Progesterone appears to play an important role in cardiovascular physiology, however, little is known about its effects on coronary circulation in different sexes. Thus, our aim was to investigate the acute action of progesterone in the coronary bed of normotensive animals of both sexes and the possible endothelial mediators involved. Female (F) and male (M) Wistar rats, with 10 weeks-old, were used. Experimental protocols on isolated hearts were conducted using the Langendorff method. Increasing doses of progesterone were administered (1-50 ?M, in bolus) before and after perfusion with L-NAME, indomethacin, catalase and Tiron, alone or in combination. NO and O2?- levels were obtained using DAF-2 and DHE, respectively. Data were expressed as mean ± standard deviation. Unpaired t-test and one-way or two-way ANOVA were used, followed by Bonferroni or Tukey post-test (p < 0.05). Progesterone promoted similar vasodilation in females and males (F = 10.8 ± 3.6 %; M = 10.2 ± 5.1 %), which was increased in both after inhibition with L-NAME (F = 23.5 ± 8.6 %, n = 10; M = 26.6 ± 6.7 %, n = 9). Only males showed a reduction in the vasodilator response after inhibition with indomethacin (M = 4.3 ± 2.5 %, n = 8), while females showed a reduction with combined perfusion of L-NAME, indomethacin and catalase (F = 6.7 ± 2.2 %, n = 8) or Tiron perfusion (F = 1.9 ± 3.2 %, n = 7). NO levels increased in females and males after stimulation with progesterone, while O2?- levels increased only in females. Our results suggest that progesterone is able to modulate coronary reactivity through a sex-specific vasodilator response mediated by different endothelial pathways. These results can contribute to better understanding of progesterone actions in the coronary bed from rats.
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