Effect of arterial pH alterations on metabolic activity of norepinephrine

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Abstract
Arterial pH (pHa) was altered in 3 groups of 19 young beagles by intravenous administration of ammonium chloride (NH4CI), alkali (bicarbonate or tris(hydroxymethyl)-amino methane (THAM), and by hyperventilation. Decrease in pHa to 7.0 induced by iv NH4CI administration exerted an inhibitory effect on norepinephrine (NE)-induced lipolysis and calorigenesis comparable to that which occurs whenpHa is decreased by hypercapnia. Alterations of the metabolic effects of NE during acidemia were best related to the decrease in pHa rather than to changes in arterial PCO2 or [HCO3-]a. Increase in pHa to 7.55 by hyperventilation or administration of alkali was accompanied by consistent rise in VO2, free fatty acids, and glycerol concentrations. The further increases in these factors, when NE was administered at alkaline pHa, were comparable to the increase observed at normal pHa. Marked arrhythmias occurred when NE was administered at alkaline pHa. The inhibitory effect of acid pHa on NE-induced lipolysis also occurs in vitro. Increased [H+] has an inhibitory effect comparable to that of [beta] -blocking agents. The ability of the body to mobilize fuel stores and to increase metabolism above basal levels is inhibited by acid pHa.