BAROREFLEX CONTROL OF RENAL SYMPATHETIC-NERVE ACTIVITY IS POTENTIATED AT EARLY PHASE OF 2-KIDNEY, ONE-CLIP GOLDBLATT HYPERTENSION IN CONSCIOUS RABBITS

Conscious normotensive and two-kidney, one-clip Goldblatt hypertensive rabbits were studied to determine the sensitivity of the arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate. The relations of the mean arterial pressure-RSNA and mean arterial pressure-heart rate were examined over a wide range of blood pressures produced by infusions of phenylephrine and nitroglycerin. The maximum slope obtained by logistic function analysis was considered to represent the baroreflex sensitivity. In the early hypertensive group (n = 8; mean arterial pressure ± SEM, 88 ± 2 mm Hg) on day 5 after renal clip application, the maximum slope of the mean arterial pressure-RSNA relation was -11.3 ± 1.2, which was significantly greater than that of the sham normotensive group (-6.9 ± 0.3, p < 0.05). The maximum slope (-4.3 ± 0.2) of the mean arterial pressure-RSNA relation in the late hypertensive group (n = 8; mean arterial pressure, 96 ± 3 mm Hg) on day 21 after renal clipping was significantly smaller than that of another sham group (-7.2 ± 0.2, p < 0.05). In contrast to these changes in the baroreflex control of RSNA, the control of heart rate was attenuated according to the magnitude of mean arterial pressure. To elucidate the mechanisms underlying the potentiated baroreflex, the effects of endogenous neuropeptides were investigated. First, plasma concentrations of angiotensin II and arginine vasopressin that are known to affect the baroreflex were determined. Plasma concentrations of vasopressin (3.1 ± 0.6 pg/ml) as well as of angiotensin II (34 ± 7 pg/ml) were increased in the early hypertensive group, and the plasma vasopressin returned to a similar level to the sham group in the late hypertensive group (1.3 ± 0.4 pg/ml). Second, to study endogenous effects of these neuropeptides on the baroreflex, the maximum slopes of the baroreflex curves during infusions of antagonists for the peptides were determined in the early hypertensive group. The maximum slope of mean arterial pressure-RSNA during intravertebral arterial [Sar1, Ala8]-angiotensin II (-16.4 ± 1.5) was significantly greater (p < 0.05), whereas the maximum slope during intravertebral arterial infusion of d(CH2)5Tyr(Me)arginine vasopressin (-4.7 ± 0.5) was significantly smaller (p < 0.05) than that during vehicle infusion (-11.3 ± 1.2). These results suggest that the baroreflex control of RSNA was potentiated in the early phase of two-kidney, one-clip hypertension in conscious rabbits and that endogenous arginine vasopressin and angiotensin II, which counteract each other, were apparently involved in the potentiated baroreflex mechanism.