Involvement of K(Ca2+) channels in the local abnormalities and hyperkalemia following the ischemia-reperfusion injury of rat skeletal muscle.

Patch-clamp technique was used to investigate the properties of the muscular Ca2+-activated K+ channel (K(Ca2+)) in the ischemic and ischemic-reperfused rat muscle fibers and the possible involvement of this ion channel in the reperfusion-dependent hyperkalemic state. The properties of the muscular K(Ca2+) channel were unaltered following 4 h of ischemia of the lower limbs and that the serum K+ level did not change following ischemia. In contrast, after 3 h of reperfusion an over-activation of K(Ca2+) channel was observed which was related to the increase in the number of functional channels per patch area.

Insulin modulation of ATP-sensitive K+ channel of rat skeletal muscle is impaired in the hypokalaemic state.

In the present work, we examined the effects of in vivo administration of insulin to rats made hypokalaemic by feeding a K+-free diet. The i.p.

The biophysical and pharmacological characteristics of skeletal muscle ATP-sensitive K+ channels are modified in K+-depleted rat, an animal model of hypokalemic periodic paralysis.

We evaluated the involvement of the sarcolemmal ATP-sensitive K+ channel in the depolarization of skeletal muscle fibers occurring in an animal model of human hypokalemic periodic paralysis, the K+-depleted rat. After 23-36 days of treatment with a K+-free diet, an hypokalemia was observed in the rats. No difference in the fasting insulinemia and glycemia was found between normokalemic and hypokalemic rats.