{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T17:16:54Z","timestamp":1776446214730,"version":"3.51.2"},"reference-count":65,"publisher":"MDPI AG","issue":"6","license":[{"start":{"date-parts":[[2025,3,15]],"date-time":"2025-03-15T00:00:00Z","timestamp":1741996800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"American Heart Association","award":["0235258N"],"award-info":[{"award-number":["0235258N"]}]},{"name":"American Heart Association","award":["EY018420"],"award-info":[{"award-number":["EY018420"]}]},{"name":"American Heart Association","award":["HL71761"],"award-info":[{"award-number":["HL71761"]}]},{"name":"National Institutes of Health","award":["0235258N"],"award-info":[{"award-number":["0235258N"]}]},{"name":"National Institutes of Health","award":["EY018420"],"award-info":[{"award-number":["EY018420"]}]},{"name":"National Institutes of Health","award":["HL71761"],"award-info":[{"award-number":["HL71761"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Metabolic stress on the heart can cause dilation of coronary arterioles for blood flow recruitment. Although potassium ions (K+) released from the myocardium are a major mediator for this response, the underlying signaling pathways for vasodilation are incompletely understood. Herein, the roles of smooth muscle inward-rectifier K+ channel subtype 2.1 (Kir2.1) and Na+\/K+-ATPase were examined. Porcine coronary arterioles were isolated, cannulated, and pressurized for vasomotor study. Vessels developed basal tone and dilated concentration-dependently to extraluminal K+ from 7 to 20 mM. Higher K+ concentrations (25\u201340 mM) caused graded vasoconstriction. Vasodilation to K+ (10 mM) was not altered by endothelial removal, and blockade of ATP-sensitive K+ channels, voltage-sensitive K+ channels, or calcium-activated K+ channels did not affect K+-induced vasodilation. However, sustained but not abrupt transient vasodilation to K+ was reduced by the nonspecific Kir channel inhibitor Ba2+ or Kir2.1 channel blocker chloroethylclonidine. The Na+\/K+-ATPase inhibitor ouabain attenuated K+-elicited vasodilation, and ouabain with Ba2+ abolished the response. Transfection of arterioles with Kir2.1 antisense oligonucleotides abolished sustained but not transient dilation. It is concluded that extraluminal K+ elevation within the physiological range induces initial transient dilation of porcine coronary arterioles by activating smooth muscle Na+\/K+-ATPase and sustained dilation via smooth muscle Kir2.1 channels.<\/jats:p>","DOI":"10.3390\/ijms26062654","type":"journal-article","created":{"date-parts":[[2025,3,17]],"date-time":"2025-03-17T06:36:23Z","timestamp":1742193383000},"page":"2654","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Activation of Smooth Muscle Kir2.1 Channels and Na+\/K+-ATPase Mediates Dilation of Porcine Coronary Arterioles at Physiological Levels of Potassium"],"prefix":"10.3390","volume":"26","author":[{"given":"Travis W.","family":"Hein","sequence":"first","affiliation":[{"name":"Department of Medical Physiology, Cardiovascular Research Institute, College of Medicine, Texas A&M University Health Science Center, Bryan, TX 77807, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Habib M.","family":"Razavi","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology, Cardiovascular Research Institute, College of Medicine, Texas A&M University Health Science Center, Bryan, TX 77807, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xin","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology, Cardiovascular Research Institute, College of Medicine, Texas A&M University Health Science Center, Bryan, TX 77807, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sonal","family":"Somvanshi","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology, Cardiovascular Research Institute, College of Medicine, Texas A&M University Health Science Center, Bryan, TX 77807, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mariappan","family":"Muthuchamy","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology, Cardiovascular Research Institute, College of Medicine, Texas A&M University Health Science Center, Bryan, TX 77807, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4912-6910","authenticated-orcid":false,"given":"Lih","family":"Kuo","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology, Cardiovascular Research Institute, College of Medicine, Texas A&M University Health Science Center, Bryan, TX 77807, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2025,3,15]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"155","DOI":"10.1152\/ajplegacy.1938.124.1.155","article-title":"The action of excess Na, Ca and K on the coronary vessels","volume":"124","author":"Katz","year":"1938","journal-title":"Am. 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