Abstract
In urinary bladder and gall bladder of guinea-pig, the application of hyperosmotic 65.4 mM K solution induced a tonic contraction and increased the rate of oxygen consumption two or three times. The increased O2 consumption maintained steady level during 120 min. In isosmotic 154 mM K, Na-deficient solution, the tonic contraction gradually decreased and oxygen consumption also showed a transient increase followed by a small one. In the urinary bladder, the addition of pyruvic acid completely prevented the decline of the tonic contraction by iso-154K solution at 120 min, but this addition partially prevented it in the gall bladder. Hyperosmotic application of sucrose partially prevented it in the urinary bladder, but completely recovered it in the gall bladder. When NaCl was applied to iso-154K solution, the decrease of tonic contraction was prevented by half in both the muscles. The application of pyruvic acid and NaCl prevented the reduction of oxygen consumption by iso-154K solution in the urinary bladder, but in the gall bladder, this had little effect. There was a close correlation (r=0.950) between the muscle tension and the rate of oxygen consumption in the urinary bladder at 120 min under various conditions. In the gall bladder, a correlation (r=0.875) was also found between both when the results by hyperosmotic addition of NaCl and sucrose were omitted. In the urinary bladder, tension cost, a ratio of O2 consumption rate (μmol O2/g/min) to developed tension (kg force/cm2), was large (0.206) and similar to that of taenia coli; and that of gall bladder was small (0.130) and almost similar to that of vascular smooth muscle. In summary, the inhibition of contraction and rate of oxygen consumption induced by high K, Na-deficient solution in the urinary bladder is probably caused by inhibition of Na-glucose symport and similar to that in taenia coll. On the other hand, that of the gall bladder seems to be mainly caused by cell swelling, similar to that of vascular smooth muscle, but partially caused by inhibition of the glucose symport.
