HYPERTENSION AND IMPAIRED RENAL ANGIOTENSIN-II RESPONSE IN RATS AFTERCHRONIC NEURONAL NITRIC-OXIDE SYNTHASE INHIBITION

Nitric oxide (NO) produced by the macula densa cells is important for the control of tubuloglomerular feedback (TGF). Reduced production of NO by these cells activates TGF and could result in hypertension, alth ough the TGF activity is then normalized in the hypertensive slate. Th e normalization of TGF in this form of hypertension might be explained by an impaired ability of angiotensin II to constrict renal vessels o r by up-regulation of some other vasodilator not affected by NO syntha se inhibitors.