Key result
Deletion of Rcn2 lowered basal blood pressure and attenuated ANG II-induced hypertension in mice, suggesting Rcn2 regulates blood pressure through actions on endothelial NO synthase.
Why the study?
Hypertension affects over 1 billion people worldwide, but its etiology remains poorly understood for most hypertensive cases.
Does deletion of Rcn2 lower blood pressure and attenuate ANG II-induced hypertension in mice?
Does deletion of Rcn2 lower blood pressure and attenuate ANG II-induced hypertension in mice?
Deletion of Rcn2 lowers basal blood pressure and attenuates ANG II-induced hypertension in mice, identifying it as a novel regulator of blood pressure via endothelial NO synthase.
Hypertension affects over 1 billion people worldwide and increases the risk for heart failure, stroke, and chronic kidney disease. Despite high prevalence and devastating impact, its etiology still remains poorly understood for most hypertensive cases. Rcn2, which encodes reticulocalbin 2, is a candidate gene for atherosclerosis that we have previously reported in mice. Here, we identified Rcn2 as a novel regulator of blood pressure in mice. Rcn2 was abundantly expressed in the endothelium and adventitia of normal arteries and was dramatically upregulated in the medial layer of the artery undergoing structural remodeling. Deletion of Rcn2 lowered basal blood pressure and attenuated ANG II-induced hypertension in C57BL/6 mice. siRNA knockdown of Rcn2 dramatically increased production of the nitric oxide (NO) breakdown products nitrite and nitrate by endothelial cells but not by smooth muscle cells. Isolated carotid arteries from Rcn2 −/− mice showed an increased sensitivity to the ACh-induced NO-mediated relaxant response compared with arteries of Rcn2 +/+ mice. Analysis of a recent meta-data set showed associations of genetic variants near RCN2 with blood pressure in humans. These data suggest that Rcn2 regulates blood pressure and contributes to hypertension through actions on endothelial NO synthase.
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Li et al. (2019) studied Hypertension. Deletion or knockdown of Rcn2 vs. Wild-type (Rcn2 +/+) mice or control cells was evaluated on Blood pressure and ANG II-induced hypertension. Deletion of Rcn2 lowered basal blood pressure and attenuated ANG II-induced hypertension in mice, suggesting Rcn2 regulates blood pressure through actions on endothelial NO synthase.
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