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)

The effects of somatostatin and vasopressin on blood gases, pulmonary and systemic hemodynamics, and portal pressure assessed by the gradient between occluded and free hepatic vein pressures, were investigated in 18 patients with liver cirrhosis. In the first 10 patients, an iv bolus of 250 microgram somatostatin, followed by an infusion of 125 microgram somatostatin over 30 min, caused a sudden rise in pulmonary and systemic vascular pressures lasting 2 to 5 min and accompanied by bradycardia. There was a slight and transient increase in venous admixture (Qsp/Qt) and alveolar-arterial oxygen tension gradients (P(A-a)O2), and a transient reduction in O2 delivery (O2 del) (-11% of the baseline values) and portal pressures (-14%). In the next 8 patients, vasopressin, 0.4 U/min infused over 30 min, caused a more persistent pulmonary and systemic hypertension and bradycardia, a slight increase in P(A.a)O2 and Qsp/Qt, a reduction in O2 del (-27%) and a decrease in portal pressures (-32%). These effects were marked during the entire vasopressin infusion period. Both somatostatin and vasopressin had vasoconstrictive properties and exerted negative effects on hemodynamics and blood gases. Vasopressin appeared to be a more potent drug than somatostatin.
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PMID:Effect of vasopressin and somatostatin on hemodynamics and blood gases in patients with liver cirrhosis. 612 42

Twelve male patients were given high dose fentanyl (75-100 microgram.kg-1) anaesthesia with oxygen during elective aorto-coronary bypass operations, and their haemodynamic and vasopressin responses were determined during induction, sternotomy, cardiopulmonary bypass, post-bypass and recovery periods. For comparison, a group of 12 male patients were anaesthetized with morphine, halothane 0.5 per cent, nitrous oxide and oxygen, and were similarly studied. Significant alterations in haemodynamics included increased mean arterial pressure after sternotomy in the fentanyl group, increased heart rate in both groups, increased systemic vascular resistance after sternotomy only in the halothane group, and decreased left ventricular stroke work index in both groups following induction, bypass, and during the recovery periods. Plasma vasopressin levels increased significantly in both groups during the bypass period, but returned to baseline levels following bypass. Serum sodium and osmolality did not change significantly, and urinary sodium and potassium excretion rose with the progress of the operation in both groups. A positive correlation was found between mean arterial pressure and vasopressin only in the halothane group. Systemic vascular resistance was correlated to vasopressin levels in both groups. Vasopressin response in both groups was similar, with significant but relatively low increases in levels during cardiopulmonary bypass. Fentanyl-oxygen anaesthesia did not provide haemodynamic stability in eight of 12 patients.
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PMID:Haemodynamic and plasma vasopressin responses with high-dose fentanyl anaesthesia during aorto-coronary bypass operations. 612 67

Cysteamine given subcutaneously to rats decreases brain concentrations of somatostatin-like immunoactivity (SLI) but does not affect vasopressin-like immunoactivity as determined by radioimmunoassay and immunocytochemistry. Since somatostatin-related peptides act within the central nervous system (CNS) to increase body temperature and decrease adrenal epinephrine secretion, changes in these parameters were assessed following cysteamine administration. Cysteamine administration lowers oxygen consumption and body temperature, and elevates plasma concentrations of epinephrine, glucose, insulin and glucagon. The lowering of body temperature and elevation of plasma epinephrine is prevented by CNS administration of the CNS-selective somatostatin analog desAA1,2,4,5,12,13[D-Trp8 ))somatostatin. The CNS actions of somatostatin-related peptides are opposite to the effects of cysteamine. The observations are consistent with the possibility that brain somatostatin-related peptides are involved in regulation of body temperature and adrenal epinephrine secretion.
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PMID:Biological effects of cysteamine: relationship to somatostatin depletion. 613 1

