Why the study?
Does benidipine reduce cardiac remodeling and renal injury in Dahl salt-sensitive rats on a high-salt diet?
Does benidipine reduce cardiac remodeling and renal injury in Dahl salt-sensitive rats on a high-salt diet?
In a Dahl salt-sensitive rat model, benidipine significantly reduced systolic blood pressure, cardiac hypertrophy, and renal lesions, suggesting both hemodynamic and non-hemodynamic protective effects.
Benidipine attenuated cardiac and renal injury in salt-sensitive rats; hypothesis-generating and should not yet change clinical practice.
Interest in cardiovascular protection by calcium channel antagonists has grown over the past decade. We investigated the prevention of cardiac remodeling and renal injury by the long-acting calcium channel antagonist benidipine using 12 week-old Dahl salt-sensitive (Dahl S) rats fed a high-salt (4% NaCl) diet. Six-week benidipine treatment (10 mg/kg chow) decreased systolic blood pressure by 22% in Dahl S rats. This blood pressure reduction was associated with decreases in cardiac mass and weight of the aortic wall. Collagen content in the left ventricle tended to decline with benidipine treatment. In addition, glomerular filtration rate increased by 33% and arterial and glomerular lesions improved morphologically with this treatment. Regression of cardiac mass and collagen content in the left ventricle was due mainly to blood pressure reduction; however, collagen content in the low-pressure right ventricle was not only related to systemic blood pressure but to the severity of renal lesions. These data suggest that the calcium channel antagonist benidipine attenuates cardiac and renal injury in hypertensive Dahl S rats, and that part of the cardiac hypertrophy is due to a non-hemodynamic mechanism that might be responsible for, or be a consequence of, the lesions in the kidney.
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Uehara et al. (1995) studied this question.
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