Hypertension preserves the magnitude of microvascular flow‐mediated dilation following transient elevation in intraluminal pressure. Issue 3 (15th February 2021)

• Record Type: Journal Article
• Authors: Hughes, William E.; Zinkevich, Natalya; Gutterman, David D.; Beyer, Andreas M.
• Is Part Of: Physiological reports. Volume 9:Issue 3(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-02-15
• Subjects: flow‐mediated dilation -- hypertension -- intraluminal pressure; Physiology -- Periodicals; 571
• DOI: 10.14814/phy2.14507
• Languages: English
• ISSNs: 2051-817X

Abstract

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 cmH2 O). In contrast, arterioles from non‐CAD hypertensive subjects exhibited no reduction in maximal FMD following IILP ( p = .84 at 100 cmH2 O). FMD was reduced by L‐NAME prior to IILP in non‐CAD hypertensive patients ( p < .05 at 100 cmH2 O); however, following IILP, FMD was inhibited by peg‐cat ( p < .05 at 100 cmH2 O), indicating a switch from NO to H2 O2 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 H2 O2 as the mechanism of dilation.