Acute hypovolemia induced by bleeding (5 ml/300 g body weight) halothane-anesthetized (0.8% in oxygen) rats is attended by hypotension, bradycardia, and increases in plasma renin, vasopressin, and catecholamine levels. Infusion of prostacyclin (PGI2, O.03 microgram/kg.min) to acutely hemorrhaged rats enhanced recuperation of heart rate, and potentiated the sympathetic response and vasopressin release without altering blood pressure of plasma renin concentration (PRC). Bleeding of bilaterally adrenal demedullated, splanchnicectomized rats resulted in prolonged hypotension and increased plasma levels of vasopressin and renin; epinephrine in the plasma was not detectable, and plasma norepinephrine concentration was not increased after hemorrhage. Prostacyclin infusion to the demedullated, splanchnicectomized rats had no effect on heart rate but enhanced blood pressure recovery after hemorrhage; in this experimental group, PRC was markedly elevated but prostacyclin had no effect on plasma vasopressin or catecholamine concentrations. In rats exposed to severe bleeding, resulting in a nonreversible shock and high mortality, PGI2 infusion after the bleeding increased the survival rate without effect on blood pressure, heart rate, or circulating levels of vasopressin and catecholamines. This study suggests that prostacyclin, through stimulation of the sympathoadrenal axis, enhances heart rate recuperation and vasopressin release in response to acute hemorrhagic shock. Furthermore, prostacyclin may stimulate renin secretion in sufficient amount to compensate for the inadequate sympathetic response during hemorrhagic shock. It is also shown that prostacyclin improves the survival rate to severe hemorrhage without overt hemodynamic or sympathetic effects.
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PMID:Alteration of cardiovascular, neurogenic, and humoral responses to acute hypovolemic hypotension by administered prostacyclin. 617 8

The epithelial cells of the toad bladder have been isolated by brief exposure to ethylenediaminetetraacetic acid followed by treatment with collagenase, DNAse, and the application of shearing forces. This approach eliminates the need for scraping of the mucosal surface and reduces mechanical damage during harvesting of the epithelium. The method yields intact, isolated epithelial cells and few clumps. The three major types of epithelial cells described in the intact toad bladder were present in the final preparation. The cellular contents of nucleic acids and proteins (in pg/cell) were: DNA 22.5 +/- 1.1; RNA, 12.9 +/- 0.6; and protein, 192 +/- 9. The isolated cells possess rates of oxygen consumption and amino acid incorporation higher than those of epithelial sheets obtained by collagenase treatment and scraping of the intact bladder. However, the production of cyclic nucleotides in response to stimulation by vasopressin and carbachol is comparable in both preparations.
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PMID:Isolation of epithelial cells from toad bladder. 624 42

The hydro-osmotic response of the toad bladder to antidiuretic hormone and cyclic AMP was inhibited by the methoxyflurane metabolite, fluoride. The osmotic transfer of water in the absence of hormone was unaffected by fluoride as was the hydroosmotic response due to hypertonicity of the serosal bathing media. Osmotic water movements across N-ethylmaleimide-"fixed" vasopressin or cyclic AMP-stimulated bladders were likewise unchanged by fluoride, suggesting that fluoride is exerting an action subsequent to the endogenous formation of cyclic AMP but before the final effector mechanism. Fluoride increased intracellular cyclic AMP concentrations even in the presence of added hormone. Fluoride suppressed calmodulin activity and prevented its activation of phosphodiesterase. Fluoride had no effect on oxygen consumption of toad urinary bladder cells but reduced lactate formation and anerobic metabolism. This decrease in the glycolytic energy source did not contribute to the inhibition of the hormonal response since 2-deoxyglucose was without effect on hormonal mediated osmotic-water flow. It is postulated that the fluoride-induced polyuria after methoxyflurane anesthesia may be due in part to the ability of fluoride to interfere with calcium and calmodulin-initiated processes (other than phosphodiesterase activity) that may occur in the stimulus-reabsorption coupling response of antidiuretic hormone.
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PMID:Fluoride inhibition of the hydro-osmotic response of the toad urinary bladder to antidiuretic hormone. 627 Mar 9

These studies were implemented to assess the relationship between fetal vasopressin secretion and the progression of parturition as well as the contribution of specific stimuli to vasopressin release during labor. In chronically catheterized fetal lamb preparations, labor was induced by infusion of adrenocorticotropin (12.5 mg/kg/hr) to seven fetuses at 130 +/- 1 day of gestation. Before labor, fetal plasma vasopressin concentrations were 2.1 +/- 1.4 pg/ml and remained low (5.3 +/- 3.4 pg/ml) during prodromal and early phases of labor, but rose significantly in the active and expulsive phases (39.6 +/- 27.5 and 173.3 +/- 152.9 pg/ml) to reach peak values at delivery (584.2 +/- 433 pg/ml) and decrease by 30 min after birth (359.8 +/- 90.0 pg/ml). At delivery, fetal plasma vasopressin concentrations were strongly correlated (P less than 0.001) with hormone values obtained during the latter phases of labor. Fetal arterial pH and oxygen tension was inversely correlated with plasma vasopressin (P less than 0.01). No similar correlations were found with arterial PCO2, K, Na, Cl, osmolality, or packed cell volume. Unexpectedly, we observed a significant (P less than 0.001) and progressive decrease in fetal oxygen tension during the induction process. Other characteristics of adrenocorticotropin-induced parturition seemed to mimic those of spontaneous labor.
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PMID:Release of vasopressin by the fetal lamb during premature parturition induced with corticotropin. 627 Jun 23

