were performed on anesthetized (chloral hydrate) Wistar rats to determine the effect of vasopressin (VP) on cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), cerebrovascular resistance (CVR), and mean arterial blood pressure (MAP) before and after V1 or V2 VP receptor blockade. Influence of synthetic V2 receptor agonist (dVDAVP) on these variables was also tested. Intracarotid administration of 5 mU VP (Pitressin, n = 15) significantly increased CBF by 28% and CMRO2 by 27% and reduced CVR by 20% of control value. Intravenous (i.v.) infusion of dEt2AVP (V1 antagonist, 15 micrograms kg-1 h-1, n = 7) did not influence the effect of VP on CBF, CMRO2, and CVR but abolished MAP increase after VP. Intravenous (i.v.) infusion of d(CH2)5[D-Ile2,Abu4] AVP (V2 antagonist, 15 micrograms kg-1 h-1, n = 8) abolished the effect of VP on CBF, CMRO2, and CVR without changing its influence on MAP. Intracarotid administration of 12.5 ng dVDAVP (n = 7) increased CBF by 43% and CMRO2 by 29% and decreased CVR by 29% of control value. MAP was not affected. The results suggest that VP-induced CBF increase is, at least partly, caused by the rise of CMRO2 and mediated by V2-like receptors.
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PMID:V2-like receptors mediate cerebral blood flow increase following vasopressin administration in rats. 169 87

The effects of infusion of arginine vasopressin (20 mU.kg-1.min-1) on coronary blood flow and the proportion of the coronary microvasculature perfused was studied in rabbit myocardium. Fluorescein isothiocyanate--dextran was injected into anesthetized open-chest rabbits to identify the perfused vessels and an alkaline phosphatase stain was employed to locate the total microvasculature. Coronary blood flow (radioactive microspheres) was studied in separate groups of rabbits. Vasopressin infusion caused bradycardia (243 +/- 19 to 165 +/- 22 beats/min, mean +/- SD) and an increase in mean blood pressure (92 +/- 18 to 104 +/- 12 mmHg) (1 mmHg = 133.32 Pa). Coronary blood flow decreased significantly with vasopressin from 209 +/- 68 to 97 +/- 36 mL.min-1.100 g-1. The proportion of the arteriolar bed per millimeter squared perfused decreased significantly after vasopressin from 54 +/- 13 to 44 +/- 21%, while the percentage of capillaries per millimeter squared increased significantly from 57 +/- 6 to 67 +/- 11%. There were no subepicardial versus subendocardial differences in any measured parameter. Thus, both coronary blood flow and the proportion of the arteriolar bed perfused decreased with vasopressin. However, compensation occurred in that the proportion of capillaries perfused increased. This indicated an independent level of control of the coronary arteriolar and capillary beds. These microvascular changes may help to maintain oxygen supply-demand balance with vasopressin in the heart.
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PMID:Effect of vasopressin on myocardial capillary recruitment and coronary blood flow in the anesthetized rabbit. 171 7

Changes in perfusate Ca2+ (measured with a Ca(2+)-selective electrode) and changes in bile calcium (measured by atomic absorption spectroscopy) were continuously and simultaneously monitored after infusion of (a) vasopressin, (b) glucagon and (c) both vasopressin and glucagon together to the perfused rat liver. Also monitored were perfusate glucose and oxygen concentrations and bile flow. Vasopressin induces a sharp, transient, pulse of increased bile flow and increased bile calcium within 1 min of infusion, concomitant with rapid changes in perfusate Ca2+ fluxes, glucose output and oxygen uptake. This is immediately followed by a decrease in both bile flow and bile calcium for as long as the hormone is administered. Changes induced by glucagon are a relatively slow onset of perfusate Ca2+ efflux and oxygen uptake, but rapid glucose output, and a small but significant and transient decrease in bile flow and bile calcium which, despite the continued infusion of the hormone, spontaneously and rapidly returns to normality. However, the greatest responses are observed after co-administration of both hormones. Coincident with the augmented perfusate Ca2+ fluxes (influx) seen in earlier work, there occurs within 1 min of vasopressin infusion a sharp increase in bile secretion and bile calcium greater in magnitude than that produced by vasopressin alone. Immediately thereafter bile secretion and bile calcium decline below basal values and remain there for as long as the hormones are administered. Glucagon and vasopressin therefore each have opposing effects on bile flow and bile calcium. However, the action of vasopressin is enhanced by the prior administration of glucagon. The data thus reveal features about the actions of glucagon and Ca(2+)-mobilizing hormones on bile flow and bile calcium not previously recorded and provide a novel framework around which the whole issue of hepato-biliary Ca2+ homoeostasis can be assessed in normal and diseased liver.
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PMID:Concomitant stimulation by vasopressin of biliary and perfusate calcium fluxes in the perfused rat liver. 173 88

