Autoregulation of blood flow during sympathetic nerve stimulation in the arteriolar network on cat sartorius muscle.

Abstract

Autoregulation is the tendency for blood flow to remain constant despite a change in arterial perfusion pressure. Flow regulation is achieved by adjustment of arteriolar caliber to the pressure change. The responses of arterioles are most commonly explained by either the metabolic or myogenic hypothesis. According to the metabolic hypothesis, the initial decrease in blood flow that accompanies a reduction in arterial pressure would reduce oxygen delivery and decrease tissue oxygen tension. We reasoned that the contribution of this mechanism to autoregulation of flow would be increased during sympathetic nerve stimulation because the latter causes arteriolar constriction and decreases tissue oxygen tension. However, the elevated vascular tone might also influence the myogenic response (i.e., arteriolar constriction to elevated intravascular pressure). In these experiments, we examined flow and diameter changes in arterioles of the exteriorized cat sartorius muscle during sympathetic nerve stimulation and tested the contribution of both metabolic and myogenic factors. Without sympathetic nerve stimulation, autoregulation was weak, flow fell coincident with reduced perfusion pressure. Sympathetic nerve stimulation caused significant constriction of arterioles, enhancing autoregulation, and increasing flow about 20% to 60% during perfusion pressure reduction from 110 to 80, 60, and 40 mmHg. With sympathetic nerve stimulation, arteriolar dilation to arterial pressure reduction was enhanced. This enhanced dilation was not abolished by 20% oxygen in a suffusate over the muscle, suggesting that it was not due to an enhanced metabolic response. On the other hand, arteriolar constriction to venous pressure elevation (which raises arteriolar intravascular pressure), was increased during sympathetic nerve stimulation, indicating an enhanced myogenic response. Arteriolar dilation to pressure reduction was also enhanced during norepinephrine infusion, showing that prejunctional inhibition of neurotransmitter release was not involved. Vasopressin and BayK8644 had similar effects, indicating the enhanced myogenic response did not require adrenergic or receptor mediated vasoconstriction. The autoregulatory response was also examined for all the orders of arterioles in the network. Third and fourth order arterioles showed significantly more dilation during pressure reduction under both with and without sympathetic nerve stimulation. With sympathetic nerve stimulation, arteriolar dilation during pressure reduction was significantly enhanced in first through fourth order arterioles and also appeared to be enhanced in fifth and sixth orders. Enhanced autoregulation appears due to generalized increase in dilation in all orders.