Contribution of ATP-sensitive potassium channels to β-adrenoceptor-mediated responses

Abstract

Contribution of ATP-sensitive potassium channels to B-adrenoceptor-mediated responses Husken, B.C.P.; Pfaffendorf, M.; van Zwieten, P.A. Published in:Naunyn-Schmiedeberg's Archives of Pharmacology Link to publication Citation for published version (APA):Husken, B. C. P., Pfaffendorf, M., & van Zwieten, P. A. (1997). Contribution of ATP-sensitive potassium channels to B-adrenoceptor-mediated responses. Naunyn-Schmiedeberg's Archives of Pharmacology, 355, 97-102. General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Abstract In isolated hearts the inotropic response to the b -adrenoceptor agonist isoproterenol is known to be abolished after ischaemia and reperfusion. The aim of this study was to investigate whether at decreased glucose levels the b -adrenoceptor-mediated responses in vascular smooth muscle would be depressed, since low glucose conditions mimick the influence of ischaemia. Accordingly, we investigated the influence of low glucose levels in the extracellular space on the vasorelaxation induced by isoproterenol and salbutamol in rat isolated thoracic aortic ring preparations with an intact endothelium and we attempted to further analyze the underlying mechanisms. Therefore, forskolin, dibutyryl-cAMP and glibenclamide (an ATP-sensitive K + -channel blocker) were studied as well.In a glucose-free medium the concentration-response curve for isoproterenol was shifted to the left compared to that obtained under normal glucose conditions. The maximal relaxation induced by isoproterenol was not affected by the absence of glucose. In contrast, the maximal relaxation induced by salbutamol in glucose-free medium decreased by 50% compared to that obtained under normal glucose conditions. Glibenclamide caused a concentrationdependent decrease of the maximum relaxation by isoproterenol in a glucose-free medium, but had no effect under normal glucose conditions. Glibenclamide did not influence the concentration-response curves for salbutamol, neither in the presence nor in the absence of glucose in the medium. The relaxation caused by forskolin and dibutyryl-cAMP was not influenced by glibenclamide in a medium devoid of glucose. In endothelium-denuded preparations glibenclamide did not affect isoproterenol-induced responses neither in the presence nor in the absence of g...

Contribution of glibenclamide-sensitive, ATP-dependent K+ channel activation to acetophenone analogues-mediated in vitro pulmonary artery relaxation of rat

“…In different vascular beds, it has been reported that isoprenaline-mediated vascular relaxation involved activation of glibenclamide-sensitive, ATP-dependent K + (IK ATP ) channel (Nakashima and Vanhoutte, 1995;Husken et al, 1997;Wellman et al, 1998). Hence, the participation of IK ATP activation was evaluated.…”

Impaired β-Adrenergic Hyperpolarization in Arteries From Prehypertensive Spontaneously Hypertensive Rats

“…[22][23][24] Defective ␤-adrenoceptor-mediated hyperpolarization might therefore permit enhanced contractile responses to sympathetic nerve stimulation in vascular smooth muscle, possibly leading to an increase in total peripheral resistance.…”

Effet de la concentration du glucose circulant sur la fonction vasculaire au cours du vieillissement. Action sur les flux calciques et la vasomotricité induite par les peptides d’élastine

“…Il a été observé que l'importation par les CMLV de la leucine présente dans le milieu extracellulaire, c'est-à-dire une étape de la synthèse des protéines, est sti mulée par l'hypoglycémie (Low et al, 1994). Il a aussi été montré que l'hypoglycémie et l'hypoxie induisent une altération de la fonction des canaux K+ sensibles à l'ATP (KATP) diminuant la sensibilité de l'aorte de rat au levcromakalim, un ouvreur de canaux KATP de référence induisant une vasodilatation (Husken et al, 1997).…”

“…Exemple de l'action des peptides d'élastine sur les cellules endothéliales : effet de la modification de la concentration de glucose extracellulaire sur l'activité des canaux calciques membranaires et sur la réactivité vasculaire L'hyperglycémie ou l'hypoglycémie sont des situations qui ont déjà été montrées comme induisant des dysfonc tionnements de canaux ioniques membranaires. Les canaux K+ des cellules vasculaires ont déjà été évoqués plus haut dans la présente revue (Husken et al, 1997), mais d'autres types de canaux voient également leur acti vité modifiée en présence de taux élevés de glucose. Par exemple, l'hyperglycémie diminue l'influx de Na+ dans des cellules de neuroblastome (Yorek et al, 1994) et diminue, dans le système cardiovasculaire, l'activité de certains canaux Ca2+ de cardiomyocytes néonataux (Pang et al, 2002).…”