Cardiovascular and hormonal responses to reconstructive abdominal aortic surgery were studied in 20 patients anaesthetized either with moderate-dose fentanyl (20 micrograms kg-1) combined with isoflurane, nitrous oxide and oxygen (n = 10), or with thoracolumbar epidural bupivacaine combined with isoflurane, nitrous oxide and oxygen (n = 10). After the start of operation, hypotension occurred in four patients in the epidural group. In both groups, the aortic cross-clamping caused slight increases both in mean arterial pressure and in calculated systemic vascular resistance, and a significant decrease in cardiac index. At the same time, a marked increase in plasma vasopressin was seen in the fentanyl group. Plasma catecholamines were low in both groups. After aortic declamping, the cardiac index improved in both groups, although two patients in the fentanyl group and four patients in the epidural group were hypotensive. Post-operatively, eight patients in the fentanyl group were hypertensive, versus none in the epidural group, in which bupivacaine-fentanyl was administered epidurally. At the same time, plasma vasopressin and adrenaline increased significantly in both groups, whereas plasma noradrenaline did so only in the fentanyl group. The results suggest that thoracolumbar epidural bupivacaine combined with low-dose isoflurane in nitrous-oxide-oxygen prevents intra-operative hypertension and tachycardia, but it may cause hypotension. Post-operative hypertension and tachycardia as well as the increase in plasma noradrenaline are prevented by epidural administration of bupivacaine-fentanyl.
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PMID:Thoracolumbar epidural anaesthesia and isoflurane to prevent hypertension and tachycardia in patients undergoing abdominal aortic surgery. 176 40

Previous work indicates that the magnitude and direction of renal responses to exercise depend on the exercise intensity. To examine mechanisms responsible for these findings, renal and hormonal responses were studied in eight healthy male subjects (29.6 +/- 1.9 yr) before and immediately after four 20-min bouts of submaximal exercise (cycle ergometry) at work loads representing 25, 40, 60, and 80% of maximal oxygen consumption. Urine flow, osmotic clearance, glomerular filtration rate, and sodium excretion (UNa+V) all tended to rise at the 25% work load but were markedly reduced at the higher work intensities. Changes in urine flow paralleled changes in glomerular filtration rate (r = 0.91). Plasma vasopressin (ADH), aldosterone, and plasma renin activity tended to increase progressively with increases in work load, with the increases for all hormones reaching statistical significance when the level of exercise reached greater than or equal to 60% of maximal oxygen consumption. However, atrial natriuretic peptide was elevated (P less than 0.05) at all work loads from greater than 1.6-fold of control levels at the 25% work load to greater than 7-fold at the 80% work load. The increase in urine flow (6 of 8 subjects) and UNa+V (7 of 8 subjects) may be due to the increase in atrial natriuretic peptide and/or a 10% suppression (P less than 0.05) of ADH at the 25% work load.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hormonal, electrolyte, and renal responses to exercise are intensity dependent. 182 9

When men are exposed to a hyperbaric environment, urine flow increases. In order to elucidate the mechanism of this hyperbaric diuresis, a dry saturation dive experiment was carried out. Five male subjects were exposed to a 16-21 ATA (atmospheric pressure absolute) helium-oxygen (He-O2) environment for 4 days. Five blood samples were obtained in the early morning (0600-0630 h): once at predive 1 ATA air, 3 times at 16-21 ATA He-O2, and once at postdive 1 ATA air. Eight-hour timed urine samples, 0600-1400 h, 1400-2200 h, and 2200-0600 h (night urine), were collected throughout the experimental period. Urine flow markedly increased by the exposure to hyperbaria in the presence of constant creatinine clearance. The increase was mostly attributable to the urine flow during 2200-0600 h. The secretion of antidiuretic hormone (ADH) was suppressed at daytime and night during the exposure. On the other hand, the secretion of atrial natriuretic polypeptide (ANP) increased solely at night during hyperbaria and correlated with the increases of both the nocturnal urine flow and the nocturnal urinary excretion of sodium. These results suggest that both suppressed ADH secretion and stimulated ANP secretion cause hyperbaric diuresis.
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PMID:Hyperbaric diuresis is associated with decreased antidiuretic hormone and increased atrial natriuretic polypeptide in humans. 183 Mar 48


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