Key result
Angiotensin II and high-salt diet caused early restriction of pulmonary flow, reduced left ventricular filling, and lower cardiac output in Balb/CJ mice compared with C57BL/6J mice.
Why the study?
Heart failure symptoms in Balb/CJ mice led to the hypothesis that angiotensin II and high-salt diet impairs cardiac function and induces cardiac remodeling in male Balb/CJ but not male C57BL/6J mice.
Does angiotensin II and high-salt diet induce different cardiac and pulmonary vascular responses in Balb/CJ mice compared to C57BL/6J mice?
Does angiotensin II and high-salt diet induce different cardiac and pulmonary vascular responses in Balb/CJ mice compared to C57BL/6J mice?
Balb/CJ mice treated with angiotensin II and high salt develop early pulmonary flow restriction and reduced cardiac output, providing a novel model for pulmonary hypertension-induced cardiorenal syndrome.
Strain-specific responses in mice suggest genetic modifiers of pulmonary flow restriction; hypothesis-generating and leaves open human translation.
The genetic background of a mouse strain determines its susceptibility to disease. C57BL/6J and Balb/CJ are two widely used inbred mouse strains that we found react dramatically differently to angiotensin II and high-salt diet (ANG II + Salt). Balb/CJ show increased mortality associated with anuria and edema formation while C57BL/6J develop arterial hypertension but do not decompensate and die. Clinical symptoms of heart failure in Balb/CJ mice gave the hypothesis that ANG II + Salt impairs cardiac function and induces cardiac remodeling in male Balb/CJ but not in male C57BL/6J mice. To test this hypothesis, we measured cardiac function using echocardiography before treatment and every day for 7 days during treatment with ANG II + Salt. Interestingly, pulsed wave Doppler of pulmonary artery flow indicated increased pulmonary vascular resistance and right ventricle systolic pressure in Balb/CJ mice, already 24 h after ANG II + Salt treatment was started. In addition, Balb/CJ mice showed abnormal diastolic filling indicated by reduced early and late filling and increased isovolumic relaxation time. Furthermore, Balb/CJ exhibited lower cardiac output compared with C57BL/6J even though they retained more sodium and water, as assessed using metabolic cages. Left posterior wall thickness increased during ANG II + Salt treatment but did not differ between the strains. In conclusion, ANG II + Salt treatment causes early restriction of pulmonary flow and reduced left ventricular filling and cardiac output in Balb/CJ, which results in fluid retention and peripheral edema. This makes Balb/CJ a potential model to study the adaptive capacity of the heart for identifying new disease mechanisms and drug targets.
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Becirovic‐Agic et al. (2019) studied Heart failure and cardiorenal syndrome. Angiotensin II and high-salt diet vs. C57BL/6J mice was evaluated on Cardiac function and pulmonary vascular resistance. Angiotensin II and high-salt diet caused early restriction of pulmonary flow, reduced left ventricular filling, and lower cardiac output in Balb/CJ mice compared with C57BL/6J mice.
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