Effect of phenylephrine and endothelium on vasomotion in rat aorta involves potassium uptake.

Vasomotion is defined as the rhythmic contractions in blood vessels, consisting of two components: vasoconstriction and oscillations of the plasma membrane potential. To determine whether vasomotion is associated with changes in K(+) uptake, we measured the effect of phenylephrine (PE) and acetylcholine (ACh) on the K(+) uptake and vascular reactivity in rat aortic rings. We found that the incubation of aortic rings with 10(-7) M PE (210 ± 28 mg maximum amplitude), and 10(-6) M ACh (177 ± 6 mg maximum amplitude) produced the highest rhythmic contractions. Both 10(-7) M PE and 10(-6) M ACh significantly increased K(+) uptake in endothelium-intact aorta versus control (121 % PE, 117 % ACh). Removal of the endothelium blunted rhythmic contractions and decreased K(+) uptake in presence of vasoactive substances (88 % PE, 81 % ACh). The inhibition of nitric oxide synthase with 10(-4) M L-NNA significantly reduced the rhythmic contractions, and it was reversed in the presence of 10(-8) M sodium nitroprusside (SNP; a nitric oxide donor). Also, we found that 10(-4) M L-NNA significantly decreased the effect of 10(-7) M PE on K(+) uptake in aortic rings (104 % PE + L-NNA vs. control). The incubation of endothelium-denuded rings with 10(-8) M SNP significantly increased the K(+) uptake (116 % SNP vs. control), similar to those observed in the presence of 10(-6) M ACh. The inhibition of protein kinase G with KT-5823 blocked SNP-mediated increase in K(+) uptake. In conclusion, these data suggest that a certain range of K(+) uptake is necessary to induce the rhythmic contractions in response to vasoactive substances.