ABSTRACT
An "in vitro" experimental line was designed to study the dependence of the canine detrussor's contractile activity on extracellular calcium, or whether on the contrary there are intracellular sources of this element. If dependence from extracellular calcium could be demonstrated, the capacity of calcium channel blockers to block the input the this ion would be studied. The conclusions arrived at were: 1. Ach- and KCl-induced activity is dependent from extracellular calcium. 2. This activity is also sensitive to the action of calcium channel blockers. 3. Calcium channel blockers block Ach-activated calcium channels completely, but only partially dose activated by KCl. 4. While the activity induced by Ach and resistant to action from calcium channel blockers is probably due to calcium released from the intracellular reservoirs, the activity induced by KCl and resistant to the calcium channel blockers action can be better explained by the activation of the transmembrane channels which cannot be blocked by this agents.
Subject(s)
Acetylcholine/pharmacology , Calcium Channel Blockers/pharmacology , Calcium/physiology , Muscle Contraction/drug effects , Muscle, Smooth/drug effects , Urinary Bladder/drug effects , Animals , Dogs , Electrophysiology , In Vitro Techniques , Muscle Contraction/physiology , Muscle, Smooth/physiology , Statistics as Topic , Urinary Bladder/physiologyABSTRACT
The ultimate mechanism of action for all substances with the ability of modifying the activity of smooth muscle is an increased or decreased intracellular concentration of Ca2+. This report presents an "in vitro" study where the dependency on extracellular Ca2+ for the spontaneous activity of the detrusor muscle was investigated, and also the changes that calcium channel blockers can exert on it. The study concludes that the tonic component of the spontaneous activity depends on the Ca2+ intracellular deposits while the physical activity depends on Ca2+ entry from extracellular space. This entry of Ca2+ from the outside is not inhibited by the action of Ca2+ channel blocking agents.