Desaggregation by Verapamil, Sodium Nitroprusside and PGE₁, of Rabbit Platelets Aggregated by PAF-acether. A Morphological and Biochemical Study

Abstract

The action of sodium nitroprusside, an activator of guanylate cyclase, on rabbit platelets stimulated with PAF-acether, was studied singly or in combination with verapamil. Not only did sodium nitroprusside in the range 10⁻⁶ to 10⁻⁴ M inhibit PAF-acether induced aggregation, but it also brought about desaggregation of previously aggregated platelets, as also did verapamil. The results were compared with those obtained with PGE₁, when used alone and in combination with verapamil. Morphological studies were carried out on control and aggregated platelets, and on platelets treated with verapamil either to inhibit aggregation or to bring about desaggregation. The platelets that had been desaggregated by verapamil were discoid in shape, had very few pseudopodia and exhibited a near normal internal morphology, except that the open canalicular system was swollen and contained an electron dense material resembling the contents of the alpha granules. The morphology of platelets desaggregated by PGE₁ was similar to that of platelets desaggregated by verapamil, including a swollen canalicular system containing electron dense material.