Central cholinergic modulation of the exercise pressor reflex in anesthetized cats

Effects of central administration of a cholinesterase inhibitor, physostigmine, on cardiovascular responses to static contraction and passive stretch of the triceps surae were studied using anesthetized cats. Contraction increased mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) by 44 ± 5 mmHg, 18 ± 1 beats/min, and 86 ± 6%, respectively. MAP, HR, and RSNA increased during stretch by 44 ± 5 mmHg, 15 ± 1 beats/min, and 61 ± 4%, respectively. Administration of physostigmine (100 μg; 5 μl) into the third ventricle decreased resting MAP by 22 ± 3 mmHg and RSNA by 32 ± 4%, with no effect on HR. Physostigmine attenuated the contraction-evoked responses as MAP, HR, and RSNA increased by 17 ± 2 mmHg, 3 ± 1 beats/min, and 31 ± 6%, respectively. Also, physostigmine blunted MAP, HR, and RSNA responses to stretch (16 ± 2 mmHg, 4 ± 1 beats/min, and 9 ± 6%, respectively). Posterior hypothalamic stimulation increased MAP by 39 ± 3 mmHg, which was unaffected by physostigmine, despite a lower baseline. Cardiovascular and RSNA responses to contraction and stretch returned to control 90-120 min after physostigmine. Preadministration of the muscarinic antagonist, atropine sulfate (100 μg; 5 μl), blocked the effects of physostigmine. Results suggest central cholinergic stimulation can inhibit the exercise pressor reflex in anesthetized cats.