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The interaction between the effects of oxygen and adenosine on acetylcholineinduced contractile tension was observed in helical coronary arterial strips suspended in physiological salt solution. It was found that (1) steady-state contractile tension was unaffected or depressed 5-20% when oxygen pressure (Po 2 ) was diminished to levels as low as 5-10 mm Hg, (2) contractile tension was markedly depressed at a Po 2 of 0 mm Hg, (3) adenosine-induced relaxation of contractile tension was inversely proportional to Po 2 in the tissue bath, and (4) in the presence of adenosine at a concentration just adequate to inhibit contractile tension at a Po 2 of 10 mm Hg, contractile tension was directly proportional to bath Po o . The latter two observations were usually most apparent at a Po 2 between 10 and 40 mm Hg. It is proposed that the vasodilating effect of adenosine on the intact coronary vasculature may be most effective during myocardial hypoxia and that physiological control of coronary vascular tone may be more closely related to variations in local Po 2 than to variations in local concentrations of adenosine.KEY WORDS adenosine anoxia critical Po 2 rabbit arteries local control of blood flow metabolites and myocardial hypoxia From the Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03755.

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The relationship between oxygen pressure measured in a tissue bath (PBO2) and the contractile tension produced by an agonist (contractile responsiveness) was studied in a series of experiments using helical strips cut from thoracic aortas, femoral and deep femoral arteries, and small arteries taken from red and white skeletal muscle of the rabbit. The wall thicknesses of these samples ranged from 200 micron for aortas down to approximately 20 micron for the smallest skeletal muscle arteries. Contractile responsiveness of all samples became progressively depressed when PBO2 was reduced stepwise. The depression produced in the large thick-walled samples occurred at higher PBO2 levels than that produced in the small thin-walled samples. Responsiveness of all of the artery samples was depressed by hypoxia more at low than at high levels of stimulation. In a second series of experiments PO2 at the surface of artery samples (PSO2) was measured using an oxygen-sensitive microelectrode. These measurements in conjunction with calculations of the PO2 within the arterial wall (PWO2) indicated that contractile responsiveness of both large and small artery samples became depressed when PWO2 fell below a lowest-value estimate of 50 Torr. From these findings it is concluded that 1) the sensitivity of vascular smooth muscle cells to hypoxia is similar for large and small arteries; 2) this sensitivity occurs in a range of PO2 that is physiologic for resistance vessels in situ; and 3) this sensitivity to hypoxia cannot be explained by an anoxic core hypothesis and may or may not involve restricted energy metabolism.