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)

When sodium transport (JNa) and CO2 production (JCO2) were measured simultaneously in the toad urinary bladder in the absence of electrochemical gradients under conditions of spontaneous variation of JNa, the curve of JNa on JCO2, phiJNa/phiJCO2, was found to be highly linear in an individual epithelium. However, no unique value appeared to characterize a population of bladders. In an effort to investigate the nature of this variation, phiJNa/phiJCO2 was examined under a variety of conditions. It was found that agents that affect sodium entry into the active transport pool, e.g. vasopressin and amiloride, or those that influence the energy-linked exit step, e.g. ouabain and insulin, have no effect on the phiJNa/phiJCO2. To investigate the possibility of the presence of a significant backleak from the serosal side into the cell, the sodium concentration was changed to 75 and 160 mM. Neither of these maneuvers influenced phiJNa/phiJCO2 or (JCO2)JNa=O. Furthermore, in the absence of mucosal sodium, ouabain had no effect on JCO2, suggesting that no significant recirculation is occurring. It is concluded that for each individual epithelium JNa is coupled to JCO2, and their ratios appear, within experimental error, to be invariant. It is suggested that sodium traverses the active transport pathway largely or entirely in one direction.
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PMID:Further studies on coupling between sodium transport and respiration in toad urinary bladder. 96 63

The mechanism whereby an increase in left atrial pressure (LAP) causes a water diuresis in the anesthetized dog remains controversial. In the present study LAP was increased by inflation of an atrial balloon in two groups of animals. In the first group of eight intact dogs, mean LAP was increased from 3.4 to 17.6 mm Hg (P less than 0.001). The rise in LAP was associated with a mean increase in urine flow (V) from 0.70 to 1.29 ml/min (P less than 0.001), a decrease in urinary osmolality (Uosm) from 808 to 490 mOsm/kg of H2O (P less than 0.001) and an increase in free water clearance (CH2O) from -0.684 to -0.200 ml/min (P less than 0.025). This diuresis was associated with a mean decrease in antidiuretic hormone concentrations in plasma as measured by radioimmunoassay from 27.6 to 12.3 pg/ml (P less than 0.02). The changes in the urinary indexes and in the antidiuretic hormone concentrations were reversible and returned to control levels when the LAP was allowed to return to normal. A second group of dogs was acutely hypophysectomized, steroid replaced and given a constant infusion of vasopressin. In these animals, mean LAP was increased from 3.0 to 16.0 mm Hg (P less than 0.001) but no significant change in V (0.49 to 0.56 ml/min), Uosm (878 to 845 mOsm/kg of H2O) or CH2O (-0.750 to -0.620 ml/min) occurred. Cardiac output, renal arterial pressure, glomerular filtration rate and solute excretion were comparable in the two groups. We therefore conclude that suppression of antidiuretic hormone release is the primary mechanism whereby increased LAP causes a water diuresis in the anesthetized dog.
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PMID:Mechanism of diuretic response to increased left atrial pressure in the anesthetized dog. 110 39

Although chronic lithium therapy has been associated with a defect in the urinary concentrating mechanism, short-term renal effects of lithium have received little attention in the intact animal. Solute-free water reabsorption (T-cH2O) and free water clearance (CH2O) were measured in primates of the genus Galago under control conditions and while animals were receiving either 0.5 mmol/kg-h or 1.0 mmol/kg-h lithium chloride (135 mM) intravenously. CH2O was unchanged by lithium infusion (P greater than 0.10), whereas T-cH2O was significantly depressed at all levels of osmolal clearance (P smaller than 0.01). Spontaneous recovery of near-normal T-cH2O was documented in two animals within 1 wk following acute lithium infusion. In addition it was observed that lithium-induced depression of T-cH2O could be partially prevented by pretreatment with intravenous amiloride. These results suggest that alterations in the renal concentrating mechanism can occur rapidly following the onset of lithium administration. They also imply that impairment of the renal concentrating mechanism by lithium is due at least in part to antagonism of the action of vasopressin on the collecting duct.
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PMID:Acute effects of lithium on the renal concentrating mechanism in a primate. 111 55

Renal function studies were done in five children with infantile polycystic disease (IPCD)of kidneys and liver and in four with congenital hepatic fibrosis (CHF). Glomerular filtration rate was reduced in all IPCD patients and in two of four CHF patients. Urinary concentrating ability following water deprivation and vasopressin administration was impaired in all IPCD patients and in three of four CHF patients. During control period, all patients had asymptomatic metabolic acidosis with total carbon dioxide content less than or equal to 20.5 millimols/liter, and net acid excretion (NAE) was reduced in all but one. Ammonium chloride was administered to seven patients; NAE increased in all, but the increments were subnormal in four. The inability to excrete maximally concentrated urine and an adequate amount of net acid may best be explained by abnormal tubular structure or alterations in medullary architecture secondary to progressive scarring, or both.
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PMID:Polycystic disease and hepatic fibrosis in children. Renal function studies. 114 74

