The present study examined the mechanisms responsible for the hindlimb vasodilation produced by elevating core body (colonic) temperature (T(co)) of α-chloralose-anesthetized rats from 37 to 39°C. Elevating T(co) to 39°C produced equivalent decreases in hindlimb vascular resistance in sham- operated (-48 ± 2%) and sinoaortic baroreceptor-denervated rats (-44 ± 3%) rats. There were no changes in mean arterial blood pressure, heart rate, or lumbar sympathetic nerve activity in either group. The prior administration of the α1-adrenoceptor antagonist prazosin (100 μg/kg iv) did not prevent the heat-induced decrease in hindlimb resistance in sham-operated rats (-52 ± 7% vs. baseline). In contrast, the fall in hindlimb resistance was markedly attenuated (-20 ± 5% vs. baseline) in sham-operated rats that had received a prior injection of the nitric oxide synthase (NOS) inhibitor N(G)- nitro-L-arginine methyl ester (100 μmol/kg iv). Dexamethasone (1 mg/kg iv), administered to prevent the possible induction of inducible NOS, did not modify the heat-induced hindlimb vasodilation in sham-operated rats (-41 ± 5%). These results demonstrate that the elevation of T(co) to 39°C in α- chloralose-anesthetized rats produces a relative vasodilation in the hindlimb that is not obviously linked to an alteration in lumbar sympathetic nerve activity. Because the vasodilation occurred in the presence of prazosin, it is unlikely that the decline in resistance is due to the loss of the vasoconstrictor potency of neurally derived catecholamines. The finding that N(G)-nitro-L-arginine methyl ester, but not dexamethasone, diminished the heat-induced hindlimb vasodilation suggests that the fall in resistance is due in part to constitutive NOS and supports a role for NOS as a mediator of thermoregulatory active vasodilation.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||3 42-3|
|State||Published - 1997|
- N(G)-nitro-L-arginine methyl ester
- Nitric oxide
- Sympathetic nervous system