The Role of Extracellular Cations in the Development of Myogenic Contraction in Isolated Rat Small Arteries

Abstract

The purpose of this study was to determine the roles of extracellular cations (Na⁺, Ca²⁺ and K⁺), membrane K⁺ channels and Na⁺/K ⁺ ATPase in the development of myogenic contraction (transmural pressure-induced contraction) in isolated rat skeletal muscle and mesenteric small arteries. The vessels were pressurized under no-flow conditions in a tissue bath. Lumen diameter was measured with a videomicroscopic system. Myogenic contraction was evoked by increasing the lumen pressure from 40 to 100 mmHg. The vessels demonstrated myogenic contraction in low-Na⁺ (Na⁺ 1.18 mmol/L) physiological salt solution (PSS), and this was abolished by removing Ca²⁺ or by applying nifedipine or nisoldipine (10 μmol/L). Neither tetraethylammonium (TEA, 1 mmol/L), Ba²⁺ (10 μmol/L) nor glibenclamide (1 μmol/L) affected the magnitude of the myogenic contraction. K⁺-free PSS and ouabain (0.1 mmol/L) partially depressed myogenic contraction. In conclusion, myogenic contraction was triggered by a cellular process that requires extracellular Ca²⁺, but not Na⁺ or K⁺. This triggering process is not affected by TEA, Ba²⁺ or glibenclamide. (Jpn Circ J 1996; 60: 239 - 246)