These findings challenge the view that elevated blood pressure itself causes endothelial dysregulation in hypertension, suggesting instead that adaptations in NCX1 expression compensate for alterations in cytosolic Ca2+ and blood pressure.
Challenges prevailing view that hypertension directly impairs endothelium; leaves open NCX1 compensation in human vascular disease.
Endothelium-dependent, ACh-induced vasodilation (EDV) is attenuated, and arterial myocyte Na+/Ca2+ exchangers (NCX1) are upregulated in many forms of hypertension. Surprisingly, mildly hypertensive smooth muscle-specific (SM)-NCX1 transgenic mice exhibited modestly enhanced EDV and augmented endothelium-independent vasodilation (EIV). Conversely, mildly hypotensive SM-NCX1-knockout mice had greatly attenuated EIV. These adaptations help compensate for NCX1 expression-induced alterations in cytosolic Ca2+ and blood pressure (BP) and belie the view that elevated BP, itself, causes the endothelial dysregulation in hypertension.
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Wang et al. (2020) studied this question.
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