This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Weintraub, N. L. Search for Related Content PubMed PubMed Citation Articles by Weintraub, N. L. Related Collections Other diabetes Coronary circulation Other Vascular biology

(Circulation Research. 2003;92:127.)
© 2003 American Heart Association, Inc.

Editorials

Impaired Hypoxic Coronary Vasodilation and ATP-Sensitive Potassium Channel Function

A Manifestation of Diabetic Microangiopathy in Humans?

Neal L. Weintraub

From the Department of Internal Medicine, Cardiovascular Division, University of Iowa College of Medicine, and VA Medical Center, Iowa City, Iowa.

Correspondence to Neal L. Weintraub, MD, Dept of Internal Medicine, Cardiovascular Division, University of Iowa College of Medicine, 200 Hawkins Dr, E329 GH, Iowa City, IA 52242. E-mail neal-weintraub@uiowa.edu

Key Words: coronary microcirculation • potassium channels • smooth muscle cells • diabetes • glibenclamide

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Hypoxic coronary vasodilation contributes to the maintenance of oxygen supply to the working heart during increased metabolic demand. Mechanisms of hypoxic coronary dilation have been studied extensively and differ considerably depending upon the species and experimental model. In isolated coronary vessels, several mechanisms have been implicated either alone or in combination, including release of vasodilatory factors (ie, nitric oxide, prostaglandins, and adenosine), activation of ATP-sensitive potassium (K_ATP) channels and Ca²⁺-activated K⁺ channels, and inhibition of voltage-gated Ca²⁺ channels.^1–5 To date, however, relatively few studies have been conducted in human blood vessels. Furthermore, whereas most prior studies have examined hypoxic dilation in conduit coronary arteries, coronary microvessels (<150 µm in diameter) are considered to be the principal regulators of coronary blood flow in response to metabolic stress.⁶ Thus, despite extensive studies conducted over the past several decades, surprisingly little is known about mechanisms of hypoxic coronary microvascular dilation in humans, and how it might be altered in disease states.

In this issue of Circulation Research, Miura and colleagues⁷ provide evidence that hypoxic dilation of human coronary microvessels is mediated primarily by activation of K_ATP channels in vascular smooth muscle cells (SMCs), independent of the endothelium. Moreover, they report that both hypoxic dilation and vasodilation induced by the K_ATP opener aprikalim are attenuated in microvessels from patients with diabetes mellitus, suggesting impaired K_ATP function. These findings provide new insight into mechanisms of coronary vasoregulation in humans, and they suggest that impaired microvascular K_ATPchannel function might contribute to increased . . . [Full Text of this Article]

This article has been cited by other articles:

				K. M. Gauthier Hypoxia-induced vascular smooth muscle relaxation: increased ATP-sensitive K+ efflux or decreased voltage-sensitive Ca2+ influx? Am J Physiol Heart Circ Physiol, July 1, 2006; 291(1): H24 - H25. [Full Text] [PDF]