Mechanism of vasoconstriction in the rat's tail when warmed locally.

The vascular response of the tail to local warming was investigated in urethan-anesthetized rats whose colonic temperature was maintained at 39.5 degrees C with an intravenous thermode at an ambient temperature of 23 degrees C. The tail, covered with thin latex tubing, was immersed in temperature-controlled water initially kept at 35 degrees C. The tail was warmed by raising the water bath temperature from 35 to 44 degrees C at a constant rate. Tail blood flow (BF), mean arterial blood pressure (BP), and tail skin temperature (Tsk) were measured before and during the local warming. Tail vascular conductance (VC) was computed as 100 x tail BF/BP. When Tsk exceeded 37 degrees C, tail BF and VC significantly decreased from the levels at Tsk of 35 degrees C, and significant reductions in tail BF and VC occurred until Tsk reached 42 degrees C. Surgical deafferentation of the tail, chemical sympathectomy with 6-hydroxydopamine (100 mg/kg), and alpha-blockade with phentolamine (7 or 40.1-45.5 mg/kg) or phenoxybenzamine (5 mg/kg) failed to stop the decrease in tail BF and VC during the local warming. These results suggest that a reflex via the central nervous system and the alpha-adrenergic sympathetic nervous system is not indispensable for heat-induced vasoconstriction (HIVC). It is therefore assumed that, at least in the rat's tail, HIVC predominantly originates from a local vascular response to high temperature.