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)

To evaluate the role of vasopressin in the renal changes during combined acute hypoxemia and acute hypercapnic acidosis, eight conscious female mongrel dogs prepared with controlled sodium intake at 80 meq/24 h for 4 days were studied in one of the following six protocols: acute hypoxemia (80 min, arterial PO2 34 +/- 1 mmHg) followed by combined acute hypoxemia and hypercapnic acidosis (40 min, arterial PO2 35 +/- 1 mmHg, arterial PCO2 58 +/- 1 mmHg, pH = 7.20 +/- 0.01) during 1) intrarenal vehicle at 0.5 ml/min (N = 8); or 2) intrarenal infusion of vasopressin V1-receptor antagonist [d(CH2)5Tyr(Me)]AVP at 5 ng.kg-1.min-1 (N = 5); and with normal gas exchange during 3) intrarenal vasopressin at 0.05 mU.kg-1.min-1 (N = 8); 4) simultaneous infusion of intrarenal vasopressin and [d(CH2)5Tyr(Me)]AVP, 5 ng.kg-1.min-1 (N = 4); 5) intrarenal [d(CH2)5Tyr(Me)]AVP, 5 ng.kg-1.min-1 (N =4); and 6) intrarenal vehicle at 0.5 ml/min (N = 7). Intrarenal infusion of a subpressor dose of vasopressin resulted in a transient decrease in glomerular filtration rate and effective renal plasma flow over the first 20 min of infusion, suggesting that vasopressin induced nonsustained vasoconstriction of the renal vasculature. Intrarenal administration of [d(CH2)5Tyr-(Me)]AVP failed to block the fall in glomerular filtration rate or effective renal plasma flow when renal arterial blood vasopressin levels were elevated by intrarenal administration of exogenous vasopressin or by elevated systemic arterial endogenous circulating vasopressin during combined acute hypoxemia and hypercapnic acidosis. These data suggest that vasopressin (V1-receptor stimulation) does not play an important role in the renal vasoconstriction during combined acute hypoxemia and hypercapnic acidosis in conscious dogs.
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PMID:Role of vasopressin in renal vascular changes with hypoxemia and hypercapnic acidosis in conscious dogs. 214 77

The aim of this study was to examine the effect of i.v. methadone on the plasma arginine-vasopressin (AVP) levels and urine production in 9 conscious dogs. A highly significant increase from the baseline plasma AVP values of below 3 pg/ml occurred within 5 min following methadone administration. Maximum levels were reached within 30-50 min post-injection and varied from 18.5 to 100 pg/ml. A significant decrease in urine production was not seen under these experimental conditions. Mean arterial blood pressure did not change significantly during the experiment. Apart from the partial influence of the methadone-induced respiratory acidosis, we postulate a direct relationship between i.v. administration of methadone and the increased plasma AVP levels in dogs.
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PMID:Effect of methadone on plasma arginine vasopressin level and urine production in conscious dogs. 360 22

The effects of acute hypercapnic acidosis (PaCO2 = 52 +/- 2 mm Hg, pH = 7.23 +/- 0.01) of 40-80 min duration on renal water excretion and circulating vasopressin were examined in conscious dogs during stable diuresis in protocols either with hypotonic water loading (n = 6) or in the euvolemic state (n = 7). The mean arterial pressure increased (p less than 0.05) during acute hypercapnic acidosis in euvolemic dogs, but was unchanged in the dogs given a water load. However, the free water clearance decreased (p less than 0.05), and urine osmolality increased during acute hypercapnic acidosis in both water-loaded and euvolemic dogs despite stable renal hemodynamic function and osmolar clearance. Plasma vasopressin concentrations increased (p less than 0.05) during hypercapnic acidosis in euvolemic but not in water-loaded dogs. The plasma renin activity increased with hypercapnic acidosis in both water loaded and euvolemic dogs. These observations indicate that acute hypercapnic acidosis results in diminished renal water excretion and increased urine osmolality in conscious dogs.
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PMID:Acute hypercapnic acidosis diminishes renal water excretion in conscious dogs. 388 17

This study examined the cardiovascular, respiratory, and sympathetic effects of selective mu and delta opioid agonists microinjected into the hypothalamic nucleus preopticus medialis (POM) of conscious SHR and WKY rats. The mu receptor agonist D-Ala2-MePhe4-Gly5-ol-enkephalin (DAGO) at a dose of 0.6 or 6.0 nanomoles (Nmol) increased the blood pressure and heart rate in WKY rats. In SHR rats, the lower dose of DAGO similarly had a pressor effect whereas the higher dose was depressor; heart rat was increased only by the 6.0 nmol dose in these animals. In both SHR and WKY rats, this opioid caused respiratory acidosis and elevation of plasma norepinephrine (NE) and epinephrine (E); plasma vasopressin was reduced by the higher dose of DAGO. All of these effects of the mu agonist were reversed by the opiate receptor antagonist naloxone (0.5 mg/kg, i.a.). The delta opiate-receptor agonist D-Ala2-D-leu5-eukephalin at a dose of 6.0 or 20.0 nmol increased blood pressure and heart rate in both SHR and WKY rats without affecting respiratory variables. Plasma NE and EPI were elevated at the peak of the pressor period. These studies suggest that the anteroventral hypothalamic region may be an important site in central autonomic regulation by opioid peptides. The mu-receptor agonist was more potent than the delta agonist in eliciting cardiovascular and respiratory effects and associated sympatho-adrenomedullary activation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Opiate receptors and cardiovascular control in conscious SHR and WKY rats. 631 37

