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

Farrell, Daniel; Bishop, V. S.

doi:10.1152/ajpheart.1995.269.5.h1613

Cited by 40 publications

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“…Although the foregoing studies showed a role for NO in human cutaneous active vasodilation, there remained two possible mechanisms: 1) levels of diffusible NO could increase to effect cutaneous vasodilation or 2) NO levels could remain unchanged so that NO acted only as a permissive factor as in the rabbit ear (9,12,23). The latter mechanism was initially suggested by Farrell and Bishop (9), who proposed that NO acted as a "permissive factor" that need not vary in concentration, but had to be present for vasodilation to occur.…”

Section: Discussionmentioning

confidence: 99%

“…Instead, their studies led them to the provocative conclusion that NO served a "permissive" role in active vasodilation in the rabbit ear. According to their hypothesis, NO maintained a basal level of cGMP-mediated phosphodiesterase inhibition that was required for an unknown neurotransmitter to effect cutaneous vasodilation by a cAMPdependent mechanism (9). This implied that NO had to be present for vasodilation to be effected by the neurotransmitter of active vasodilation but that the absolute concentration of NO need not increase in heat stress in the rabbit ear.…”

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confidence: 99%

“…These studies demonstrated that NOS activity, and therefore the presence of NO, was required during heat stress for complete cutaneous active vasodilation. They did not distinguish whether concentrations of NO increased (suggesting an active effector role for NO) or remained unchanged [suggesting a role as a permissive factor (9,12,23)]. …”

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confidence: 99%

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Nitric oxide concentration increases in the cutaneous interstitial space during heat stress in humans

Kellogg

Zhao

Friel

et al. 2003

Journal of Applied Physiology

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. Nitric oxide concentration increases in the cutaneous interstitial space during heat stress in humans. J Appl Physiol 94: 1971Physiol 94: -1977Physiol 94: , 2003 10.1152/japplphysiol.00826. 2002To examine the role of nitric oxide (NO) in cutaneous active vasodilation, we measured the NO concentration from skin before and during whole body heat stress in nine healthy subjects. A forearm site was instrumented with a NO-selective, amperometric electrode and an adjacent intradermal microdialysis probe. Skin blood flow (SkBF) was monitored by laser-Doppler flowmetry (LDF). NO concentrations and LDF were measured in normothermia and heat stress. After heat stress, a solution of ACh was perfused through the microdialysis probe to pharmacologically generate NO and verify the electrode's function. During whole body warming, both SkBF and NO concentrations began to increase at the same internal temperature. Both SkBF and NO concentrations increased during heat stress (402 Ϯ 76% change from LDF baseline, P Ͻ 0.05; 22 Ϯ 5% change from NO baseline, P Ͻ 0.05). During a second baseline condition after heat stress, ACh perfusion led to increases in both SkBF and NO concentrations (496 Ϯ 119% change from LDF baseline, P Ͻ 0.05; 16 Ϯ 10% change from NO baseline, P Ͻ 0.05). We conclude that NO does increase in skin during heat stress in humans, attendant to active vasodilation. This result suggests that NO has a role beyond that of a permissive factor in the process; rather, NO may well be an effector of cutaneous vasodilation during heat stress. skin blood flow; vasodilation; amperometric electrode; thermoregulation THE HUMAN CUTANEOUS CIRCULATION is a major effector of thermoregulatory homeostasis. During periods of whole body heat stress, this circulation undergoes a profound reflex vasodilation to deliver blood, and hence heat, to the body's surface for removal to the environment. During periods of cold stress, the cutaneous blood vessels are intensely vasoconstricted to reduce loss of heat from the body to the environment. These reflex changes in skin blood flow (SkBF) occur in response to changes in internal temperature and skin temperature (T sk ) and are mediated by two branches of the sympathetic nervous system: an active vasodilator system and an active vasoconstrictor system (17).The mechanisms by which the active vasodilator system causes increases in SkBF during heat stress have been the subject of numerous investigations since the system was first described over 70 years ago (18). A number of these studies demonstrated that muscarinic-receptor blockade with atropine could slightly delay (10, 17, 19, 22) and attenuate (17, 19) the reflex increase in SkBF during heat stress. This finding of partial reductions in the active vasodilator response despite complete muscarinic-receptor blockade established a role for cholinergic nerves in the process of active vasodilation, but it left open to question the exact nature of this involvement. In 1995, our laboratory showed that thermoregulatory active vasodilation involve...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Nitric oxide concentration increases in the cutaneous interstitial space during heat stress in humans

