Abstract
Background: While apelin and its endogenous receptor APJ have been reported to play roles in pathophysiology of the cardiovascular system, the relationship of apelin-APJ system with cardiac hypertrophy is still not well understood. Recently, Kuba et al. have reported that the degree of cardiac hypertrophy induced by pressure overload in apelin-deficient and wild type (WT) mice are not significantly different (2007, Circ Res). Since we had generated APJ-deficient (APJ KO) mice, we examined whether apelin-APJ system affected the pathogenesis of catecholamine-induced cardiac hypertrophy. Materials and Methods: APJ KO mice and WT mice at 3-month old (n=11, respectively) received chronic infusion of isoproterenol (ISO, 60mg/kg/day) for 7 days. Echocardiography was performed before and after infusion. Results: In the absence of ISO infusion, the heart of APJ KO mice was not morphologifcally different from that of WT mice. Excessive β-adrenergic stimulation developed significant cardiac hypertrophy in both strains, but to a greater extent in APJ KO mice (the ratio of heart weight to tibial length: 8.1±0.7 versus 7.5±0.7 mg/mm, p<0.05). Conclusion: The present study demonstrated that apelin-APJ system played an important role in preventing catecholamine-induced cardiac hypertrophy. [J Physiol Sci. 2008;58 Suppl:S59]
