Hypertension is not related to suppressed lymphocyte proliferation but to elevated NO synthesis in vascular smooth muscle cells of borderline hypertensive rat.

Abstract

Hypertensive individuals often exhibit immune abnormalities. We have previously reported that spontaneously hypertensive rats (SHR) had a severely depressed lymphocyte proliferation response caused by excessive nitric oxide (NO) from macrophages and vascular smooth muscle cells (VSMC). However, the development of hypertension was not correlated with the lymphocyte depression and elevated NO synthesis in macrophages. In this study, we investigated the effect of hypertension on lymphocytes and the NO synthesis system in borderline hypertensive rats (BHR). BHR became significantly hypertensive after receiving a high sodium diet. The proliferation response of lymphocytes in hypertensive BHR was similar to that of normotensive BHR fed a normal diet or of Wistar Kyoto rats (WKY). NO production in macrophages of hypertensive BHR was not different from that of normotensive BHR or WKY. However, NO production in VSMC was significantly elevated in hypertensive BHR. A positive correlation between blood pressure and VSMC NO production exists in hypertensive BHR. These results suggested that high blood pressure neither affected the lymphocyte function nor influenced the activation of NO synthesis in macrophages. Hypertension, however, may influence the activation of VSMC NO synthesis. In conclusion, hypertension is not causally associated with immune dysfunction as seen in SHR but is related to enhanced NO synthesis in VSMC.