The involvement of AQP1 in myocardial edema induced by pressure overload in mice

OBJECTIVE: To investigate the effect of aquaporin-1 (AQP1) on heart edema in- duced by transverse aortic constriction (TAC) in mice, and to explore whether inhibiting the ex- pression of AQP1 could attenuate myocardial edema and improve cardiac function. MATERIALS AND METHODS: The C57BL/6 mice were divided into four groups: (1) the sham group; 2) the sham + acetazolamide group: mice were orally gavaged with acetazolamide (20 mg/ kg/day) after sham operation; (3) the TAC group: a mouse model of pressure overload induced by TAC for two weeks; (4) the TAC + acetazolamide group: mice were orally gavaged with acetazol- amide (20 mg/kg/day) after TAC. Cardiac func- tion was detected by echocardiography after 2 weeks’ TAC. The ratio of heart weight to body weight (HW/BW) and myocardial water content were calculated. The mRNA and protein expres- sions of AQP1 were measured by reverse tran- scriptase-polymerase chain reaction (RT-PCR) and Western blot, respectively. RESULTS: Significant myocardial hypertrophy and dysfunction were found in TAC mice. The ratio of HW/BW, myocardial water content, and the mRNA and protein expression of AQP1 of the TAC group were markedly higher than those of the sham group. By contrast, acetazolamide administration reduced the ratio of HW/BW and myocardial water content, whereas improved cardiac dysfunction induced by TAC. Moreover, acetazolamide reduced the mRNA and protein expression of AQP1 in TAC mice. CONCLUSIONS: The expression of AQP1 was closely related to myocardial edema induced by TAC. The inhibition of AQP1 could reduce myocardial edema and improve cardiac dys- function.