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 Authors studied the effects of e.v. Salbutamol evaluating the acute "in vivo" variations of acid-base and hydro-electrolitic balance in 16 chronic obstructive lung patients undergoing e.v. drug administration, and also ionic variations "in vitro" of venous blood samples incubated and tonometrated with the drug. The results "in vivo" do not show variations of acid-base equilibrium (paO2, paCO2, pH, HCO3-); whereas diminution of haematocrit (Ht), rise of urinary osmolarity and variations of hydro-electrolitic balance (Na+, K+, Cl-) are demonstrated. The results "in vitro" do not show considerable variations on ionic assessment. These data, according to the other latest result, indicate the possible role of haemodilution. We think that the explanation of these phenomena could be a modification of renal water and electrolytes reabsorption, likely under the influence of antidiuretic hormone (ADH), stimulated in the hypothalamus and activated also by the beta-stimulant drug at tubular cell receptors.
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PMID:[Changes in the acid-base and water-electrolyte balance induced by salbutamol. "In vivo" studies in patients with chronic broncho-pulmonary disease and "in vitro" by tonometry of venous blood]. 3 12

With pithed normotensive rats we studied the interaction between beta 2-adrenoceptor-mediated vasodilation and pressor responses elicited by vasopressin, the selective alpha 2-adrenoceptor agonists B-HT 920 and UK 14,304, and the alpha 2-adrenoceptor-mediated pressor responses of (--)-norepinephrine, tyramine [via neuronally released (--)-norepinephrine], alpha-methylnorepinephrine, and (--)-epinephrine. Salbutamol was used as a selective agonist of beta 2-adrenoceptors. The selective beta 2-adrenoceptor antagonist ICI 118,551 was employed to reveal the intrinsic beta 2-adrenoceptor activation induced by alpha-methylnorepinephrine and (--)-epinephrine, measured as a potentiation of the increase in diastolic pressure. Two types of interaction between beta 2-adrenoceptor-mediated vasodilation and alpha 2-adrenoceptor-mediated vasoconstriction were found. The effect of the alpha 2-adrenoceptor agonists was attenuated in most cases. However, intravenously administered (--)-norepinephrine elicited an alpha 2-adrenoceptor-mediated vasoconstriction not attenuated by beta 2-adrenoceptor-mediated vasodilation. These results are interpreted as indications for two different populations of vascular alpha 2-adrenoceptors. Neuronally released (--)-norepinephrine activated alpha 2-adrenoceptors, and its effect was attenuated by beta 2-adrenoceptor-mediated vasodilation in contrast to that of intravenously administered (--)-norepinephrine. Therefore, an intrasynaptic and extrasynaptic population of vascular alpha 2-adrenoceptors as postulated. In contrast to (--)-norepinephrine, intravenously administered (--)-epinephrine seems to activate predominantly intrasynaptic alpha 2-adrenoceptors.
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PMID:Interaction between beta 2-adrenoceptor-mediated vasodilation and alpha 2-adrenoceptor-mediated vasoconstriction in the pithed normotensive rat. 619 71

1. The aim of the study was to measure the regional haemodynamic responses to vasodilators, and the effects of nitric oxide (NO) synthase inhibition, in conscious, hypertensive, transgenic ((mRen-2)27) rats (TG rats) and normotensive, Hannover Sprague-Dawley (SD) rats. 2. The hypotensive response to acetylcholine was greater in TG than in SD rats, but the renal vasodilator responses were not different. 3. The responses to bradykinin were similar in the two strains, except that hindquarters vasodilatation occurred only in SD rats. 4. Salbutamol caused smaller renal and hindquarters vasodilatation in TG rats than in SD rats, and there was mesenteric vasodilatation only in the latter strain. 5. The hypotensive response to sodium nitroprusside was smaller, but the accompanying mesenteric vasodilatation was greater, in SD than in TG rats. 6. The contribution of NO to the vasodilator responses was taken as the difference between the responses in the presence of the NO synthase inhibitor, NG-nitro-L-arginine methylester (L-NAME), compared to those in the presence of a co-infusion of angiotensin II and vasopressin (to match the haemodynamic effects of L-NAME). 7. In TG rats, L-NAME caused a greater absolute pressor effect, but a smaller mesenteric vasoconstriction, than in SD rats. 8. L-NAME affected the vasodilator responses to all the challenges similarly in the two strains. 9. Collectively, the results provide no direct evidence for impaired NO-mediated vasodilator mechanisms in TG rats. It is feasible that the reduced hindquarters response to bradykinin and the reduced renal and hindquarters responses to salbutamol, in TG rats are due to abnormal beta2-adrenoceptor-mediated processes.
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PMID:The contribution of nitric oxide to cardiovascular status and responses to vasodilators in conscious, hypertensive, transgenic ((mRen-2)27) rats. 964 46