Pitetti K H, Iwamoto G A, Mitchell J H, Ordway G A
Department of Physiology, University of Texas Southwestern Medical Center, Dallas 75235.
Am J Physiol. 1989 Jun;256(6 Pt 2):R1331-9. doi: 10.1152/ajpregu.1989.256.6.R1331.
We used a constant flow preparation to study the changes in left circumflex coronary arterial (LCCA) pressure and resistance evoked by electrical stimulation of branches of muscle, cutaneous, and mixed nerves in the hindlimb of anesthetized dogs. Stimulation (20 Hz) of all three nerve types at 20, 70, 100, and 200 times the voltage threshold that evoked compound action potentials significantly (P less than 0.05) increased LCCA resistance. Stimulation at three and five times threshold had no effect on this same variable. Cooling the nerve to 2-4 degrees C, temperatures that block myelinated nerve fibers, attenuated but did not abolish the increase in LCCA resistance. Combinations of beta- and alpha-adrenergic and cholinergic blockade established that the biphasic change evoked by nerve stimulation was due to an initial alpha-adrenergic vasoconstriction followed by a metabolite-induced vasodilation. These data demonstrate that stimulation of muscle, cutaneous, or mixed nerve afferent C-fibers increases coronary arterial resistance by alpha-adrenergic vasoconstriction.