Physiological reports · 2021
Hypertension preserves the magnitude of microvascular flow-mediated dilation following transient elevation in intraluminal pressure.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Hughes William E, Zinkevich Natalya, Gutterman David D, Beyer Andreas M
Аннотация
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.
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.