AJP - Heart and Circulatory Physiology, Vol 250, Issue 2 221-H225, Copyright © 1986 by American Physiological Society
Skeletal muscle vasodilation during electrical stimulation of the preoptic recess
K. G. Proctor and S. L. Bealer
Transverse (3rd-order) arterioles (diam 12 +/- 2 micron, n = 6) in rat
spinotrapezius muscle were observed with video microscopy during electrical
stimulation of preoptic recess in periventricular region of hypothalamus
(AV3V region) to test whether active skeletal muscle vasodilation was
mediated by a beta-adrenergic mechanism. Bipolar wire electrodes were
implanted in AV3V 3-7 days before an experiment. Continuous superfusion of
propranolol (10(-5) M) caused steady-state reduction (3 +/- 1 microns) in
arteriolar diameter and reduced steady-state vasodilation (26 +/- 2 vs. 11
+/- 2 microns) caused by a continuous superfusion of isoproterenol (10(-6)
M). Six arterioles were observed with and without propranolol during four
frequencies of AV3V stimulation (8-15 V, 0.2-0.5 ms pulse duration; 10, 15,
20, and 25 Hz; 1 min stimulus duration). Stimulation caused
frequency-related reductions in arterial blood pressure (10-20 mmHg), which
were sustained and not altered by propranolol. Transient peak diameters
were observed after 30 +/- 7 s; the time was not related to stimulus
frequency or affected by propranolol. Peak diameters averaged 14-17 microns
during vehicle and 11-12 micron during propranolol (maximum diam 32 +/- 3).
Peak vasodilations were significant but identical with vehicle or
propranolol (avg 3 +/- 1 microns) and not related to stimulus frequency.
Diameters stabilized at steady-state values above base line only during 15
and 20 Hz with vehicle and only during 20 Hz with propranolol. We conclude
that AV3V stimulation causes transient vasodilation in spinotrapezius
muscle that is probably not mediated by beta-adrenergic receptors.(ABSTRACT
TRUNCATED AT 250 WORDS)
