| Summary: | Abstract Objective The objective of this study was to measure flow‐mediated dilation (FMD) prior to and following transient increases in intraluminal pressure (IILP) in resistance arterioles isolated from subjects with and without coronary artery disease (CAD) (CAD and non‐CAD) and non‐CAD subjects with hypertension. Methods Arterioles were isolated from discarded surgical tissues (adipose and atrial) from patients without coronary artery disease (non‐CAD; ≤1 risk factor, excluding hypertension), with CAD, and non‐CAD patients with hypertension (hypertension as the only risk factor). To simulate transient hypertension, increased IILP was generated (150 mmHg, 30 min) by gravity. Arterioles were constricted with endothelin‐1, followed by FMD and endothelial‐independent dilation prior to and following exposure to IILP. Results IILP reduced FMD in non‐CAD and CAD arterioles relative to pre‐IILP (p <.05 at 100 cmH2O). In contrast, arterioles from non‐CAD hypertensive subjects exhibited no reduction in maximal FMD following IILP (p = .84 at 100 cmH2O). FMD was reduced by L‐NAME prior to IILP in non‐CAD hypertensive patients (p < .05 at 100 cmH2O); however, following IILP, FMD was inhibited by peg‐cat (p < .05 at 100 cmH2O), indicating a switch from NO to H2O2 as the mechanism of dilation. Conclusions Acute exposure (30 min) to IILP (150 mmHg) attenuates the magnitude of FMD in non‐CAD and CAD resistance arterioles. The presence of clinically diagnosed hypertension in non‐CAD resistance arterioles preserves the magnitude of FMD following IILP as a result of a compensatory switch from NO to H2O2 as the mechanism of dilation.
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