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Inhibitory effect of insulin on bradykinin-induced venodilation
M Kimura1, H Watanabe, R Takahashi
1Department of Clinical Pharmacology, Hamamatsu University School of Medicine, Japan.
Journal of Hypertension
|March 22, 2000
Summary
Insulin reduces the vasodilating effects of bradykinin by decreasing calcium signaling in endothelial cells. This interaction may contribute to hypertension in individuals with high insulin levels.
Area of Science:
- Endocrinology
- Vascular Biology
- Cardiovascular Physiology
Background:
- Excessive insulin (hyperinsulinemia) is linked to hypertension and arteriosclerosis.
- Insulin's vasodilative properties are known, but its interactions with other vasoactive substances remain unclear.
Purpose of the Study:
- To investigate the effect of insulin on bradykinin-mediated vasodilation.
Main Methods:
- Assessed bradykinin-induced vasodilation in human dorsal hand veins with and without insulin.
- Measured bradykinin-stimulated intracellular calcium increase in cultured porcine aortic endothelial cells before and after insulin exposure.
Main Results:
- Insulin significantly reduced bradykinin-induced venodilation in human veins.
- Insulin attenuated the bradykinin-induced rise in intracellular calcium in endothelial cells.
Conclusions:
- Insulin dampens bradykinin's effect on endothelial cells by reducing calcium signaling.
- This may decrease vasodilative substance production, leading to reduced vasodilation and potentially contributing to hypertension in hyperinsulinemia.