Baroreflex depression persists in the early phase after hypertension reversal

The baroreflex control of heart rate (HR) was evaluated in conscious chroni c renal hypertensive rats (RHR; 1K-1C, 2 mo) under control conditions and a fter reversal of hypertension by unclipping the renal artery or sodium nitr oprusside infusion. Unclipping and nitroprusside infusion were both followe d by significant decreases in the mean arterial pressure (unclipping: from 199 +/- 4 to 153 +/- 8 mmHg; nitroprusside infusion: from 197 +/- 9 to 166 +/- 6 mmHg) as well as slight and significant increases, respectively, in t he baroreflex bradycardic response index (unclipping: from 0.2 +/- 0.04 to 0.6 +/- 0.1 beats. min(-1).mmHg(-1); nitroprusside infusion: from 0.1 +/- 0 .04 to 0.5 +/- 0.1 beats.min(-1).mmHg(-1)). However, this index was still d epressed compared with that for normotensive control rats (2.1 +/- 0.2 beat s.min(-1).mmHg(-1)). The index for the baroreflex tachycardic response was also depressed under control conditions and remained unchanged after hypert ension reversal. RHR possessed markedly attenuated vagal tone as demonstrat ed by pharmacological blockade of parasympathetic and sympathetic control o f HR with methylatropine and propranolol, respectively. A reduced bradycard ic response was also observed in anesthetized RHR during electrical stimula tion of the vagus nerve or methacholine chloride injection, indicating impa irment of efferent vagal influence over the HR. Together, these data indica te that 2 h after hypertension reversal in RHR, the previously described no rmalization of baroreceptor gain occurs independent of the minimal or lack of recovery of baroreflex control over HR.