Evidence for a participation of the kallikrein—kinin system in the regulation of muscle metabolism during muscular work

Dietze, Gabriele; Wicklmayr, M.

doi:10.1016/0014-5793(77)80847-8

Cited by 48 publications

(32 citation statements)

References 8 publications

(3 reference statements)

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“…synthetic bradykinin, should renormalize the hemodynamic and metabolic response. As can be seen from Figure 2 this has indeed happened [16]. The same effect could also be achieved if hypoxia was performed by a blood pressure cuff on the upper arm.…”

Section: Figuresupporting

confidence: 61%

The Kallikrein-Kinin system and muscle metabolism: Biochemical aspects

et al. 1980

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Infusion of bradykinln (BK) into the brachlal artery in front of skeletal muscle of the human forearm yielding arterial concentrations of about 10 -12 mol/I caused not only acceleration of blood flow but also of glucose and branchedchain amino acid uptake into the muscle in healthy volunteers and maturlty-onset diabetics. These effects were almost entirely abolished after inhibition of prostaglandin biosynthesis.Papaverine, although causing identical acceleration of capillary blood flow, induced no metabolic action. Apart from causing enlargement of the capillary bed, bradykinin has another metabolic effect which was underlined by results obtained in the isolated perfused rat heart, indicating increased glucose uptake at constant rates of coronary blood flOW, In order to clarify whether kinins play a physiological role in muscle carbohydrate metabolism, the well-known work-induced acceleration of muscle glucose uptake was studied during the inhibition of kinin I~eration from kinlnogen by application of a protease inhibitor (Trasylol| and during additional substitution with synthetic BK. The glucose uptake under a defined work load was almost completely abolished by the protease inhibitor; application of BK restored the normal effect. Almost identical responses have been observed concerning the well-known hypoxia-indueed acceleration of muscle glucose uptake. Furthermore, insulin-lnduced acceleration of glucose uptake into the resting forearm was reduced by half when kinin liberation from kinlnogen was inhibited by Trasylol| additional application of synthetic BK restored the normal response.From the data presented, one may suggest that kinins are involved in carbohydrate and amino acid metabolism of skeletal muscle, most probably by improving the action of insulin.

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Section: Figuresupporting

confidence: 61%

The Kallikrein-Kinin system and muscle metabolism: Biochemical aspects

et al. 1980

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“…First, captopril has been reported to enhance insulin sensitivity secondary to a reduction in serum catecholamines, or by a direct but unproven effect on insulin receptors, as measured by the euglycemic glucose-clamp technique, in patients with NIDDM and IDDM [13]. Second, it has been demonstrated that bradykinin enhances peripheral glu cose uptake, and it has been suggested that the kallikreinkinin system participates in the physiologic regulation of muscle substrate [20]. Retts et al [21] reported that in type II diabetics, captopril raised the insulin-stimulated glu cose uptake of the whole organism, predominantly due to an increased glucose uptake by the skeletal musculature.…”

Section: Discussionmentioning

confidence: 99%

Beneficial Effects of Angiotensin-Converting Enzyme Inhibitor on Renal Function and Glucose Homeostasis in Diabetics with Hypertension

Ueda

Aoi²,

Yamachika³

et al. 1990

Nephron

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The antihypertensive efficacy of enalapril and its effects on renal function and glucose homeostasis were investigated in 9 hypertensive patients with non-insulin-dependent diabetes mellitus. Enalapril therapy produced a significant fall in blood pressure (BP) (p < 0.05) and a significant increase in renal blood flow (p < 0.05) without a change in glomerular filtration rate. Furthermore, fasting plasma glucose was significantly reduced (p < 0.01). Similarly, M value, as an index of plasma glucose control in diabetes, was significantly reduced from 19.6 to 10.1 (p < 0.01). These findings suggested that the angiotensin-converting enzyme inhibitor enalapril was effective in reducing BP and improving renal function, and might improve glucose homeostasis in hypertensive diabetics.

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“…There are other findings which favour this view. Prostaghurdins are known to exhibit insulinlike activity in myocardial [ 18-201 and adipose tissue [2 1,221 . Furthermore, kinins, the most likely candidates for the muscular activity factor [2,3,23] (which themselves display insulin-like activity [4,24]) are no longer effective ifprostaglandin synthesis is blocked by indomethacin [4] . Further support has come from the finding that prevention of endogenous kinin liberation by a kallikrein inhibitor also reduced the action of insulin on glucose uptake into the human forearm [ 11.…”

Section: Discussionmentioning

confidence: 99%

“…A crucial role of kinin liberation has been demonstrated for the acceleration of glucose uptake which occurs during muscle work [2] and hypoxia [3]. Since evidence had been obtained [4] that the effect of kinins on glucose uptake into muscle was mediated via the synthesis of prostaglandins, it was of interest to investigate whether insulin action on glucose uptake into skeletal muscle of the human forearm might be impaired after indomethacin pretreatment which prevents prostaglandin synthesis in man [S].…”

Section: Introductionmentioning

confidence: 99%