抄録
We set out to study if changes of Ca2+-activated K+ (KCa) channels and associated signaling pathways can alter vascular reactivity during cardiac hypertrophy induced by isoprenaline. In vascular smooth muscles cells isolated from coronary artery, the whole-cell current density, single channel conductance, and open probability of KCa channels were significantly reduced during hypertrophy. Furthermore, KCa channels exhibited decreased sensitivity to [Ca2+]i but pronounced block by external TEA. Consistent with the electrophysiological data, biochemical data indicated no changes in KCa channel expression. Furthermore, the degree of resting tension contractility increased with high [K+]out and decreased with external TEA during hypertrophy. In cerebral artery, vasomotion during cardiac hypertrophy was qualitatively similar to that observed in controls but vasoconstrictor response on Angiotensin II (Ang II) was attenuated. The electrophysiological properties of KCa channels were significantly changed by Ang II during hypertrophy. The protein expression of Ang II receptors and associated signaling molecules also changed significantly during hypertrophy. Our findings suggest novel mechanisms for reduced coronary reserve and impaired cerebrovascular contractility during cardiac hypertrophy by modulating KCa channel properties and altering the gene expression of related proteins. [Jpn J Physiol 55 Suppl:S52 (2005)]
