PubMed1991
1. When the web of the anaesthetized Xenopus laevis was perfused with Ringer solution maintained at 20 degrees C, radio frequency (RF) burst-type electromagnetic (EM) field radiation not only dilated arterioles of the web which had been preconstricted with noradrenaline, but also dilated arterioles under non-stimulated conditions. The EM field-induced vasodilatation increased slowly and reached a plateau 60 min after the onset of radiation. After the cessation of radiation, vasodilatation remained for 10-20 min, then slowly subsided. 2. When a 10 MHz, 1 V (peak to peak) generator voltage induced a 7.3 milliGauss, 2.19 V cm-1 EM field, the vasodilatory effect was optimum when bursts were applied 50% of the total time at 10 kHz burst rate. 3. The vasodilatory effect was not secondary to dielectric heat in the web, because the EM field was too weak to have produced enough heat to dilate the arterioles and heat would have been constantly conducted away by the perfusion solution. 4. During perfusion with Ringer solution warmed to 30 degrees C, no vasodilatation was found, but perfusion with Ringer solution warmed to 35 degrees C induced only 11% vasodilatation. Perfusion with Ringer solution warmed to 37 degrees C induced irreversible vasoconstriction. The pattern of vasodilatation induced by warm Ringer solution was different from the vasodilatory effect of weak EM field radiation. 5. The extent of the vasodilatory effect was influenced by Ca2+ concentration of the perfusion medium. Under normal Ca2+ conditions arterioles dilated to 126% of the control diameter, while under Ca(2+)-free conditions arterioles dilated to 131% of the control value and under high-Ca2+ conditions (twice the normal level) arterioles dilated to 111% of the control value. This suggests that the vasodilatory effect may be caused by facilitation of Ca2+ outflow, and the extent of this flow may settle down to the equilibrium level of countercurrent flux between Ca2+ influx and outflow. 6. The vasodilatory effect was not inhibited under perfusion with Na(+)-free Ringer solution, suggesting that Na(+)-Ca2+ exchange system may not be involved in the vasodilatory effect. The vasodilatory effect was inhibited by vanadate, an inhibitor of Ca(2+)-ATPase, and was abolished by Methylene Blue, an inhibitor of guanylate cyclase. The evidence suggests that the mechanism of the vasodilatory effect may depend on an increase in Ca2+ outflow through the plasma membrane of the smooth muscle and/or an increase in Ca2+ influx into the sarcoplasmic reticulum.(ABSTRACT TRUNCATED AT 400 WORDS)