Abstract
In this study, the subcellular mechanism of impaired prostacyclin (PGI2) synthesis in the vascular system of Dahl salt-sensitive (Dahl S) rats was investigated. Arachidonate liberation in response to PDGF or bradykinin was decreased in cultured aortic smooth muscle cell (VSMC) from Dahl S rats, compared with Dahl salt-resistant (Dahl R) rats. Phospholipase C (PIP2-PLC) activity was lowered and the inositol 1, 4, 5-triphosphate content was also decreased in the VSMC from Dahl S rats. In fact, cytosolic calcium levels in basal and angiotensin-II stimulated conditions were significantly decreased in VSMC from Dahl S rats, compared with those in Dahl rats. There was no difference, however, in phospholipase A2 (PLA2) activity in the two strains. Moreover, the PLA2 enzyme properties, e.g., its Ca2+ requirement, pH profile, Km value and Vmax, were equal in Dahl S and Dahl R rats. The level of functional PLA2 messenger RNA was found to be greater in the VSMC from Dahl S rats. Similarly, PGI2 synthesis was reduced in Dahl S rats and this was associated with an unaltered PLA2 concentration and decreased PIP2-PLC activity in the arterial wall. Thus, these data indicate that dysfunction of receptor-mediated PLA2 activation is responsible for altered PGI2 synthesis in Dahl S rats. This finding is likely mediated by a decrease in phosphoinositides metabolism. (Hypertens Res 1993; 16: 105-111)
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