Mechanisms underlying cardiovascular defense reaction evoked by dorsal periaqueductal gray stimulation

Hemodynamic and autonomic mechanisms underlying the cardiovascular defense reaction elicited by electrical stimulation of the dorsolateral periaqueductal gray region were evaluated in pentobarbital sodium-anesthetized Sprague-Dawley rats. Stimulation of this area produced transient increases in mean arterial pressure and more sustained increases in heart rate, hindlimb blood flow, and plasma catecholamine levels. The pressor component of the defense reaction was due entirely to increased total peripheral vascular resistance; elevations in cardiac output occurred only at the end of the stimulation period when blood pressure had returned to resting values. The hindlimb vasodilatory response included distinct early and late components. The late component was produced by epinephrine-mediated activation of beta 2-receptors because it was abolished by bilateral adrenalectomy or treatment with butoxamine, a beta 2-receptor selective antagonist. In contrast, the early component was only partially reduced by adrenalectomy or butoxamine treatment. During conditions of constant flow provided by a pump-perfused hindlimb preparation, the early hindlimb vasodilatory response was eliminated and a neurogenic vasoconstrictor response revealed. This finding suggests that the early hindlimb blood flow response may result from shunting of blood from highly vasoconstricted vascular beds to relatively less constricted hindlimb vasculature.