The roles of cgmp and camp in active thermoregulatory
vasodilation.
Farrell, Diane M., and Vernon S. Bishop.
Department of Physiology, The University of Texas Health Science
Center at San Antonio, San Antonio, TX 78284-7756
APStracts 3:0384R, 1996.
This study was designed to test the hypothesis that active
thermoregulatory vasodilation (AVD) is the result of a
neurotransmitter-induced cAMP pathway interacting with a nitric
oxide-induced cGMP pathway. Rabbits were instrumented for measurement
of arterial pressure and ear blood flow and the infusion of drugs. In
four groups of conscious animals, whole body heating increased ear
blood flow (EBF) from 0.5 +/- 0.3 kHz to 8.3 +/- 1.3 kHz. In group 1
(n=6), Nw-nitro-L-arginine methyl ester (L-NAME, a nitric oxide
synthase inhibitor, 10-40 mg) reduced EBF from 7.1 +/- 0.9 to 1.9 +/-
0.5 kHz. Subsequent infusion of 8-bromo-cGMP (a cGMP analog, 5-10 mg)
returned EBF to 6.2 +/- 0.7. In group 2 (n=3), Rp-adenosine 3',5'
-cyclic monophosphothioate (a cAMP-dependent protein kinase inhibitor,
10mg) reduced EBF to 1.6 +/- 0.4 kHz. In group 3 (n=6), nerve
blockade of the ear (procaine, 20mg/ml, 1.5 ml) reduced EBF from 8.6
+/- 1.3 to 1.6 +/- 0.3 kHz. Subsequent infusion of 8-bromo-cAMP (a
cAMP analog, 5-10 mg) returned EBF to 8.3 +/- 2.0 kHz. In group 4
(n=6), the infusion of L-NAME caused EBF to fall from 9.0 +/- 1.1 to
1.2 +/- 0.3 kHz. Infusion of the cAMP phosphodiesterase inhibitor Ro
20-1724 (0.2-0.5 mg) raised EBF to 5.5 +/- 0.7 kHz. These results
suggest that cGMP plays a permissive role in AVD and indicate that
the transmitter acts through cAMP.
Received 5 August 1996; accepted in final form 1 October 1996.
APS Manuscript Number R451-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996