To test the hypothesis that ACTH and vasopressin responses are quantifiable as functions of induced changes in central venous or arterial pressures, we produced various degrees of vena caval obstruction in fetal sheep (118--134 days gestation). In seven experiments, vena caval obstruction increased heart rate 18 +/- 7 beats/min and carotid arterial oxygen saturation 8.4 +/- 2.1%, but did not alter any measured vascular pressure or hormones. More severe vena caval obstruction (n = 10) decreased mean arterial pressure 13 +/- 2 mmHg, central venous pressure 1.3 +/- 0.3 mmHg, and heart rate 47 +/- 12 beats/min, and increased fetal plasma ACTH 1,047 +/- 448 pg/ml, cortisol 4.4 +/- 2.2 ng/ml, and vasopressin 47.9 +/- 24.2 pg/ml, but did not alter 11-deoxycortisol. The stimulus increased plasma cortisol (radioimmunoassay after chromatography) 100% and "corticosteroids" (radiotransinassay without chromatography) 20%, demonstrating the nonlinear relationship between these two variables. End-inflation plasma ACTH and vasopressin concentrations were significantly related to the induced decreases in mean arterial and central venous pressures, suggesting that the hormonal responses to vena caval obstruction were mediated by cardiovascular mechanoreceptors. Plasma vasopressin concentrations were linearly related to plasma ACTH concentrations (4 = 0.94; P less than 0.001), suggesting parallel release of the two hormones.
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PMID:Hormonal and hemodynamic responses to vena caval obstruction in fetal sheep. 628 73

Many of the neurochemical changes associated with aging brain, particularly lower choline acetyltransferase and higher monoamine oxidase, occur with greater severity in senile dementia, Alzheimer's type (SDAT). These alterations correlate with neuropathologic indices, e.g., the number of senile plaques and tangles. Although many different treatment techniques have been used, most have been unsuccessful. No strong data have supported the use of stimulants, Gerovital H3, or hyperbaric oxygen. Among the vasodilators, cyclandelate and hydergine may be of value in some but not most patients. Much recent work has focused on techniques to increase acetylcholine brain concentrations. To date, precursors, such as choline, seem to have very limited value. Postsynaptic treatments, e.g., physostigmine, hold more hope for future benefit, if longer acting oral preparations are developed. Other compounds, such as ACTH, vasopressin, and piracetam, may have some value but need better definition and treatment indications. Recent discoveries on the influences of lecithin on membrane fluidity and receptor binding, may affect the focus of future pharmacologic investigation.
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PMID:Chemotherapy of cognitive disorders in geriatric subjects. 632 57

The effects of age and chronic caffeine use (approximately 300 mg/day) on the cardiovascular and humoral responses to 250 mg of oral caffeine (the equivalent of 2 to 3 cups of coffee) were examined. Older subjects had greater increases in blood pressure than younger subjects (p less than 0.03), and caffeine nonusers had greater blood pressure increases than caffeine users, regardless of age (p less than 0.05). Caffeine increased the product of systolic blood pressure and heart rate (an estimate of myocardial oxygen demand) in older caffeine nonusers, but this effect was absent in older caffeine users (p less than 0.01). Cardiovascular effects of caffeine could not be related temporally to changes in plasma epinephrine, which were greater in caffeine nonusers and younger subjects, or to plasma norepinephrine, renin activity or vasopressin, which did not change. Thus, age accentuates and moderate prior caffeine use attenuates the cardiovascular effects of oral caffeine; these effects are not mediated solely through the sympathoadrenal system.
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PMID:Age and prior caffeine use alter the cardiovascular and adrenomedullary responses to oral caffeine. 635 97


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