Modulation by physostigmine of head-up tilt- and bilateral carotid occlusion-induced baroreflexes in rats.

In anesthetized normotensive rats, 45 degrees head-up tilt induced a transient marked drop followed by a long-lasting slight drop in mean arterial pressure (MAP), and with cessation of tilt there is a transient pressor response. Heart rate (HR) did not change appreciably by tilting. Bilateral occlusion of common carotid arteries (BCO) induced pressor responses with tachycardia. Physostigmine (5 and 15 micrograms i.c.v.) attenuated the tilt-induced decreases in MAP. Neither the HR during tilt nor the restoration-related transient pressor response was altered by physostigmine. Acetylcholine (ACh, 5 micrograms i.c.v.) exhibited a similar attenuation of tilt-induced changes in MAP. Physostigmine enhanced BCO-induced pressor responses whereas not affecting BCO-induced HR responses. The time for onset of these changes in arterial pressure was slower than that of physostigmine-induced pressor response. Depletion of brain ACh with hemicholinium-3 (20 micrograms i.c.v.) or its derivative A-5 (20 micrograms i.c.v.) or blockade of muscarinic-receptors with atropine (1 microgram i.c.v.) blocked physostigmine-elicited modulation of both tilt- and BCO-induced reflexes. These results suggest involvement of central cholinergic systems for modulation not only of BCO-induced but also tilt-induced cardiovascular reflexes. In particular, ACh appears to enhance these reflexes by acting within the central nervous system.