Cardiovascular control by cholinergic mechanisms in the rostral ventrolateral medulla

The cardiovascular effects associated with the microinjection (100 nl) of carbachol, physostigmine and atropine into the pressor area in the ventrolateral medulla (VLPA) were studied. In urethane anesthetized rats, VLPAs were functionally identified bilaterally by microinjection of the neuroexcitatory amino acid L-glutamate (300 ng/site). L-Glutamate microinjections into the VLPA cause a transient rise in blood pressure (BP) and heart rate (HR). The bilateral microinjection of carbachol into the VLPA caused a prolonged dose-related increase in BP and HR in the dose range of 0.8 to 400.0 ng/site. At higher doses (1-10 micrograms), carbachol caused a decrease in BP and HR; indicative of depolarization blockade. Acetylcholine esterase inhibition by physostigmine microinjections in the VLPA caused cardiovascular effects similar to those observed with carbachol. The hypertensive responses evoked by muscarinic receptor stimulation in the VLPA were mediated by increasing sympathetic outflow. The pathway by which cholinergic receptor stimulation in the VLPA activates vasomotor outflow appears to be entirely descending as coronal knife cuts at the level of the trapezoid body failed to alter the hypertensive responses. Pressor responses elicited by both physostigmine and carbachol were reversed completely by the i.v. administration of atropine sulfate (0.5-3 mg/kg i.v.). Muscarinic receptor blockade in the VLPA after atropine sulfate microinjection caused a dose-related (0.4-15.0 micrograms/site) fall in the BP and HR suggesting that cholinergic mechanisms in the VLPA are tonically active.