Hypertension and beneficial treatment with beta-blocking agents does not change the platelet sensitivity to the antiaggregatory prostaglandins.
Recent publications have described increased vascular prostacyclin synthesis in vascular tissue from both spontaneous and experimental hypertensive animals and hypertensive humans. The only paper dealing with the platelet sensitivity reported that the cells are not abnormally sensitive to PGI2 in spontaneously hypertensive rats. In 22 patients with essential hypertension the platelet sensitivity to the antiaggregatory prostaglandins PGI2, PGE1, and PGD2 was studied on admission and two weeks after successful treatment with a beta-blocking agent. In all the age groups and in both sexes no differences in platelet sensitivity could be detected. These findings suggest that increased vascular PGI-2 synthesis is not counterbalanced by a change in platelet sensitivity in men.
D000328:Adult; D000527:Alprostadil; D011464:Epoprostenol / Q000494:pharmacology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D010869:Pindolol / Q000627:therapeutic use*; D010974:Platelet Aggregation / Q000187:drug effects*; D011453:Prostaglandins / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology
D011453:Prostaglandins; D011458:Prostaglandins E; D010869:Pindolol; D011464:Epoprostenol; D000527:Alprostadil