Julian H. Lombard
>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?
Drs. Imig and Nurkiewicz,
Your discussion regarding NO/prostaglandin interactions and the effect of high dietary salt on prostaglandin release is quite interesting. We do have some information related to the question of the effect of dietary salt intake on the release of dilator prostaglandins [Liu et al., Am J Physiology 273 (Heart and Circulatory Physiology 42): H869-H877, 1997]. In that study, prostacyclin release during normoxic conditions, and hypoxia induced prostacyclin release was unaffected in normotensive animals on a high salt diet.