Effect of histamine on the energy metabolism of K+-depolarized hog carotid artery.

Abstract

In a previous study (Peterson and Glück, 1982), activation of hog carotid artery with high-K+ medium caused no increase in aerobic glycolysis (lactic acid production). In contrast, histamine alone is found to stimulate aerobic glycolysis in a tension-dependent fashion (GLück and Paul, 1977). In this study, the addition of histamine to the already K+-depolarized hog carotid artery induced additional contraction, elevated tissue cyclic adenosine 3',5'-monophosphate [cAMP] levels, coupled the rate of aerobic glycolysis to external [Ca++] and isometric tension, and caused suprabasal energy utilization to exceed that required to support the contraction alone by approximately 25%. Increased cytoplasmic free-[Ca++] per se does not stimulate aerobic glycolysis. In the presence of histamine, however, aerobic glycolysis is Ca++-sensitive. Whereas a cycle of Ca++ depletion and restoration has only a small effect on basal metabolic rates in arteries activated with high-K+ alone, the same procedure with arteries stimulated by high-K+ with added histamine causes a dramatic shift in basal metabolic rates toward higher levels of glycolysis.