Before giving clonidine the cardiac sympathetic and vagus each exerted similar effects on resting heart rate in unanaesthetized normotensive and renal hypertensive rabbits, suggesting that the resting activity of these effectors was not altered in renal hypertension. Administration of clonidine resulted in resetting of the mean arterial pressure (MAP)-heart period (HP; pulse interval) curves. The resetting was dose dependent and was due to alterations in excitability of cardiac autonomic pathways receiving baroreceptor projections and also of baroreflex-independent pathways. In each group the relationship between dose and change in appropriate MAP-HP curve parameter expresses the characteristic changes in excitability which the drug induces in the cardiac autonomic pathways. Comparison of such dose-response curves between hypertensive and normotensive animals then provides a measure of relative excitability of clonidine-sensitive pathways in these groups. In vagotomized hypertensive rabbits (with only cardiac sympathetic functioning), a given i.v. dose of clonidine evoked less reduction in median blood pressure and in gain of the MAP-HP curve than in normotensive rabbits, the baroreflex-independent sympathoinhibitory effects were smaller and complete inhibition of the sympathetic required higher doses of clonidine. The smaller baroreflex-dependent changes in MAP-HP curves produced by clonidine were partly due to functional impairment of the peripheral baroreceptors in hypertensives. However the less pronounced baroreflex-independent sympatho-inhibitory effects and higher doses of drug needed for complete inhibition in hypertensives suggested that they had a small increase in central cardiac sympathetic excitability. In hypertensive and normotensive rabbits with vagus and sympathetic both intact, the effects of i.v. clonidine on the MAP-HP curve were identical, with the same degree of facilitation of the baroreceptor-heart rate reflex. This implies a small increase in vagal excitability in renal hypertensive rabbits which masked the increase in sympathetic excitability when both effectors were intact.
- Autonomic excitability
- Baroreceptor-heart rate reflex
- Heart rate
- Renal hypertension