Abstract
Effects of nifedipine (Nif) and nisoldipine (Nis), dihydropyridine Ca 2+ channel blockers (DHPs) on membrane potential and currents of endothelial cells, which are enzymatically dispersed (dis-ECs) from or exist in arterial segments (seg-ECs) of rabbit and rat aorta, were examined. Outward currents induced by 1–10 μM acetylcholine (ACh) in dis-ECs were neither affected by a receptor operated Ca 2+ channel blocker, SK&F 96365 (SKF), nor DHPs. ACh hyperpolarized dis-ECs and seg-ECs by 15–20 mV, whereas phenylephrine (Phe) elicited oscillatory depolarization in seg-ECs but not in dis-ECs. The Phe-induced response in seg-ECs was significantly inhibited by treatment with 18β-glycyrrhetinic acid, a disrupter of gap junctions. Application of 0.3 μM Nif or Nis effectively inhibited the Phe-induced oscillatory depolarization, while these DHPs did not affect ACh-induced hyperpolarization in seg-ECs. The lack of effect on dis-ECs indicates that DHPs have little effect on dis-ECs themselves, nevertheless DHPs inhibit the Phe-induced endothelial potential oscillation which is conducted from smooth muscle cells via a myo-endothelial pathway.
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