Some of the biochemical changes which occur at the menopause can be attributed to an increased rate of loss of bone but others cannot be explained in this way. Data, collected through literature search, are presented which suggest that the rise in plasma phosphate concentration at the menopause is not due primarily to increased breakdown of bone but rather to the following sequence of events: progesterone deficiency----respiratory hypoventilation----mild respiratory acidosis and hypoxia----compensatory metabolic alkalosis----altered carbohydrate metabolism----rise in plasma phosphate concentration. Increases in the concentration of many plasma constituents occur at the menopause, which appear to be due to fluid loss and haemoconcentration. A possible cause of these changes is a reduced secretion of vasopressin by the pituitary gland as a result of oestrogen deficiency. Increases in the fasting urinary excretion of phosphate, sodium and magnesium also occur at the menopause. These changes cannot be attributed to increased bone loss but could be due to the effects of oestrogen deficiency on circadian rhythms in the hypothalamus.
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PMID:Hypothesis. Biochemical changes at the menopause: possible role of the central nervous system. 639 28

The physiological relationship of increased circulating angiotensin II and vasopressin to circulatory changes during combined hypoxemia and hypercapnic acidosis is unclear. To evaluate the role(s) of angiotensin II and vasopressin, seven unanesthetized female mongrel dogs with controlled sodium intake (80 meq/24 h X 4 d) were studied during 40 min of combined acute hypoxemia and hypercapnic acidosis (PaO2, 36 +/- 1 mmHg; PaCO2, 55 +/- 2 mmHg; pH = 7.16 +/- 0.04) under the following conditions: (a) intact state with infusion of vehicles alone; (b) beta-adrenergic blockade with infusion of d,l-propranolol (1.0 mg/kg bolus, 0.5 mg/kg per h); of the vasopressin pressor antagonist d-(CH2)5Tyr(methyl)arginine-vasopressin (10 micrograms/kg); and (d) simultaneous vasopressin pressor and angiotensin II inhibition with the additional infusion of 1-sarcosine, 8-alanine angiotensin II (2.0 micrograms/kg per min). The rise in mean arterial pressure during the combined blood-gas derangement with vehicles appeared to be related to increased cardiac output, since total peripheral resistance fell. Beta-adrenergic blockade abolished the fall in total peripheral resistance and diminished the rise in cardiac output during combined hypoxemia and hypercapnic acidosis, but the systemic pressor response was unchanged. In addition, the rise in mean arterial pressure during the combined blood-gas derangement was unaltered with vasopressin pressor antagonism alone. In contrast, the simultaneous administration of the vasopressin pressor and angiotensin II inhibitors during combined hypoxemia and hypercapnic acidosis resulted in the abrogation of the overall systemic pressor response despite increased cardiac output, owing to a more pronounced fall in total peripheral resistance. Circulating catecholamines were increased during the combined blood-gas derangement with vasopressin pressor and angiotensin II blockade, suggesting that the abolition of the systemic pressor response in the last 30 min of combined hypoxemia and hypercapnic acidosis was not related to diminished activity of the sympathetic nervous system. These studies show that vasopressin and angiotensin II are major contributors to the systemic pressor response during combined acute hypoxemia and hypercapnic acidosis.
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PMID:Role of arginine vasopressin and angiotensin II in cardiovascular responses to combined acute hypoxemia and hypercapnic acidosis in conscious dogs. 654 29

To determine the effects of acute blood gas derangements on renal water and solute excretion and vasopressin secretion, six unanesthetized mongrel dogs were studied during 1) combined acute hypoxemia and hypercapnic acidosis [arterial O2 partial pressure (PaO2) 36 +/- 1 Torr, arterial CO2 partial pressure (PaCO2) 54 +/- 2 Torr, pH 7.18 +/- 0.01], 2) acute hypoxemia (PaO2 33 +/- 2 Torr, PaCO2 33 +/- 1 Torr, pH 7.34 +/- 0.01), and 3) acute hypercapnic acidosis (PaO2 83 +/- 3 Torr, PaCO2 53 +/- 1 Torr, pH 7.19 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis increased (P less than 0.05) mean arterial pressure, but renal hemodynamic function deteriorated with decreased (P less than 0.05) glomerular filtration rate and increased (P less than 0.05) renal vascular resistance. Moreover free water clearance became more negative (P less than 0.05) and urine osmolality increased (P less than 0.05). During acute hypoxemia or acute hypercapnic acidosis alone, mean arterial pressure and renal hemodynamic function were unchanged but free water clearance became more negative (P less than 0.05). During acute hypoxemia, urine osmolality increased (P less than 0.05) comparably with values observed during combined acute hypoxemia and hypercapnic acidosis. Plasma vasopressin concentrations increased profoundly (P less than 0.05) during combined hypoxemia and hypercapnic acidosis and during acute hypoxemia alone and were significantly elevated (P less than 0.05) above the increased plasma vasopressin concentrations observed during acute hypercapnic acidosis. We conclude that acute hypoxemia and hypercapnic acidosis result in impairment of renal water excretion, probably mediated through vasopressin secretion.
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PMID:Antidiuresis and vasopressin release with hypoxemia and hypercapnia in conscious dogs. 674 23