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(Circulation Research. 2000;86:824.)
© 2000 American Heart Association, Inc.

Editorials

Making Sense out of Oxygen Sensor

Michael S. Goligorsky

From the Departments of Medicine and Physiology and Biophysics, State University of New York, Stony Brook, NY.

Correspondence to Michael S. Goligorsky, Health Science Center, Division of Nephrology, State University of New York, Stony Brook, NY 11794-8152. E-mail mgoligorsky@mail.som.sunysb.edu

Key Words: oxygen • sensor • mitochondria • nitric oxide • heme proteins

	Introduction

 
Autoregulatory mechanisms that adjust the diameter of a vascular bed and the blood flow through it to the intrinsic parameters of tissue oxygen demand have become a cornerstone of vascular physiology.^{1 2 3 4} Although examples of hypoxia-induced vasoconstriction do exist (such as pulmonary microvasculature), most blood vessels respond to hypoxic or ischemic environment with vasodilation. Coronary arteries are not an exception to this rule; in fact, autoregulation in this vascular bed is of paramount importance. Increased myocardial demand for oxygen cannot be met by increasing oxygen extraction, because coronary arteriovenous difference is already high under normal conditions. Therefore, matching the supply depends almost entirely on the ability to increase coronary blood flow.

Although the occurrence of hypoxia- and ischemia-induced coronary vasodilation has been well established, the number of theories attempting to explain the phenomenon has multiplied. Proposed physiological models include (1) direct sensing of reduced PO₂ by different cellular elements of the vascular wall⁵ ; (2) production and release of vasodilatory metabolites by the oxygen-deprived myocardium; (3) changes in intracellular calcium or proton metabolism and distribution, or a rapidly developing deficiency in high-energy phosphates, which suppress the contractile apparatus of the smooth muscle cells^{5 6} ; and (4) a shift in the affinity of hemoglobin for nitric oxide (NO).⁷ In this issue of Circulation Research, Shimizu et al⁸ provide further insight into the mechanisms of hypoxic vasorelaxation in porcine coronary arteries.

Previous studies by Daut et al,⁹ performed in guinea pigs, demonstrated the existence of glibenclamide-inhibitable coronary vasodilation in response to . . . [Full Text of this Article]

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