A novel platelet-derived renal vasoconstrictor agent in normotensives and essential hypertensives.

Platelet homogenates from 200 ml blood of essential hypertensives (n = 28) and normotensives (n = 13) were deproteinized and separated by gel chromatography. The fractions obtained were then tested for vasopressor activity in the isolated perfused rat kidney. In both normotensives and hypertensives, two vasopressor fractions appeared. There was no difference in vasopressor activity in the first vasoactive fraction between normotensives and hypertensives. In the second vasoactive fraction, the hypertensive patients showed a significant higher activity than the normotensive subjects (increase in perfusion pressure by 35.9 +/- 11.5 vs. 6.8 +/- 5.3 mmHg, p less than 0.01). This vasopressor fraction was not inhibited by saralasin, phentolamine, ketanserin, nitroprusside and daltroban and was effective after pretreatment with indomethacin and reserpine and in enzymatically deendothelialized kidneys. The effect was reduced by nifedipine and unchanged by heating the fraction at 100 degrees C and by incubation with proteinase K. It is concluded that a yet unidentified platelet-derived vasopressor agent may contribute to the enhanced vasoconstriction in essential hypertension.