Differential effects of clonidine on renal sympathetic nerve activity and heart rate at onset of static exercise

Abstract

The effects of the α 2-adrenergic agonist clonidine on the increase in renal sympathetic nerve activity (RSNA) and heart rate (HR) at the onset of voluntary static exercise were studied using conscious cats. Five cats were trained to press a bar with one forelimb. A total of 60 exercise trials were performed before and after injection of clonidine (5–10 μg/kg i.v.). Before clonidine, RSNA and HR increased immediately before or at the onset of exercise, which was followed by a rise in arterial blood pressure (AP). The initial increases in RSNA and HR are likely to be caused by descending input from higher brain centers. After clonidine, baseline RSNA was decreased to 21 ± 5% of the control before clonidine, probably due to a central action of clonidine. HR and AP were decreased from 221 ± 4 to 178 ± 5 bpm and from 108 ± 2 to 82 ± 4 mmHg, respectively. The increase in RSNA at the onset of exercise and the rise in AP during exercise were blunted to 56–57% of the responses before clonidine injection. In contrast, the increase in HR at the onset of exercise was not altered by clonidine. Thus, it is suggested that clonidine, administered intravenously, attenuates the centrally-induced increase in RSNA at the onset of static exercise but does not affect the increase in HR.