title: Endothelin modulates calcium channel current in neurones of rabbit pelvic parasympathetic ganglia.
abstract: 1. The effects of endothelin were studied, in vitro, on neurones contained in the rabbit vesical pelvic ganglion by use of intracellular and single-electrode voltage clamp techniques under conditions where sodium and potassium channels were blocked. 2. In the current-clamp experiments, endothelin (1 microM) caused a depolarization followed by a hyperpolarization of the membrane potential. In the voltage-clamp experiments, endothelin (0.01-1 microM) caused an inward current followed by an outward current in a concentration-dependent manner. 3. Membrane conductance was increased during the endothelin-induced depolarization and inward current. Membrane conductance was decreased during the endothelin-induced hyperpolarization and outward current. 4. The endothelin-induced inward and outward currents were not altered by lowering external sodium concentration or raising external potassium concentration. 5. The endothelin-induced inward current was depressed (mean 72%) in a Krebs solution containing nominally zero calcium and high magnesium. These results suggest that a predominent component of the endothelin-induced inward current is mediated by calcium ions. 6. The calcium-insensitive component of the inward current was abolished by a chloride channel blocker, 4-acetamide-4'-isothiocyanostilbene-2,2'-disulphonic acid. The mean reversal potential for the calcium-insensitive component of the inward current was -18 mV. This value is near the equilibrium potential for chloride. Thus, it is presumed that the calcium-insensitive component of the inward current is carried by chloride ions. 7. Endothelin caused an initial depression followed by a long lasting facilitation of both rapidly and slowly decaying components of high-threshold calcium channel currents (N- and L-type). 8. In summary, the data show that for neurones in the vesical pelvic ganglia, endothelin causes membrane depolarization and activates an inward current. The ionic mechanisms involve receptor-operated calcium and chloride currents. Also, endothelin causes an initial depression followed by a long-lasting facilitation of the voltage-dependent calcium current.
authors.affiliation: Department of Physiology, Kurume University School of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nishimura
authors.forename: T
authors.initials: T
authors.lastname: Akasu
authors.forename: J
authors.initials: J
authors.lastname: Krier
mesh_terms: D000818:Animals; D001464:Barium / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects*; D016232:Endothelins / Q000494:pharmacology*; D005726:Ganglia, Parasympathetic / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D066298:In Vitro Techniques; D008297:Male; D008566:Membranes / Q000187:drug effects / Q000378:metabolism; D008839:Microelectrodes; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D010388:Pelvis / Q000294:innervation; D015221:Potassium Channels / Q000187:drug effects; D011817:Rabbits; D015222:Sodium Channels / Q000187:drug effects
chemical_list: D015220:Calcium Channels; D016232:Endothelins; D015221:Potassium Channels; D015222:Sodium Channels; D001464:Barium