Key result
Monocrotaline-induced pulmonary hypertension in rats drives a 57-fold increase in RV ANP correlating with RVSP.
Why the study?
The time course and triggers for synthesis of atrial natriuretic peptide in the right ventricle during development of right ventricular hypertrophy were not well defined.
Answers are grounded in this paper and cite their sources.
In a rat model of monocrotaline-induced pulmonary hypertension, pressure overload triggers significant synthesis and storage of atrial natriuretic peptide in the right ventricle.
To determine the time course and potential triggers for synthesis of atrial natriuretic peptide (ANP) in right ventricle during the development of right ventricular hypertrophy (RVH), we measured mean right atrial pressure, right ventricular systolic pressure (RVSP), immunoreactive ANP (iANP) concentrations in plasma, and cardiac iANP concentrations and contents of monocrotaline (MCT)-induced pulmonary hypertensive rats treated with a subcutaneous injection of MCT (40 mg/kg). Following the development of RVH and pulmonary hypertension, iANP concentrations in plasma and iANP concentrations and contents in ventricular tissues increased with time. At the third week after treatment, iANP concentrations in MCT rats increased 6-fold in plasma, 57-fold in the right ventricular free wall, 20-fold in the ventricular septum and 10-fold in the left ventricular free wall compared with those in controls. At the third week, iANP contents of total ventricular tissues in MCT and control rats were 29% and 0.8%, respectively, of the corresponding atrial contents. The iANP concentrations and contents of right ventricular free walls in MCT rats were greater than those of any other parts of ventricular tissues. The iANP concentrations in right ventricular free walls were very closely related to RVSP (r = 0.93, P < 0.001). In MCT rats, iANP concentrations in right atrial tissues decreased with time. This study shows that ventricular ANP contributes to the amount of ANP stored within the heart in MCT rats and that pressure overload may be one of the triggers for ANP synthesis in the right ventricle.
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Ohie et al. (1993) studied Pulmonary hypertension and right ventricular hypertrophy. Monocrotaline (MCT) vs. Controls was evaluated on Immunoreactive ANP (iANP) concentrations in the right ventricular free wall (57-fold increase). Monocrotaline-induced pulmonary hypertension in rats led to a 57-fold increase in right ventricular free wall ANP concentrations at 3 weeks, which closely correlated with right ventricular systolic pressure (r=0.93, P<0.001).
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