WEDNESDAY, Oct. 28 (HealthDay News) -- Lack of adiponectin, an adipose-derived plasma protein that exerts anti-inflammatory and anti-hypertrophic effects, in aldosterone-induced hypertension worsens left ventricular hypertrophy and heart function in mice, according to a study published online Oct. 22 in Endocrinology.
Noting that aldosterone is associated with left ventricular hypertrophy, hypertension, and diastolic heart failure, while adiponectin is associated with the development of hypertension and systolic heart failure, Flora Sam, M.D., and colleagues from Boston University School of Medicine treated normal and adiponectin-deficient mice lacking one kidney with saline or aldosterone.
After four weeks of feeding with one percent salt water, the researchers found that aldosterone treatment significantly increased blood pressure, left ventricular hypertrophy, and two measures of diastolic function in normal mice, and even more so in adiponectin-deficient mice. Aldosterone treatment had no effect on left ventricular ejection fraction, renal function, or cardiac fibrosis in normal and adiponectin-deficient mice. Pulmonary congestion was significantly worse in adiponectin-deficient mice. In addition, aldosterone-treated normal mice had increased expression of several proinflammatory proteins and a protein involved in breaking down the extracellular matrix.
"Therefore, hypoadiponectinemia in hypertension-induced diastolic heart failure exacerbates left ventricular hypertrophy, diastolic dysfunction, and diastolic heart failure," Sam and colleagues conclude. "This interaction between adiponectin and aldosterone in hypertension and obesity may be useful for future therapeutic interventions for severe and/or resistant hypertension and to prevent the progression to diastolic dysfunction and diastolic heart failure."
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