Affiliation:
1. Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland
2. Department of Physical Education, Shaanxi Normal University, Xi’an, Shaanxi, China
3. Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland
Abstract
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.
Funder
University of Maryland Baltimore Foundation, Center for Heart, Hypertension and Kidney Disease
Natural Science Basic Research Program of Shaanxi Province
Fundamental Research Funds for the Central Universities
College Students' Assistantship Project of Shaanxi Normal University
HHS| NIH|National Heart, Lung and Blood Institute
HHS|NIH|National Heart, Lung and Blood Institute
American Heart Association
HHS | NIH | National Heart, Lung, and Blood Institute
National Natural Science Foundation of China
Publisher
American Physiological Society
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology
Cited by
11 articles.
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