Role of thromboxanes in alterations of the diabetic β-adrenergic system

The inotropic effects of isoproterenol (ISO), as well as the β-adrenoceptors population, were measured in cardiac tissues from normal and short-term (3 days) diabetic rats. ISO increased the tension of both normal and diabetic ventricles, but the efficacy (Emax) of the concentration-response curve w...

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Publicado:	1989
Materias:	7 [5 (4 biphenylylmethoxy) 2 morpholino 3 oxocyclopentyl] 4 heptenoic acid adenosine triphosphatase (potassium sodium) beta adrenergic receptor bucladesine cyclic amp dihydroalprenolol imidazole insulin isoprenaline nictindole propranolol radioisotope theophylline thromboxane b2 verapamil animal cell animal experiment animal model drug concentration drug receptor binding enzyme activity heart ventricle contractility male nonhuman priority journal rat receptor density streptozocin diabetes Animal Biphenyl Compounds Diabetes Mellitus, Experimental Dihydroalprenolol Isoproterenol Male Myocardial Contraction Na(+)-K(+)-Exchanging ATPase Rats Rats, Inbred Strains Receptors, Adrenergic, beta Support, Non-U.S. Gov't Thromboxane B2
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00062952_v38_n19_p3347_Wald http://hdl.handle.net/20.500.12110/paper_00062952_v38_n19_p3347_Wald
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_00062952_v38_n19_p3347_Wald
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spelling	paper:paper_00062952_v38_n19_p3347_Wald2023-06-08T14:30:32Z Role of thromboxanes in alterations of the diabetic β-adrenergic system 7 [5 (4 biphenylylmethoxy) 2 morpholino 3 oxocyclopentyl] 4 heptenoic acid adenosine triphosphatase (potassium sodium) beta adrenergic receptor bucladesine cyclic amp dihydroalprenolol imidazole insulin isoprenaline nictindole propranolol radioisotope theophylline thromboxane b2 verapamil animal cell animal experiment animal model drug concentration drug receptor binding enzyme activity heart ventricle contractility male nonhuman priority journal rat receptor density streptozocin diabetes Animal Biphenyl Compounds Diabetes Mellitus, Experimental Dihydroalprenolol Isoproterenol Male Myocardial Contraction Na(+)-K(+)-Exchanging ATPase Rats Rats, Inbred Strains Receptors, Adrenergic, beta Support, Non-U.S. Gov't Thromboxane B2 The inotropic effects of isoproterenol (ISO), as well as the β-adrenoceptors population, were measured in cardiac tissues from normal and short-term (3 days) diabetic rats. ISO increased the tension of both normal and diabetic ventricles, but the efficacy (Emax) of the concentration-response curve was greater on ventricles from diabetic rats than in those from the normal control. This phenomenon was accompanied by a decrease in the number of β-adrenoceptor sites (Bmax) during diabetes. Insulin-treated diabetic hearts partially reversed the phenomenon. Propanolol blocked, in a competitive manner, the positive inotropic action of ISO in both types of ventricles. Inhibition of the synthesis and receptors of thromboxane (TX) reduced the hyperreactivity to ISO and increased the number of β-adrenoceptors during diabetes, producing Bmax values almost similar to those of the normal heart. Additionally, the diabetic heart generated and released a greater amount of TXB2 than the normal heart, even in the presence or absence of ISO. The stimulatory effect of ISO upon TXB2 release was altered by the specific β-adrenergic blockade and by verapamil. In addition, the drugs able to induce a sustained increase of endogenous cAMP also inhibited the release of TXB2 by diabetic ventricles. Exogenous TXB2 exerted the same type of hyperreactivity in diabetic ventricles. This phenomenon was accompanied by an inhibition of Na+ + K+-ATPase activity. These results suggest that β-adrenergic inotropic stimulation is secondary to receptor-mediated hydrolysis of arachidonic acid with subsequent release of thromboxanes, which, in turn, may be responsible for both the superreactivity and the decrease in the number of β-adrenoceptors during diabetes. The abnormal reactivity to β-agonists also could be associated with alterations of the diabetic cardiac Na+ + K+-ATPase activity induced by TXB2 whose production is increased during diabetes. © 1989. 1989 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00062952_v38_n19_p3347_Wald http://hdl.handle.net/20.500.12110/paper_00062952_v38_n19_p3347_Wald
