Salt-induced and spontaneous hyperactivity of phospholipase C in primary hypertension.

Previous studies from our laboratory have shown that platelets from both spontaneously hypertensive rats and essential hypertensive patients exhibited an increased thrombin-triggered phospholipase C activity compared with normotensive subjects. In order to determine the relationship between phospholipase C and hypertension we investigated this enzymatic activity in Dahl salt-resistant (Dahl R/Jr) and salt-sensitive (Dahl S/Jr) rats fed either a low- or a high-NaCl diet, and in DOCA-NaCl hypertensive rats. Phospholipase C activity was increased in the Dahl S/Jr rats fed a high-NaCl diet compared to a low-NaCl diet. This difference was not observed in the Dahl R/Jr rats, irrespective of diet. Likewise, phospholipase C activity was similar in the DOCA-NaCl hypertensive rats compared with their controls. Our results indicate that the increased platelet phospholipase C activity was not a consequence of either the blood pressure elevation or the high NaCl intake and was probably of genetic origin. While the increased phospholipase C activity was not correlated with blood pressure, the enhanced enzymatic activity in Dahl S/Jr hypertensive rats may be involved in the elevation of blood pressure and may be NaCl-regulated.