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.

Energy cost of membrane depolarization in hog carotid artery.

“…Activation by K + for Na + substitution in hog carotid artery stimulates only a small and not significant increase in tissue cAMP (Peterson 1982), whereas no effect on cAMP has been reported for K + depolarization of rabbit aorta (van Breeman, 1976). Thus, it is reasonable to expect, under these conditions, that the same level of steady isometric tension reflects similar cytoplasmic freeCa ++ levels.…”

“…Experiments were performed at the muscle length optimal for isometric tension generation and at 37°C. (Ore Res 50: 839-847, 1982) \N THIS and a subsequent report (Peterson 1982), we compare the metabolic energy cost of isometric tension maintenance in the isolated hog carotid artery under three sets of activating conditions by which the level of isometric tension development may be altered in a stable graded fashion. In all three conditions, activation with high extracellular K + is used.…”

“…In this report, we focus on the metabolic energy cost due to membrane depolarization per se, whereas a subsequent report (Peterson 1982) examines the excess metabolic energy cost of hormonal activation. In whole frog skeletal muscle, it has long been known that membrane depolarization by even moderately elevated extracellular [K + ] results in a dramatic (up to 20-fold) increase in resting energy metabolism (Solandt, 1936) which is not completely reversed even after 6 hours of exposure.…”

Metabolic factors influencing lower urinary tract function

“…However, the magnitude of this contraction-independent energy utilization is not as great as that induced by bethanechol (Levin et al , 1991bRuggieri et al 1988). Similar observations have been made in vascular smooth muscle; histamine stimulated glycolysis to a significantly greater extent than did KCl (Peterson, 1982). …”

Effects of in vivo Ischemia on Contractile Responses of Rabbit Bladder to Field Stimulation, Carbachol, ATP and KCl

“…Muscarinic stimulation of cell-surface receptors activates a membrane-bound G-protein signaling pathway to the intracellular contractile apparatus, whereas KCl stimulation depolarizes the cell membrane, initiating contraction more directly [5,16]. Similar to these observations of bladder smooth muscle metabolism, Peterson [17] observed that histamine stimulates vascular smooth muscle glycolysis to a greater degree than KCl.…”