Heat stress reduced endothelium-dependent relaxations in rat mesenteric artery

Objective: To investigate the mechanisms of reduced endothelium-dependent relaxation in mesenteric artery in rats after heat stress. Methods: With the myograph system, we examined the vessel dilatory responses by cumulative addition of acetylcholine (ACh) and pre-contraction with 5-hydroxytryptamine in heat stress rats and control rats. We studied the effects of nitric oxide (NO)-, prostacyclin I₂ (PGI₂)- and endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in mesenteric artery after heat stress. The responses were characterized in terms of maximum relaxant effect (R_max) and negative logarithm of the molar concentration that produced half maximum relaxation (pIC₅₀). Results: The R _max and pIC₅₀ were decreased from (97±6)% and (52±8)% in control rats to 8.67±0.59 (P<0.01) and 7.66±1.33 (P<0.05), respectively, in heat stress rats. In NO-mediated relaxation, the R_max and pIC₅₀ were (53±6)% and 6.89±0.93 in control rats, and (21±8)% (P<0.01) and 4.91±0.31 (P<0.01) in heat stress rats. In EDHF-mediated relaxation, the R_max and pIC₅₀ were (35±14)% and 6.30±0.56 in control rats, and (13±3)% (P<0.01) and 5.23±1.07 (P<0.01) in heat stress rats. In PGI₂-mediated relaxation, the R_max and pIC₅₀ were (8±3)% and 5.69±0.37 in control rats, and (10±6)% (P>0.05) and 5.74±0.79 (P>0. 05) in heat stress rats. Conclusion: The decreased endothelium-dependent relaxation in mesenteric artery induced by heat stress damages NO- and EDHF-pathways.