Kellogg

Zhao

Friel

et al. 2003

Journal of Applied Physiology

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“…In the non-adrenergic, non-cholinergic, thermoregulatory control of blood flow in the rabbit ear skin and in the heat dissipating nasal mucosa of dogs NO seems to exert a permissive function (Farrell andBishop, 1995, Watanabe et al, 1995), but not in humans (Dietz et al, 1994). NO may also be relevant in the process of cold acclimation as a local messenger in the brown adipose tissue (BAT), a heat generating thermoregulatory effector organ (Kuroshima, 1995).…”

Section: Pharmacology Of No In Temperature Regulation and Fevermentioning

confidence: 99%

Nitric oxide as a peripheral and central mediator in temperature regulation

Simón

1998

Amino Acids

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In animals including humans nitric oxide (NO) serves as a biological messenger both peripherally at neuroeffector junctions and in the central nervous system where it modulates neuronal activity. Evidence for the involvement of NO in homeostatic control is accumulating also for temperature regulation in homeotherms. In the periphery an auxiliary role in the vasomotor control of convective heat transfer to heat dissipating surfaces and modulation of thermoregulatory heat generation, especially in brown adipose tissue as the site of nonshivering thermogenesis, are discussed as NO actions. At the central level a thermolytic role of NO in thermoregulation as well as in fever is assumed, however, experimental data opposing this view suggest that topical specificity may be important. At the level of single neurons, the observed interrelationships between thermosensitivity and responsiveness to NO are still not consistent enough to reconcile these data with the effects of NO-donors and inhibitors of NO-synthase on temperature regulation.

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“…Inhibiting the synthesis of nitric oxide reduces evaporative water loss and skin blood flow [13,15,23], increases the rate at which body temperature rises during heat-exposure [17], and enhances the febrile response to endotoxin [18]. However, reducing nitric oxide synthesis also is reported to lower metabolic rate [15], cause hypothermia [34,42], and decrease fever magnitude [21,33,34,35].…”

Section: Introductionmentioning

confidence: 99%

Circadian variation in the effects of nitric oxide synthase inhibitors on body temperature, feeding and activity in rats

Kamerman

Mitchell

Laburn

2001

Pflügers Arch - Eur J Physiol

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We have investigated whether there is circadian variation in the effects of nitric oxide synthase inhibitors on body temperature, physical activity and feeding. We used nocturnally active Sprague-Dawley rats, housed at approximately 24 degrees C with a 12:12 h light:dark cycle (lights on 07:00 hours) and provided with food and water ad libitum. Nitric oxide synthesis was inhibited by intraperitoneal injection of the unspecific nitric oxide synthase inhibitor N-nitro- L-arginine methyl ester ( L-NAME, 100, 50, 25, 10 mg/kg), or the relatively selective inducible nitric oxide synthase inhibitor aminoguanidine (100, 50 mg/kg), during the day ( approximately 09:00 hours) or night ( approximately 21:00 hours). Body temperature and physical activity were measured using radiotelemetry, while food intake was calculated by weighing each animal's food before as well as 12 and 24 h after each injection. We found that daytime injection of L-NAME and aminoguanidine had no effect on daytime body temperature. However, daytime injection of both drugs did decrease nocturnal food intake ( P<0.05) and activity ( P<0.05). When injected at night, L-NAME reduced night-time body temperature ( P<0.01), activity ( P<0.05) and food intake ( P<0.05) in a dose-dependent manner, but night-time injection of aminoguanidine inhibited only night-time activity ( P<0.05). The effects of nitric oxide synthase inhibition on body temperature, feeding and activity therefore are primarily a consequence of inhibiting constitutively expressed nitric oxide synthase, and are subject to circadian variation.

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

Cited by 40 publications

References 0 publications

Nitric oxide concentration increases in the cutaneous interstitial space during heat stress in humans

Nitric oxide concentration increases in the cutaneous interstitial space during heat stress in humans

Nitric oxide as a peripheral and central mediator in temperature regulation

Circadian variation in the effects of nitric oxide synthase inhibitors on body temperature, feeding and activity in rats

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