The role of extracellular cations in the development of myogenic contraction in isolated rat small arteries.
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 mumol/L). Neither tetraethylammonium (TEA, 1 mmol/L), Ba2+ (10 mumol/L) nor glibenclamide (1 mumol/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.
Watanabe
J
J
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Horiguchi
S
S
Keitoku
M
M
Karibe
A
A
Takeuchi
M
M
Suzuki
S
S
Satoh
S
S
Shirato
K
K
D000818:Animals; D001158:Arteries / Q000502:physiology*; D002118:Calcium / Q000502:physiology*; D005110:Extracellular Space / Q000502:physiology; D017136:Ion Transport; D009119:Muscle Contraction / Q000502:physiology*; D011188:Potassium / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000502:physiology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology
D015221:Potassium Channels; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium; D002118:Calcium