Effects of tempol and candesartan on neural control of the kidney

We compared the effects of tempol (300 μmol kg− 1 plus 300 μmol kg− 1 h− 1, n = 14) and candesartan (10 μg kg− 1 plus 10 μg kg− 1 h− 1, n = 14) on renal haemodynamics, excretory function, and responses to electrical stimulation of the renal nerves (RNS) in lean and obese rabbits under pentobarbitone anaesthesia. Depressor responses to tempol (− 16 ± 2 mmHg) and candesartan (− 12 ± 1 mmHg) were similar. Candesartan, but not tempol, significantly increased basal renal blood flow (RBF; + 36 ± 7%). Tempol, but not candesartan, significantly reduced glomerular filtration rate (GFR; − 30 ± 10%) and sodium excretion (UNaV; − 44 ± 14%). RNS induced frequency-dependent reductions in RBF (− 20 ± 3% at 1 Hz), GFR (− 28 ± 6% at 1 Hz) and UNaV (− 55 ± 6% at 1 Hz). Candesartan blunted these responses. Tempol did not significantly alter RBF and GFR responses to RNS but blunted the UNaV response. Responses to RNS, and the effects of tempol and candesartan, were similar in lean compared with obese rabbits. Unlike candesartan, tempol did not induce renal vasodilatation, maintain GFR and UNaV during reductions in arterial pressure, or blunt neurally-mediated vasoconstriction. In conclusion, unlike the AT1-receptor antagonist candesartan, tempol does not blunt the effects of RNS on renal haemodynamic function. Furthermore, under the current experimental conditions superoxide appears to make little contribution to the actions of endogenous angiotensin II on baseline renal haemodynamics or excretory function, or their responses to RNS.