Tamsulosin Attenuates Cardiac Hypertrophy via Integrin-Linked Kinase: Possible Mechanisms.

BACKGROUND

Cardiac hypertrophy often transits into heart failure. Angiogenesis significantly affects the pathogenesis of cardiac hypertrophy. Cytoplasmic integrin-linked kinase (ILK) regulates cardiac angiogenesis by stimulating vascular endothelial growth factor (VEGF). There is a lack of evidence that investigates the effect of α1A-adrenoceptor blockade on ILK-related angiogenesis. Thus, the current study aims to examine the effect of tamsulosin on ILK-related angiogenesis.

METHOD: Twenty-four Wistar rats were divided into four groups as follows: control receiving 0.9% NaCl; an isoproterenol (ISO)-treated (5 mg/kg/day); tamsulosin-treated (0.4 mg/kg/day); and tamsulosin + ISO-treated group. The cardiac injuries, angiogenic biomarkers, and target proteins expressions were assessed.

RESULTS

Tamsulosin significantly attenuated the cardiac hypertrophy index and biomarkers. Tamsulosin reversed histopathological changes in cardiac tissues and mediated significant modulation in VEGF, eNOS, ILK, p-PI3K, p-Akt, Flt-1, and PECAM-1 expressions.

CONCLUSION

The data indicate that targeting α1A adrenoceptors by inhibition offers a promising therapeutic approach for preventing cardiac hypertrophy via signal-transduction pathways, including ILK-related VEGF/eNOS/PI3K/Akt.