Hypertension preserves the magnitude of microvascular flow-mediated dilation following transient elevation in intraluminal pressure.

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 cmH O). In contrast, arterioles from non-CAD hypertensive subjects exhibited no reduction in maximal FMD following IILP (p = .84 at 100 cmH O). FMD was reduced by L-NAME prior to IILP in non-CAD hypertensive patients (p < .05 at 100 cmH O); however, following IILP, FMD was inhibited by peg-cat (p < .05 at 100 cmH O), indicating a switch from NO to H O 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 H O as the mechanism of dilation.