Subject(s)
Calcium Channel Blockers , Myocardial Infarction/metabolism , Myocardium/metabolism , Nitrendipine/metabolism , Adenosine Triphosphatases/metabolism , Affinity Labels , Animals , Calcium Channels/drug effects , Membrane Proteins/metabolism , Myofibrils/enzymology , Myofibrils/metabolism , Nitrendipine/pharmacology , Sarcoplasmic Reticulum/enzymology , Sarcoplasmic Reticulum/metabolism , Swine , Swine, MiniatureABSTRACT
Hypertension may cause activation of blood platelets in vivo. One of the possible mechanisms could be adrenergic activation of platelets by catecholamines. Therefore, we have studied specific binding of the alpha 2-adrenoceptor blocker, 3H-yohimbine, to platelets in order to elucidate the role of alpha 2-adrenoceptors of platelets in hypertensive animals. Particularly, competitive inhibition of 3H-yohimbine binding to platelets by hydergine, and plasma catecholamine levels were investigated in hypertensive (stress induced) and normotensive monkeys. It was demonstrated that 3H-yohimbine binds to platelets from rhesus monkeys with high affinity and specificity. The binding was found to be saturable and reversible. Additionally, it was shown that hydergine inhibits specific binding of 3H-yohimbine to platelets from hypertensive monkeys more potent that to those from normotensive animals. The obtained data suggest that the total number of the number of available, free alpha 2-adrenoceptors were reduced on the platelets from hypertensive monkeys. The latter was confirmed by the decreased adrenaline level in the plasma of hypertensive animals.
