SYMPATHETIC NEURAL CONTROL OF VASCULAR MUSCLE IN REDUCED RENAL MASS HYPERTENSION

Vascular smooth muscle (VSM) transmembrane potentials (E(m)) were measured in situ in small branch arteries (150-300-mu-m o.d.), small branch veins (300-400-mu-m o.d.), arterioles (90-150-mu-m o.d.), and venules (80-250-mu-m o.d.) in the mesenteric and gracilis muscle and the arterioles and venules of cremaster muscle vascular beds in anesthetized rats with reduced renal mass hypertension (HT-RRM) and normotensive sham-operated RRM control rats. All rats were given a 4% NaCl diet for 2 weeks with water ad libitum. Relative to sham, HT-RRM mesenteric and gracilis arterial and venous vessels, but not the microvessels of the cremaster muscle bed, were less polarized during superfusion with normal physiological salt solution. Also relative to sham, hyperpolarization responses to local sympathetic neural (SNS) denervation with 6-hydroxydopamine were greater in mesenteric and gracilis small arteries, arterioles, veins, and venules but not in cremaster microvessels. The immediate (less than 5-minute) electrogenic depolarization response to local blockade of VSM Na+-K+ pump activity with 10(-3) M ouabain was similar between each respective HT-RRM and sham vessel pair in each vascular bed. These results suggest that in all three vascular beds: 1) significant SNS control of VSM E(m) (and active tone) exists all the way to the arterial and venous microvasculature (except cremaster venules); 2) in HT-RRM, such SNS control is elevated relative to sham in both arterial resistance and venous capacitance vessels in mesenteric and gracilis vascular beds but not in the cremaster microvessels; and 3) any circulating Na+-K+ pump inhibitors in the circulation of this volume-expanded model of hypertension do not appear to affect VSM tone in the vessels studied.