Arachidonic acid (AA) is the common precursor for several vasodilatory factors involved in the local control of blood flow. This study was designed to determine the role of phospholipase A₂ (PLA₂) and AA release in functional hyperemia in the hamster cremaster muscle. The muscle was prepared for in vivo microscopy and subjected to electrical field stimulation for 1 min. First- and second-order arterioles dilated in response from a mean diameter of 66 ± 5 to 88 ± 7 µm (n = 6). PLA₂ was then inhibited with quinacrine (3 × 10⁶ M) for 60 min. PLA₂ inhibition was verified by an attenuation of thrombin-induced vasodilation (2 U/ml). Quinacrine had no effect on resting arteriolar diameter but completely abolished functional hyperemia. Quinacrine also had no effect on dilation induced by superfusion of the preparation with 3 × 10⁶-10⁵ M AA, 10⁶-10⁴ M adenosine, or 10⁶-10⁴ M sodium nitroprusside, ruling out nonspecific effects of quinacrine on smooth muscle contractility. These results indicate that functional hyperemia in the hamster cremaster muscle is dependent on PLA₂ activation and the availability of AA.

microcirculation; arachidonic acid; arteriolar diameter

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