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(Hypertension. 1998;31:872-877.)
© 1998 American Heart Association, Inc.

Scientific Contributions

Mechanisms Responsible for Forskolin-Induced Relaxation of Rat Tail Artery

Christopher M. Rembold; ; Xiao-Liang Chen

From the Cardiovascular Division, Departments of Internal Medicine and Physiology, University of Virginia Health Sciences Center (Charlottesville).

Abstract—The goal of the present study was to determine the physiologically relevant mechanisms for forskolin-induced relaxation of intact rat tail artery. We stimulated deendothelialized rat tail artery with phenylephrine and then relaxed the tissue with the addition of forskolin, a specific activator of adenylyl cyclase. We measured membrane potential with the use of microelectrodes, estimated intracellular Ca²⁺ concentration ([Ca²⁺]_i) with the use of fura 2, and measured isometric force with a strain-gauge transducer. We found that 0.3 to 1.0 µmol/L forskolin relaxed 0.3 to 1.0 µmol/L phenylephrine-stimulated rat tail artery by decreasing the [Ca²⁺]_i sensitivity of force as well as through repolarization. There was no evidence for forskolin-induced inhibition of Ca²⁺ influx beyond that associated with repolarization. There also was no evidence for forskolin-induced enhancement of Ca²⁺ efflux or sequestration. Inhibition of ATP-activated K⁺ channels with 10 µmol/L glibenclamide, Ca²⁺-activated K⁺ channels with 50 nmol/L iberiotoxin, Ca²⁺-activated K⁺ channels with 3 or 10 mmol/L tetraethylammonium ion, inwardly rectified K⁺ channels with 20 µmol/L Ba²⁺, and voltage-activated K⁺ channels with 0.5 mmol/L 4-aminopyridine did not significantly attenuate forskolin-induced reductions in [Ca²⁺]_i or force. Forskolin-induced repolarization was not altered by 10 µmol/L glibenclamide or 0.5 mmol/L 4-aminopyridine. These data suggest that these K⁺ channels were not individually involved in forskolin-induced relaxation and that other channels and/or multiple channels are involved in forskolin-induced repolarization of intact rat tail artery. Our data also suggest that forskolin-induced relaxation of intact rat tail artery occurred primarily through repolarization and reductions in the [Ca²⁺]_i sensitivity of force.

Key Words: calcium ion concentration • repolarization • forskolin • membrane potential • potassium channels

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