Dissociation of K+-induced tension and cellular Ca2+ retention in vascular and intestinal smooth muscle in normoxia and hypoxia.

In experiments on smooth muscle preparations of rabbit aorta and guinea pig taenia coli, replacement of the external Na+ with K+ produced sustained contraction. When external K+ concentration was increased, cellular Ca2+ retention as measured by a modified lanthanum technique increased. However, when K+ concentration was above 80 mM, the tension decreased despite an increase in Ca2+ retention. Maximum amount of Ca2+ retained was 1280 nmol/g in aorta and 980 nmol/g in taenia coli while the control values for both tissues were approximately 430 nmol/g when the external Ca2+ concentration was 2.5 mM. Under hypoxia (N2 aeration), sustained contraction was induced by 80 mM K+ in aorta and by 45.4 mM K+ (and 55 mM glucose) in taenia coli. However, no increase in the cellular Ca2+ retention was observed under these conditions. During the K+-induced sustained contraction in aorta, introduction of N2 transiently increased, while readmission of O2 transiently decreased the muscle tension. In taenia coli, the introduction of N2 decreased the sustained contractile tension probably because of an ATP deficiency, while the readmission of O2 further decreased the tension transiently. From these results, it is concluded that, in the presence of a high concentration of K+, external Ca2+ enters the cell and activates the contractile machinery. A part of the cellular Ca2+ is taken up by mitochondria under normoxic but not under hypoxic conditions.