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Permissive role for nitric oxide in active thermoregulatory vasodilation in rabbit ear

Permissive role for nitric oxide in active thermoregulatory vasodilation in rabbit ear METHODS PROCEDURES THERMOREGULATORY in human forearm (10, 13, 21, 23) rabbit ear (28) occurs through an neurogenic mechanism. Thus, in response to whole body ing (WBH), a neurotransmitter is released that leads to of the cutaneous vascular bed. Previous work from our laboratory has shown that the vasodilator response to WBH in the rabbit was dependent on the synthesis of (NO) (27). In that study, administration of NO-nitro+ arginine (L-NNA) to the ear circulation inhibited the . However, the precise role of NO in thermoregulatory was not defined. NO is a potent vasodilator produced in vascular endothelium various neuronal tissue is regulated by intracellular calcium concentration (6, 9). It is, therefore, tempting to speculate that on WBH, NO release is increased in the cutaneous circulation, leading to . This increase could occur in two ways. First, NO release could be increased by a neurotransmitter released on ing. Second, NO could be the neurotransmitter itself, released from nonadrenergic, noncholiner0363-6135/95 $3.00 Copyright o 1995 Surgical procedure. New Zeal White rabbits (2-2.5 kg, either sex) were anesthetized with rabbit cocktail (45% ketamine, 14% thorazine, 43% xylazine). The surgical procedures have been previously described by Taylor et al. (28). Briefly, rabbits were http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Permissive role for nitric oxide in active thermoregulatory vasodilation in rabbit ear

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Publisher
The American Physiological Society
Copyright
Copyright © 1995 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
See Article on Publisher Site

Abstract

METHODS PROCEDURES THERMOREGULATORY in human forearm (10, 13, 21, 23) rabbit ear (28) occurs through an neurogenic mechanism. Thus, in response to whole body ing (WBH), a neurotransmitter is released that leads to of the cutaneous vascular bed. Previous work from our laboratory has shown that the vasodilator response to WBH in the rabbit was dependent on the synthesis of (NO) (27). In that study, administration of NO-nitro+ arginine (L-NNA) to the ear circulation inhibited the . However, the precise role of NO in thermoregulatory was not defined. NO is a potent vasodilator produced in vascular endothelium various neuronal tissue is regulated by intracellular calcium concentration (6, 9). It is, therefore, tempting to speculate that on WBH, NO release is increased in the cutaneous circulation, leading to . This increase could occur in two ways. First, NO release could be increased by a neurotransmitter released on ing. Second, NO could be the neurotransmitter itself, released from nonadrenergic, noncholiner0363-6135/95 $3.00 Copyright o 1995 Surgical procedure. New Zeal White rabbits (2-2.5 kg, either sex) were anesthetized with rabbit cocktail (45% ketamine, 14% thorazine, 43% xylazine). The surgical procedures have been previously described by Taylor et al. (28). Briefly, rabbits were

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Nov 1, 1995

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