Expression of β_3-adrenoceptors of Left Ventricle and Its Effect on Heart Function in Rats with Experimental Heart Failure
Zhibin Huang
Abstract
Zhibin Huang
Abstract
[Objective] To observe the expression of β3-adrenoceptors (β3-AR) of left ventricle and the effect on heart function by stimulating β3-AR in rats with experimental heart failure. [Methods] Rats were randomly distributed to heart failure group (n=8) and control group (n=8). Heart failure models were built up by ligation of coronary artery in rats. The expression of β3-adrenoceptors mRNAs was detected with RT-PCR. The change of heart function was observed after administration of BRL37344 (β3-AR agonist) by measuring LVESP (left ventricular end-systolic pressure), left ventricular end-diastolic volume (LVEDP), the maximum pressure ascending rate of left ventricle (+dp/dtmax) and the maximum pressure descending rate of left ventricle (-dp/dtmax).[Results] Both the expression of β3-AR mRNA (β3/β-actin) and the proportion [β3/(β1+β2+β3)] was increased in failure rats in comparison with control rats (0.028 vs 0.011 and 5.4% vs 1.2%); The decreased percentages of LVESP, +dp/dtmax and -dp/dtmax were 16.1%, 21.7%, and 13.2%, respectively after administration of BRL37344 in failure rats while the corresponding numbers were 12.2%, 15.8%, and 11.5% in control rats. [Conclusion] In comparison with non-failure rats, the expression of β3-AR mRNA of left ventricle was obviously increased and the negative inotropic function was obviously increased in failure groups when stimulating β3-AR.
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[Objective] To observe the expression of β3-adrenoceptors (β3-AR) of left ventricle and the effect on heart function by stimulating β3-AR in rats with experimental heart failure. [Methods] Rats were randomly distributed to heart failure group (n=8) and control group (n=8). Heart failure models were built up by ligation of coronary artery in rats. The expression of β3-adrenoceptors mRNAs was detected with RT-PCR. The change of heart function was observed after administration of BRL37344 (β3-AR agonist) by measuring LVESP (left ventricular end-systolic pressure), left ventricular end-diastolic volume (LVEDP), the maximum pressure ascending rate of left ventricle (+dp/dtmax) and the maximum pressure descending rate of left ventricle (-dp/dtmax).[Results] Both the expression of β3-AR mRNA (β3/β-actin) and the proportion [β3/(β1+β2+β3)] was increased in failure rats in comparison with control rats (0.028 vs 0.011 and 5.4% vs 1.2%); The decreased percentages of LVESP, +dp/dtmax and -dp/dtmax were 16.1%, 21.7%, and 13.2%, respectively after administration of BRL37344 in failure rats while the corresponding numbers were 12.2%, 15.8%, and 11.5% in control rats. [Conclusion] In comparison with non-failure rats, the expression of β3-AR mRNA of left ventricle was obviously increased and the negative inotropic function was obviously increased in failure groups when stimulating β3-AR.
Key concepts: Ventricle, Preload, Heart failure, Internal medicine, Inotrope, Cardiology, Medicine, Ventricular pressure