Heat attenuates vasoconstriction produced by release of endogenous neurotransmitters

We have previously shown that P2X‐agonist mediated vasoconstriction was attenuated by an increase in temperature, whereas α 1 ‐agonist mediated vasoconstriction was unaffected. Therefore, the purpose of this study was to examine the effect of temperature on vasoconstriction produced via release of endogenous neurotransmitters. Rat femoral arteries (n=14) were dissected and placed in modified Krebs‐Henseleit buffer. The arteries were cut into 2mm sections and mounted in organ tissue baths at 37 o C and pH=7.4. Maximal tension (grams) was measured during field stimulation at 60Hz, 15V and a pulse width of 2msec. Bath temperature was either maintained at 37 o C or adjusted to 41 o C 15 minutes prior to beginning the protocol. Vessels were stimulated for 144 impulses at 2, 6, 20, 60Hz and patterns consisting of pairs or sextuplets at 8Hz or 30Hz instantaneous frequencies. This protocol was repeated in the presence of the purinergic antagonist, suramin (4.7mM), or the α 1 ‐antagonist, prazosin (1.59mM). Tension increased in a frequency dependent manner. At 41 o C, tension was attenuated at all frequencies and patterns (range: −0.09±0.06g to −0.20±0.11g; p<0.05). The purinergic antagonist, suramin, and the α 1 ‐antagonist, prazosin attenuated tension. Residual tension was abolished by double blocking. From these data it appears that heat attenuates tension produced by release of endogenous neurotransmitters. The observed attenuation is likely to be attributable to P2X receptors. Supported by NHLBI and VA Medical Research.