Nitric oxide dependent neural influences on blood pressure.

For the past decade we have known of NO as vasodilator produced by the enzyme NO synthase (NOS) in the vascular endothelium. Reports have indicated that this vasodilator may be deficient in hypertension. The brain is also an important site of NOS activity. Here NO has a broad spectrum of functions, among which is an important role in the activities of the cardiovascular regulatory centers. In 1991 Shapoval et al. reported that an NO donor injected into the ventrolateral medulla caused a decrease in sympathetic nerve activity (SNA) and a fall in blood pressure. NO must be tonically active in this center since blockade of NOS activity caused an increase in SNA and blood pressure. We have observed this pressor response when we infuse an NOS blocker into the lateral ventricle (i.c.v.) of either normotensive (WKY) or hypertensive (SHRSP) rats. Conversely, when we stimulated NOS with calcium we observed a depressor response in both strains. Both the pressor and depressor responses were greater in the WKY than in the SHRSP. The NO depressor mechanism appeared to be deficient in the hypertensive rat. We have implanted cerebellar tissue (rich in NOS) from new-born WKY rats into the brains of adult SHRSP and observed a fall in pressure of 40 mmHg that persisted for over one week. We hypothesize that a deficit in NOS activity may contribute to the elevated arterial pressure of SHRSP.