β-Adrenergic Receptors and the Gs Protein in Myocardial Ischemia and Injury

Abstract

SummaryThe purpose of this study was to explore alterations in the life cycle of adrenergic receptors and the G, protein in the heart of ischemic animals. In initial experiments left anterior descending coronary artery occlusion was performed in guinea pigs. Sarcolemmal (SL) and light vesicle (LV) (presumably intracellular) fractions were prepared. Both fractions contained a substantial number of fJ-adrenergic receptors and lXI-adrenergic receptors: the relative proportion of fJ-adrenergic receptors in LV/SL was greater than for lXI-adrenergic receptors. Myocardial ischemia produced a rapid extemalization of fJ-adrenergic receptors from LV to SL. IXI -adrenergic receptors also increased in SL but without an apparent extemalization from LV. Pretreatment of animals with either the non-selective fJ-antagonist propranolol or the fJl-selective antagonist atenolol increased the number of SL fJ-receptors and blunted the ischemia-induced increase in SL fJ-adrenergic receptors. Treatment with the partial agonist pindolol did not cause up-regulation of fJ-receptors, and did not block ischemia-induced extemalization.In the second part of this study, we have begun to examine post-receptor events in a rat model of myocardial ischemia. Ligation of the distal left main coronary artery in the rat led to an increase in SL fJ-receptors. As G proteins playa pivotal role in transducing receptor occupancy to activation of effector molecules, we measured levels ofG, which stimulates adenylate cyclase activity, using an ELISA technique. In rat SL the amount of IX, markedly decreased within 15 min of coronary occlusion. There was no transfer of G, activity to the light vesicle fraction.These studies indicate the dynamic nature of adrenergic receptors and the IX, protein in the sarcolemma in myocardial ischemia. Changes in adrenergic receptor number and in G protein expression may contribute to the altered pathophysiology of the ischemic heart.

Acupuncture pretreatment protects heart from injury in rats with myocardial ischemia and reperfusion via inhibition of the β1-adrenoceptor signaling pathway

“…We determined the contents of cardiac β 1 -AR, Gs protein and cAMP, the important components of β 1 -AR signaling pathway, known to contribute to the cardiac injury induced by ischemia and reperfusion (Maisel et al, 1990;Schomig and Richardt, 1990;Hohl and Li, 1991;Anthonio et al, 2000). In agreement with the previous findings, present results showed that the elevation of ECG ST segment and myocardial infarction were induced in IR group, which was accompanied by the increases in the contents of β 1 -AR, cAMP and Gsα.…”

Effect of Strenuous, Acute Exercise on α2-Adrenergic Agonist–Potentiated Platelet Activation

“…catecholamines, after the onset of myocardial ischemia (15 minutes). 38,39 A previous study also revealed that agonistpromoted internalization and functional uncoupling of the receptors are abolished after acute myocardial ischemia. 38 In addition, strenuous, acute exercise can increase the release of endogenous catecholamines.…”

The effects of acute dynamic exercise on haemostasis in first class Scottish football referees

“…New receptors could be synthesised or pre-existing receptors could be externalised. Previous investigators have observed rapid externalisation of myocardial alpha-1 and B-adrenergic receptors accompanied by the local release of endogenous catecholamines after the onset of myocardial ischaemia 22 23…”