We examined the influence of gender and climacteric status, two coronary risk factors, on bradykinin (BK)-induced dilation in adipose arterioles from men and women of different ages (premenopausal women (preW), postmenopausal women (postW), and similar aged men (Y-M and O-M) respectively. We examined responses from both omental (more closely associated with coronary disease) and subcutaneous fat. Tissues were obtained at surgery and cannulated (60 mmHg) for measurement of internal diameter. In vessels from omental tissue, dilation to BK was more sensitive in preW than other groups while in vessels from subcutaneous tissue sensitivity to BK was greater in both preW and postW compared to Y-M and O-M. Maximal dilation was similar among groups. Indomethacin (INDO, 10^-5 M) alone had no effect on dilation to BK in any groups, but INDO and N-nitro-L-arginine methyl ester (LNAME 10^-4 M) reduced dilation to BK in Pre-W more than Y-M. LNAME increased dilation to BK in subcutaneous fat from Y-M, but had no effect in PostW and O-M. INDO- and LNAME-resistant dilation in all vessels was markedly reduced by 30 mM KCl. There was no difference in SNP-induced dilation among groups. We conclude that gender and climacteric state contribute to mechanisms of microvascular regulation in humans. Functional vascular differences in visceral and subcutaneous fat may underlie the proposed differential influence of these tissues on cardiovascular risk.