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	7 [5 (4 biphenylylmethoxy) 2 morpholino 3 oxocyclopentyl] 4 heptenoic acid adenosine triphosphatase (potassium sodium) beta adrenergic receptor bucladesine cyclic amp dihydroalprenolol imidazole insulin isoprenaline nictindole propranolol radioisotope theophylline thromboxane b2 verapamil animal cell animal experiment animal model drug concentration drug receptor binding enzyme activity heart ventricle contractility male nonhuman priority journal rat receptor density streptozocin diabetes Animal Biphenyl Compounds Diabetes Mellitus, Experimental Dihydroalprenolol Isoproterenol Male Myocardial Contraction Na(+)-K(+)-Exchanging ATPase Rats Rats, Inbred Strains Receptors, Adrenergic, beta Support, Non-U.S. Gov't Thromboxane B2
spellingShingle	7 [5 (4 biphenylylmethoxy) 2 morpholino 3 oxocyclopentyl] 4 heptenoic acid adenosine triphosphatase (potassium sodium) beta adrenergic receptor bucladesine cyclic amp dihydroalprenolol imidazole insulin isoprenaline nictindole propranolol radioisotope theophylline thromboxane b2 verapamil animal cell animal experiment animal model drug concentration drug receptor binding enzyme activity heart ventricle contractility male nonhuman priority journal rat receptor density streptozocin diabetes Animal Biphenyl Compounds Diabetes Mellitus, Experimental Dihydroalprenolol Isoproterenol Male Myocardial Contraction Na(+)-K(+)-Exchanging ATPase Rats Rats, Inbred Strains Receptors, Adrenergic, beta Support, Non-U.S. Gov't Thromboxane B2 Role of thromboxanes in alterations of the diabetic β-adrenergic system
topic_facet	7 [5 (4 biphenylylmethoxy) 2 morpholino 3 oxocyclopentyl] 4 heptenoic acid adenosine triphosphatase (potassium sodium) beta adrenergic receptor bucladesine cyclic amp dihydroalprenolol imidazole insulin isoprenaline nictindole propranolol radioisotope theophylline thromboxane b2 verapamil animal cell animal experiment animal model drug concentration drug receptor binding enzyme activity heart ventricle contractility male nonhuman priority journal rat receptor density streptozocin diabetes Animal Biphenyl Compounds Diabetes Mellitus, Experimental Dihydroalprenolol Isoproterenol Male Myocardial Contraction Na(+)-K(+)-Exchanging ATPase Rats Rats, Inbred Strains Receptors, Adrenergic, beta Support, Non-U.S. Gov't Thromboxane B2
description	The inotropic effects of isoproterenol (ISO), as well as the β-adrenoceptors population, were measured in cardiac tissues from normal and short-term (3 days) diabetic rats. ISO increased the tension of both normal and diabetic ventricles, but the efficacy (Emax) of the concentration-response curve was greater on ventricles from diabetic rats than in those from the normal control. This phenomenon was accompanied by a decrease in the number of β-adrenoceptor sites (Bmax) during diabetes. Insulin-treated diabetic hearts partially reversed the phenomenon. Propanolol blocked, in a competitive manner, the positive inotropic action of ISO in both types of ventricles. Inhibition of the synthesis and receptors of thromboxane (TX) reduced the hyperreactivity to ISO and increased the number of β-adrenoceptors during diabetes, producing Bmax values almost similar to those of the normal heart. Additionally, the diabetic heart generated and released a greater amount of TXB2 than the normal heart, even in the presence or absence of ISO. The stimulatory effect of ISO upon TXB2 release was altered by the specific β-adrenergic blockade and by verapamil. In addition, the drugs able to induce a sustained increase of endogenous cAMP also inhibited the release of TXB2 by diabetic ventricles. Exogenous TXB2 exerted the same type of hyperreactivity in diabetic ventricles. This phenomenon was accompanied by an inhibition of Na+ + K+-ATPase activity. These results suggest that β-adrenergic inotropic stimulation is secondary to receptor-mediated hydrolysis of arachidonic acid with subsequent release of thromboxanes, which, in turn, may be responsible for both the superreactivity and the decrease in the number of β-adrenoceptors during diabetes. The abnormal reactivity to β-agonists also could be associated with alterations of the diabetic cardiac Na+ + K+-ATPase activity induced by TXB2 whose production is increased during diabetes. © 1989.
title	Role of thromboxanes in alterations of the diabetic β-adrenergic system
title_short	Role of thromboxanes in alterations of the diabetic β-adrenergic system
title_full	Role of thromboxanes in alterations of the diabetic β-adrenergic system
title_fullStr	Role of thromboxanes in alterations of the diabetic β-adrenergic system
title_full_unstemmed	Role of thromboxanes in alterations of the diabetic β-adrenergic system
title_sort	role of thromboxanes in alterations of the diabetic β-adrenergic system
publishDate	1989
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00062952_v38_n19_p3347_Wald http://hdl.handle.net/20.500.12110/paper_00062952_v38_n19_p3347_Wald
_version_	1768543353144606720

Role of thromboxanes in alterations of the diabetic β-adrenergic system

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