A J Visser1, R Van Mastrigt. 1. Department of Urology-Urodynamics, Erasmus University Rotterdam, the Netherlands. visser@udn.fgg.eur.nl
Abstract
OBJECTIVE: To elucidate the role of the membrane potential in human detrusor smooth muscle contraction, by simultaneously recording mechanical and intracellular electrical activity in muscle strips. Materials and methods The agonists acetylcholine and carbachol were applied to induce a contraction on muscarinic receptor stimulation; to block the response, atropine was added to the bath. The Ca2+ necessary for activating the contractile machinery can be recruited via two pathways: release from intracellular stores or influx from the extracellular matrix. High potassium was applied to induce Ca2+ influx through voltage-sensitive Ca2+ channels. RESULTS: There were significant changes in the force when agonist, antagonist and high potassium was administered. However, there were significant changes in membrane potential only when KCl was applied to the bath and not with muscarinic agonist or antagonist application. Activity in the form of spike potentials did not change significantly on applying any of the test substances. CONCLUSION: The present results indicate that the Ca2+ mobilized on M3 receptor stimulation originates primarily from intracellular stores, with no systematic changes in membrane potential. Atropine only caused a relaxation in muscle previously contracted by M3-receptor agonist stimulation; it had no effect on relaxed muscle strips.
OBJECTIVE: To elucidate the role of the membrane potential in human detrusor smooth muscle contraction, by simultaneously recording mechanical and intracellular electrical activity in muscle strips. Materials and methods The agonists acetylcholine and carbachol were applied to induce a contraction on muscarinic receptor stimulation; to block the response, atropine was added to the bath. The Ca2+ necessary for activating the contractile machinery can be recruited via two pathways: release from intracellular stores or influx from the extracellular matrix. High potassium was applied to induce Ca2+ influx through voltage-sensitive Ca2+ channels. RESULTS: There were significant changes in the force when agonist, antagonist and high potassium was administered. However, there were significant changes in membrane potential only when KCl was applied to the bath and not with muscarinic agonist or antagonist application. Activity in the form of spike potentials did not change significantly on applying any of the test substances. CONCLUSION: The present results indicate that the Ca2+ mobilized on M3 receptor stimulation originates primarily from intracellular stores, with no systematic changes in membrane potential. Atropine only caused a relaxation in muscle previously contracted by M3-receptor agonist stimulation; it had no effect on relaxed muscle strips.