In the present study the effect of angiotensin II (AII) on renal water excretion was evaluated. In dogs undergoing a water diuresis, neither the intravenous (IV) (40ng/kg per min) nor intracarotid (5-10 ng/kg per min) infusion of AII significantly altered urinary osmolality (Uosm) or free-water clearance (CH2O). Intravenous infusion of a competitive inhibitor of AII (1-sarcosine,8-glycine AII) into hydropenic dogs also failed to alter Uosm and CH2O significantly. To examine whether AII might suppress, rather than stimulate, vasopressin release, AII was also infused into hydropenic animals. No effect on Uosm and CH2O was observed during the intracarotid infusion. A significant fall in Uosm and rise in CH2O occurred during the intravenous AII infusion, but reversal after cessation of the infusion was incomplete and statistically not significant. Some suppression of antidiuretic hormone (ADH) release during the intravenous infusion of AII, however, was suggested since no similar alteration in renal water excretion was observed during an intravenous AII infusion in hypophysectomized animals receiving a constant infusion of ADH. Taken together, the present results provide no evidence for a direct effect of AII to alter ADH release or to interfere with the peripheral action of ADH. Suppression of ADH release may sometimes occur with pressor doses of intravenous angiotensin, but this effect is clearly less consistent than previously observed with intravenous norepinephrine.
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PMID:Effect of angiotensin II on renal water excretion. 114 6

A patient with Shy-Drager syndrome exhibited a partial defect in antidiuretic hormone (ADH) release, and cluster breathing, an indication of pontomedullary respiratory center damage, with a normal CO2 response curve. This extends the spectrum of abnormalities associated with the degenerative disease of the central nervous system. The presence of a pontomedullary respiratory pattern without an impaired CO2 response curve suggests that neurons that determine respiratory rhythm function independently from those that function as chemoreceptors.
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PMID:Shy-Drager syndrome with abnormal respirations and antidiuretic hormone release. 125 43

In the present paper the effects of nonapeptide hormones and of some of their chemical analogues were investigated on progesterone and testosterone production in granulosa cells of sow ovaries; the experiments were made in vitro. This objective was given by data on potential regulatory roles of nonapeptides at the level of hypothalamus, pituitary and reproductive organs. The goal of this experiment was to analyze the effects of various doses of oxytocin (OT), arginine-8-vasopressin (AVP), arginine-8-vasotocin and of some of their analogues on progesterone and testosterone production in vitro in granulosa cells of sow ovaries. The production activity of granulosa cells was investigated which were obtained from slaughtered sows without any changes in their reproductive process and abnormalities in their reproductive organs. Follicles of the size 2-5 mm without marked paleness in the early follicular phase were selected for aspiration. Granulosa cells with determined viability (more than 75%) and concentration (2 million/ml) were cultivated in defined culture conditions (37.5 degrees C, 5% CO2) after threefold resuspension and centrifugation of follicle fluid. These hormonal preparations were used in the experiments: pFSH, synthetic OT, synthetic AVP, synthetic AVP with antidiuretic effects and synthetic AVT. Progesterone and testosterone concentrations were analyzed radioimmunoanalytically using commercial kits of the Institute of Radio ecology and Nuclear Technology at Kosice. Statistically significant differences between the groups were evaluated by Student's t-test. The administered preparations were found to influence progesterone and testosterone production in dependence on the doses applied (Figs. 1-6). OT stimulation of progesterone production in granulosa cells indicated its regulatory role in relation to secretion of this hormone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Production of progesterone and testosterone in ovarian granulosa cells in sows after administration of nonapeptide hormones in vitro]. 141 99

