Key result
Enalaprilat produced vasodilation in isolated perfused kidneys of control and diabetic rats by activating B1 receptors and stimulating nitric oxide production.
Why the study?
Does enalaprilat activate B1 receptors and induce vasodilation in isolated perfused kidneys of rats?
Does enalaprilat activate B1 receptors and induce vasodilation in isolated perfused kidneys of rats?
Enalaprilat activates B1 receptors and stimulates nitric oxide production, leading to renal vasodilation in both control and diabetic rats.
Hypothesis-generating for B1-mediated renal vasodilation; human studies required before any clinical consideration.
The present study evaluated whether enalaprilat (the active form of enalapril, an angiotensin-converting enzyme inhibitor) activates B(1) receptors. We observed that the levels of B(1) receptor mRNA and protein expression were upregulated in the kidneys of diabetic rats. Bradykinin (BK)-induced renal vasodilation decreased in isolated perfused kidneys of diabetic rats, but des-Arg(9)-BK-induced renal vasodilation increased. Enalaprilat also produced vasodilation in the isolated perfused kidneys of control and diabetic rats. The response to des-Arg(9)-BK or enalaprilat was blocked by Lys-(des-Arg(9), Leu(8))-BK (a B(1) receptor antagonist) and N-nitro-L-arginine methyl ester (an inhibitor of nitric oxide synthase). These results suggest that enalaprilat activates B(1) receptors and stimulates the production of nitric oxide in the kidneys of both control and diabetic rats.
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Bautista‐Pérez et al. (2011) studied Diabetes (animal model). Enalaprilat vs. Control rats / antagonists was evaluated on Renal vasodilation and B1 receptor activation. Enalaprilat produced vasodilation in isolated perfused kidneys of control and diabetic rats by activating B1 receptors and stimulating nitric oxide production.
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