title: Effect of phenylephrine and endothelium on vasomotion in rat aorta involves potassium uptake.
abstract: 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.
authors.affiliation: Departamento de Química, Universidad Católica del Norte, Av Angamos, 0610 Antofagasta, Chile. jpalacios@ucn.cl
authors.forename: Javier
authors.initials: J
authors.lastname: Palacios
authors.forename: José Luis
authors.initials: JL
authors.lastname: Vega
authors.forename: Adrián
authors.initials: A
authors.lastname: Paredes
authors.forename: Fredi
authors.initials: F
authors.lastname: Cifuentes
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D017869:Cyclic GMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D008564:Membrane Potentials; D009569:Nitric Oxide / Q000378:metabolism; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D010507:Periodicity; D010656:Phenylephrine / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D004791:Enzyme Inhibitors; D020030:Nitric Oxide Donors; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D014662:Vasoconstrictor Agents; D010656:Phenylephrine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D017869:Cyclic GMP-Dependent Protein Kinases; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium