Mediation of EDHF‐Induced Reduction of Smooth Muscle [Ca²⁺]_i and Arteriolar Dilation by K⁺ Channels, 5,6‐EET, and Gap Junctions

This publication has 43 references indexed in Scilit:

• Role of gap junctions and EETs in endothelium-dependent hyperpolarization of porcine coronary artery
  British Journal of Pharmacology, 2000
• Endothelium‐derived hyperpolarizing factor but not NO reduces smooth muscle Ca²⁺ during acetylcholine‐induced dilation of microvessels
  British Journal of Pharmacology, 1999
• Serotonin reuptake inhibitor, fluoxetine, dilates isolated skeletal muscle arterioles. Possible role of altered Ca²⁺ sensitivity
  British Journal of Pharmacology, 1999
• Inhibition of the gap junctional component of endothelium‐dependent relaxations in rabbit iliac artery by 18‐α glycyrrhetinic acid
  British Journal of Pharmacology, 1998
• Ryanodine receptors regulate arterial diameter and wall [Ca²⁺] in cerebral arteries of rat via Ca²⁺‐dependent K⁺ channels
  The Journal of Physiology, 1998
• Characterization and modulation of EDHF-mediated relaxations in the rat isolated superior mesenteric arterial bed
  British Journal of Pharmacology, 1997
• Evidence against a role of cytochrome P450-derived arachidonic acid metabolites in endothelium-dependent hyperpolarization by acetylcholine in rat isolated mesenteric artery
  British Journal of Pharmacology, 1997
• The Importance of the Hyperpolarizing Mechanism Increases as the Vessel Size Decreases in Endothelium-Dependent Relaxations in Rat Mesenteric Circulation
  Journal of Cardiovascular Pharmacology, 1996
• Hyperpolarizing Vasodilators Activate ATP-sensitive K ⁺ Channels in Arterial Smooth Muscle
  Science, 1989
• Electrical Transmission at the Nexus between Smooth Muscle Cells
  The Journal of general physiology, 1968