Abstract
Of the vasodilators used at present in the treatment of heart failure, only nitroprusside and phentolamine inhibit platelet aggregation at therapeutic dose levels. The other vasodilators studied, viz. nitroglycerin, isosorbide dinitrate, hydrallazine, dihydrallazine and prazosin, only inhibit platelet aggregation at relatively high concentrations, well above those reached in vivo. The exact nature of the platelet receptor, stimulation and blockade of which respectively initiate and inhibit aggregation, is not yet know, but it would appear to resemble the presynaptic alpha-receptors of other tissues.
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