A permissive role for nitric oxide in active thermoregulatory
vasodilation in the rabbit ear.
Farrell, Diane M., and Vernon S. Bishop.
Department of Physiology, The University of Texas Health Science
Center at San Antonio, San Antonio, Texas 78284-7756
APStracts 2:0220H, 1995.
We have previously shown that an increase in ear blood flow (EBF)
velocity in the rabbit during whole body heating (WBH) involves
active, neurogenic vasodilation that is abolished by treatment with
nitric oxide synthase (NOS) inhibitors. The present study was
designed to test the hypothesis that during WBH, nitric oxide (NO)
synthesized in the endothelium, acts synergistically with an unknown
neurotransmitter to elicit active vasodilation. Twelve rabbits were
instrumented for the measurement of mean arterial pressure (MAP),
heart rate (HR), and EBF (Doppler ultrasound). A catheter was placed
in the left lingual artery for administration of drugs to the left
ear. WBH was achieved by circulating warm water through a rubber pad
placed around the rabbit. Internal temperature was measured with a
rectal thermocouple. During WBH, either Nw-nitro-L-arginine methyl
ester (L-NAME, 10-40 mg over 10-15 min, 6 rabbits - Group 1), an NOS
inhibitor, or saponin (30-40 mg over 10-20 min, 6 rabbits - Group 2),
a detergent which denudes the endothelium, was given via the lingual
artery catheter until thermoregulatory vasodilation was reversed.
When EBF stabilized at the new reduced level, the NO donor, sodium
nitroprusside (SNP), was infused (0.2-1.0 mg/ml, 0.01-0.05 ml/min, 2
-5 min) via the lingual artery catheter. During WBH, EBF increased
from 0.39 +/- 0.08 kHz to 6.47 +/- 0.63 kHz in Group 1, and from 0.69
+/- 0.18 kHz to 5.72 +/- 0.49 kHz in Group 2. Infusion of L-NAME
decreased EBF in group 1 to 1.97 +/- 0.40 kHz. Infusion of saponin
decreased EBF in Group 2 to 1.23 +/- 0.40. Subsequent nitroprusside
infusion during hyperthermia returned EBF to 6.88 +/- 0.72 kHz in
Group 1 and 5.53 +/- 1.27 kHz in Group 2, but had no effect when
administered during normothermia. These results suggest that NO acts
in conjunction with another substance, presumably the
neurotransmitter released upon WBH, to elicit thermoregulatory
vasodilation.
Received 24 March 1995; accepted in final form 12 May 1995.
APS Manuscript Number H287-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 May 1995.