[Phospholipase C hypersensitivity in hypertensive rats results from innate and acquired factors].

In spontaneously hypertensive rats (SHR), enhanced activity of phospholipase C (PLase C) has been reported in various cells and tissues. In particular, the increased PLase C activity of platelets has been described as being involved in the hyperactivity to thrombin exhibited by these cells in SHR and in some patients with essential hypertension. In order to determine the relationship between such an enzymic abnormality and hypertension, the PLase C activity of platelets was investigated in various models of experimental hypertension, i.e. Dahl rats and DOCA-salt hypertensive rats. PLase C activity was determined by measuring the thrombin-induced 32P-phosphatidic acid (32P-PA) formation from 32P-prelabeled platelets. In parallel, experiments on the platelet reactivity was assessed by measuring the thrombin-induced serotonin secretion from 3H-serotonin prelabeled platelets. In Dahl salt-resistant rats (DR), the blood pressures were 123 +/- 6 and 118 +/- 7 mmHg for animals fed a low (0.3 p. 100) and high (4 p. 100) salt diet, respectively; the blood pressures of Dahl salt-sensitive rats (DS) were 159 +/- 6 and 202 +/- 11 mmHg, respectively. Hypertensive rats of the DOCA/salt--treated group exhibited a blood pressure of 210 +/- 8 mmHg compared with 137 +/- 4 mmHg for those of the control group. At rest (ie before stimulation) the platelets of all groups of animals behave similarly with respect to the incorporation of 32P and its metabolism into phospholipids as well as the uptake of serotonin. These data indicate therefore that platelets were in a similar quiescent status.(ABSTRACT TRUNCATED AT 250 WORDS)