Large-conductance, voltage- and Ca2+-activated K+ channels (MaxiK, BK) are key regulators of vascular tone. Vascular MaxiK are formed by the pore-forming subunit and modulatory 1 subunit, which imprints unique kinetics, Ca2+/voltage sensitivities and pharmacology to the channel. As age progresses, subunit functional expression and protein levels diminish in coronary myocytes. However, whether aging modifies 1 subunit expression or the mechanism of subunit reduction is unknown. Thus, we examined functional and pharmacological characteristics of MaxiK, as well as, and 1 transcript levels in coronary myocytes from young and old F344 rats. The mechanism of age-dependent subunit protein reduction involves its transcript downregulation. A corresponding loss of 1 transcripts was also detected in old myocytes, suggesting a proportional age-dependent decrease of 1 to subunit protein. Indeed, MaxiK channel properties defined by coassembly of 1 and subunits were equivalent in young vs. old, like: i) activation kinetics; ii) sensitivity to Ca2+ levels > 1 µM, iii) dehydrosoyasaponin-I induced activation, and iv) iberiotoxin blockade. Consistent with less MaxiK expression/function in older myocytes, iberiotoxin ability to contract coronary rings was reduced ~50% with aging confirming our previous findings. 5-hydroxytryptamine (5-HT) contractile efficacy was reduced by iberiotoxin pretreatment in young>old coronary arteries (explained by larger iberiotoxin-induced contraction and decreased dynamic range for 5-HT contraction in young vs. old) with no apparent differences in nitroglycerin-induced relaxation. We propose that the age-related MaxiK reduction involves a parallel decrease of and 1 functional expression via a transcript downregulatory mechanism; a major impact on basal and possibly stimulated coronary contraction may contribute to altered coronary flow regulation and coronary morbidity in the elderly.