Previous experiments have demonstrated that consumption of a glucose polymer-electrolyte (GP-E) beverage is superior to water in minimizing exercise-induced decreases in plasma volume (PV). We tested the hypothesis that elevated plasma concentrations of vasopressin and/or aldosterone above that seen with water ingestion may explain this observation. Six trained cyclists performed 115 min of constant-load exercise (approximately 65% of maximal oxygen consumption) on a cycle ergometer on two occasions with 7 days separating experiments. Ambient conditions were maintained relatively constant for both exercise tests (29-30 degrees C; 58-66% relative humidity). During each experiment, subjects consumed 400 ml of one of the following beverages 20 min prior to exercise and 275 ml immediately prior to and every 15 min during exercise: (1) distilled water or (2) GP-E drink contents = 7% carbohydrate (glucose polymers and fructose; 9 mmol.l-1 sodium; 5 mmol.l-1 potassium; osmolality 250 mosmol.l-1). No significant difference (P > 0.05) existed in mean skin temperature, rectal temperature, oxygen consumption, carbon dioxide production or the respiratory exchange ratio between treatments. Further, no significant differences existed in plasma osmolality and plasma concentrations of sodium, potassium, chloride or magnesium between treatments. Plasma volume was better maintained (P < 0.05) in the GP-E trial at 90 and 120 min of exercise when compared to the water treatment. No differences existed in plasma levels of vasopressin or aldosterone between treatments at any measurement period. Further, the correlation coefficients between plasma concentrations of vasopressin and aldosterone and change in PV during exercise were 0.42 (P < 0.05) and 0.16 (P > 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fluid replacement beverages and maintenance of plasma volume during exercise: role of aldosterone and vasopressin. 142 51

Recent studies have suggested that the renal effects of high protein intake could be mediated, at least in part, by vasopressin and/or an increase in the urinary concentrating activity. The present study investigated the influence of the level of hydration, and hence of the activity of the concentrating process, on the renal response to an acute oral protein load. Clearance studies were performed before (Control) and during three hours after a protein meal (1.5 g/kg body wt protein as cooked meat) in ten healthy volunteers. This study was performed twice at a two to three week interval under either constant low (LowH) or high (HighH) hydration. In spite of the marked difference in initial diuresis (3.1 +/- 0.3 in LowH vs. 13.9 +/- 0.7 ml/min in HighH) and urine osmolality (501 +/- 42 in LowH vs. 99 +/- 3 mOsm/kg H2O in HighH), a similar relative decrease in urine flow rate was observed following the meal in both conditions. TcH2O increased progressively by 70% in LowH whereas CH2O decreased by 40% in HighH. Plasma vasopressin showed a progressive increase with time in LowH (from 1.10 +/- 0.26 in control, to 1.98 +/- 0.35 pg/ml at the third hour after the PM, P < 0.05) but not in HighH (0.53 +/- 0.09 to 0.70 +/- 0.17 pg/ml). Glomerular filtration rate (inulin clearance) increased significantly on the second post-prandial hour under LowH but not under HighH. Excretions rates of Na, Cl, K, and urea increased after the meal, however, not to the same extent nor with the same time course in the two conditions. Significant positive correlations were observed between GFR and TcH2O, urine osmolality, or the ratio of urine-to-plasma urea concentrations in LowH. These results suggest that the protein-induced hyperfiltration is partially blunted by a high water intake, and hence is dependent, directly or indirectly, on the urine concentrating activity.
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PMID:Influence of the level of hydration on the renal response to a protein meal. 145 5

In anaesthetized rats, ventilatory stimulation induced by phentolamine, an alpha sympatholytic agent, emphasizes the role of some adrenergic mechanisms in the control of the respiratory centres activity. Phentolamine (5 and 10 mg.kg-1, iv) stimulates ventilation after a 4 s latency, tidal volume and respiratory rate being both increased. A same response can also be provoked 10 min later, by a second identical iv administration, systemic blood pressure remaining then stable at its previous low level. Hyperventilation is also observed when phentolamine is injected in totally denervated rats, without any remaining baro- or chemosensitivity. Stimulation is thus due to a central activity in relation with the release of inhibitory influences. Phentolamine also causes hyperventilation after prazosin pretreatment indicating that the alpha 1 adrenergic blockade is not involved in the post-phentolamine stimulation. This is an alpha 2 adrenergic transmission dependent mechanism. Variation of the systemic blood pressure is not the main mechanism involved in the hyperventilation induced by phentolamine. Meanwhile, baroreceptor activity modulates the central response to the drug, as shown by the negative influence of the post-vasopressin arterial hypertension. Hyperoxia is also a modulating factor acting by two ways: an inhibition of the peripheral chemoreceptors activity is added to an arterial hypertension. On the other side, activation of these chemoreceptors by almitrine bismesilate increases the respiratory responses to phentolamine. As already shown by one of us (Lagneuax, 1986), phentolamine pretreated rats are more responsive to hypoxia and to almitrine. Moreover, these phentolamine pretreated rats are protected against cardiovascular collapses and against apnea, frequently observed during hypoxia without CO2 compensation.
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PMID:[Alpha 2 adrenergic control of ventilation in the rat]. 170 84


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