Baroreflex sensitivity is impaired in Sprague‐Dawley rats with spontaneous hydronephrosis independent of angiotensin II actions in the solitary tract nucleus

Abstract

Hydronephrosis, associated with ureteral obstruction, activates the circulating renin‐angiotensin system (RAS). Elevations in the RAS impair baroreflex sensitivity (BRS) for control of heart rate (HR) involving central sites of action. We hypothesized that central cardiovascular regulation is altered in this condition. Resting arterial pressure (AP), HR and BRS for control of HR were assessed in urethane/chloralose anesthetized Sprague‐Dawley (SD) rats with normal or hydronephrotic (HN) kidneys defined by established criteria. BRS was significantly lower in rats with severe HN (0.56 ± 0.08 vs 1.06 ± 0.06 msec/mm Hg in normal rats; p < 0.01, n = 7, 8) with a trend for lower BRS in rats with mild/moderate HN (0.80 ± 0.13 msec/mm Hg, n = 8). While resting AP was similar among conditions, resting HR was significantly elevated in mild/moderate and severe HN rats (290 ± 12 normal vs 344 ± 11 mild/moderate vs 355 ± 13 bpm severe; p < 0.01). A possible site for Ang II‐mediated BRS impairment is the solitary tract nucleus (NTS). NTS administration of the Ang II AT1 receptor blocker candesartan had no significant effects on AP, HR or BRS in severe HN rats, but enhanced BRS by ~ 40% in normal rats. Thus, hydronephrosis is associated with impairments in BRS and autonomic regulation. Since Ang II provides inhibitory tone to the BRS in normal rats, the lack of Ang II actions in hydronephrosis may suggest dysregulation of the local NTS RAS. HL51952