Evidence for a participation of the kallikrein-kinin system in the regulation of muscle metabolism during hypoxia.
The effect of hypoxia on muscle metabolism was studied in the human forearm by the registration of arterial-deep venous concentration differences of oxygen, glucose, lactate, pyruvate, acetoacetate, and muscular blood flow after short, transient arrest of the forearm circulation. These studies were performed during the intravenous infusion of physiological saline (n=4), of a kallikrein-trypsin inhibitor (n=4), and of kallikrein-trypsin inhibitor plus the intrabrachial-arterial infusion of bradykinin (n=4). Infusion of the kallikrein-trypsin inhibitor significantly reduced the well known hypoxia-induced acceleration of nuscular glucose uptake due to a reduction of blood flow and of muscular glucose extraction. These changes of muscular glucose metabolism were accompanied by more or less striking effects on the balances of oxygen, lactate and acetoacetate. Physiological doses of bradykinin into the brachial artery during the infusion of a kallikrein-trypsin inhibitor restored almost completely the metabolic response during hypoxia. From these data there is further evidence for a participation of the kallikrein-kinin system in the physiological regulation of muscular substrate metabolism.
D000090:Acetoacetates / Q000097:blood; D000328:Adult; D007611:Aprotinin / Q000494:pharmacology; D001786:Blood Glucose / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000378:metabolism*; D007610:Kallikreins / Q000502:physiology*; D007705:Kinins / Q000502:physiology*; D007773:Lactates / Q000097:blood; D009132:Muscles / Q000098:blood supply / Q000378:metabolism*; D010100:Oxygen / Q000097:blood; D012039:Regional Blood Flow
D000090:Acetoacetates; D001786:Blood Glucose; D007705:Kinins; D007773:Lactates; D007611:Aprotinin; D007610:Kallikreins; D010100:Oxygen