Key result
One-hour ex vivo exposure to aldosterone impaired endothelium-dependent vasodilation in normotensive arterioles, while spironolactone reversed endothelial dysfunction in hypertensive arterioles.
Why the study?
Does ex vivo exposure to aldosterone or spironolactone modulate microvascular endothelial function in African Americans with and without hypertension?
Observational (n=33)
Does ex vivo exposure to aldosterone or spironolactone modulate microvascular endothelial function in African Americans with and without hypertension?
Aldosterone impairs and spironolactone improves microvascular endothelial function in African Americans, suggesting mineralocorticoid receptor activity contributes to hypertension-related endothelial dysfunction via G6PD suppression.
Answers are grounded in this paper and cite their sources.
May support MR antagonism for endothelial dysfunction in hypertensive African Americans; hypothesis-generating and requires prospective clinical validation.
Prior work suggests blood pressure in African Americans is more sensitive to the effects of aldosterone than in Caucasians. This mechanism may relate to a negative response of the vascular endothelium to aldosterone, including reduced glucose-6-phosphate dehydrogenase (G6PD) activity. Thirty-three African Americans (11 hypertensives, 22 controls) without evidence of diabetes or metabolic syndrome completed the protocol. The protocol included measurement of in vivo microvascular endothelial function by digital pulse arterial tonometry and ex vivo measurement of endothelial function by videomicroscopy of arterioles obtained from these same subjects with and without exposure to aldosterone or spironolactone. Systemic and arteriolar G6PD activities were also measured. In vivo and ex vivo microvascular endothelial function were impaired in African Americans with hypertension. One-hour exposure with aldosterone impaired endothelium-dependent vasodilation in arterioles from normotensive subjects, while 1 hour of spironolactone exposure reversed endothelial dysfunction in arterioles from hypertensive subjects. G6PD activity was impaired in hypertensive arterioles. Aldosterone-related endothelial dysfunction may be responsible for at least a portion of the greater blood pressure sensitivity to aldosterone in African Americans. This may be in part related to vascular suppression of G6PD activity.
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Mohandas et al. (2015) conducted an observational in Hypertension (n=33). Aldosterone or spironolactone exposure (ex vivo) vs. No exposure / normotensive controls was evaluated on In vivo microvascular endothelial function and ex vivo endothelial function. One-hour ex vivo exposure to aldosterone impaired endothelium-dependent vasodilation in normotensive arterioles, while spironolactone reversed endothelial dysfunction in hypertensive arterioles.
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