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Studies on the Effects of Drugs upon the Lactic Acid Metabolism and Contraction of Vascular Smooth Muscle
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Abstract— The effects of contracting drugs — adrenaline, noradrenaline, histamine, Ba++‐ions — and electrical stimulation upon lactic acid production and muscle contraction were investigated under anaerobic conditions in experiments on bovine mesenteric arteries. When the muscle contracted, the lactic acid production was stimulated and the increase in production showed both a quantitative and a temporal correlation to the contraction. After cessation of contraction the lactic acid production remained the same at different tone levels. Substrate depletion attenuated and glucose augmented the contracting and lactic acid‐stimulating effects of drugs. Glycolysis‐inhibiting substances and other metabolic inhibitors blocked the contractility under both anaerobic and aerobic conditions. Calculation of the energy metabolism associated with contraction of mesenteric arteries indicated that the muscle's preformed high‐energy phosphate compounds sufficed only for a fraction of a total contraction. This behavior probably accounts for the apparently far greater dependence of vascular than of striated muscle upon a continuous energy production for the contractile processes. The cause of the greater energy requirements for contraction of smooth than for contraction of striated muscle is discussed. — Adrenaline stimulated glycolysis in vascular muscle even under aerobic conditions and in the presence of glucose. Thus oxygen consumption alone cannot serve as a reliable indicator of the energy metabolism of smooth muscle.
Title: Studies on the Effects of Drugs upon the Lactic Acid Metabolism and Contraction of Vascular Smooth Muscle
Description:
Abstract— The effects of contracting drugs — adrenaline, noradrenaline, histamine, Ba++‐ions — and electrical stimulation upon lactic acid production and muscle contraction were investigated under anaerobic conditions in experiments on bovine mesenteric arteries.
When the muscle contracted, the lactic acid production was stimulated and the increase in production showed both a quantitative and a temporal correlation to the contraction.
After cessation of contraction the lactic acid production remained the same at different tone levels.
Substrate depletion attenuated and glucose augmented the contracting and lactic acid‐stimulating effects of drugs.
Glycolysis‐inhibiting substances and other metabolic inhibitors blocked the contractility under both anaerobic and aerobic conditions.
Calculation of the energy metabolism associated with contraction of mesenteric arteries indicated that the muscle's preformed high‐energy phosphate compounds sufficed only for a fraction of a total contraction.
This behavior probably accounts for the apparently far greater dependence of vascular than of striated muscle upon a continuous energy production for the contractile processes.
The cause of the greater energy requirements for contraction of smooth than for contraction of striated muscle is discussed.
— Adrenaline stimulated glycolysis in vascular muscle even under aerobic conditions and in the presence of glucose.
Thus oxygen consumption alone cannot serve as a reliable indicator of the energy metabolism of smooth muscle.
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