John D. Imig
This is a very nice study. The suppression of high dietary salt on the endogenous NO and changes in myogenic responsiveness in both normotensive and hypertensives is interesting. In the kidney, there is emerging evidence that at the level of the macula densa an interaction exist between the renin-angiotensin system, nitric oxide and prostaglandins. Recent studies suggest that NO may stimulate COX-2 to generate vasodilatory prostaglandins that particpate in modulation of renal vascular tone. Could a similar type of interaction be occuring in the skeletal muscle arterioles? Is there suppression of endogenous vasodilatory prostaglandins with high dietary salt?