SummaryLysolecithin is adsorbed to washed blood platelets and, at sufficient concentration, lyses them, inhibits their clot-retracting activity and promotes their thromboplastin-generating activity. Lysolecithin adsorption to the platelet was studied by using P32-labelled lysolecithin obtained from the liver of rats injected with labelled orthophosphate. The amount of lysolecithin adsorbed to the surface of the washed platelet in saline medium is dependent on the concentration of lysolecithin in solution and reaches saturation — 5 × 10-8 jig per platelet — at a concentration of 9—10 µg per ml. Platelet lysis in saline medium begins at a lysolecithin concentration higher than 18 jig per ml. Plasma and albumin prevent adsorption of lysolecithin to the platelet and protect the platelet from damage by lysolecithin. Albumin is able to remove previously adsorbed lysolecithin from the platelet surface. The protective action of plasma explains the lack of platelet damage in blood, the plasma lecithin of which has been converted to lysolecithin by the action of Vipera palestinae venom phosphatidase, in vitro and in vivo.
Serum renin concentration (SRC) was determined in 97 hypertensive patients under basal conditions and during stimulation of renin secretion. Renin secretion was stimulated by upright posture and by either of the following means: (a) diet containing 20 mEq Na/24 hours for 3 days; (b) 300 mg i.v. diazoxide injections; (c) oral ingestion of 80 mg furosemide; (d) oral hydrochlorothiazide (HCT), 25 mg twice daily for 3 days. HCT was used in 6 patients previously treated with daizoxide and in 8 patients previously treated with furosemide. Using pairs of basal and stimulated SRC determinations, the patients could be classified as high, normal, or low renin hypertensives. HCT proved to be the most convenient stimulus as far as efficacy, reliability and the patients' tolerance were concerned, and compared well with sodium restriction.
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