Key result
Spironolactone prevents cardiac hypertrophy driven by early local cardiac aldosterone synthesis in stroke-prone hypertensive rats.
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Aldosterone is synthesized in extra-adrenal tissues, both blood vessels and brain. We undertook the present study to determine whether the rat heart produces aldosterone and to investigate the effects of adrenalectomy, ACE inhibition, and angiotensin II on aldosterone synthesis in the heart. To clarify the pathophysiological role of cardiac aldosterone in the hypertensive heart, we compared the synthesis of aldosterone in the hearts of stroke-prone spontaneously hypertensive rats (SHRSP) with that in Wistar-Kyoto rats. The effects of the aldosterone antagonist spironolactone on myocardial hypertrophy in adrenalectomized SHRSP were also studied. Isolated rat hearts were perfused for 2 hours, and the perfusate was analyzed with HPLC and mass spectrometry. The activity of aldosterone synthase was estimated on the basis of the conversion of [(14)C]deoxycorticosterone to [(14)C]aldosterone. The levels of aldosterone synthase gene (CYP11B2) mRNA were determined with competitive polymerase chain reaction. Aldosterone production, the activity of aldosterone synthase, and the expression of CYP11B2 mRNA were increased in hearts from adrenalectomized rats and rats treated with angiotensin II. ACE inhibitors decreased cardiac aldosterone synthesis. Cardiac aldosterone, aldosterone synthase activity, and CYP11B2 mRNA levels in hearts from 2- and 4-week-old SHRSP were significantly greater than those of age-matched Wistar-Kyoto rats. Spironolactone prevented cardiac hypertrophy in adrenalectomized SHRSP. These results suggest that the rat heart produces aldosterone and that endogenous cardiac aldosterone may affect cardiac function and hypertrophy in hypertension in rats.
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Takeda et al. (2000) studied Genetic hypertension and myocardial hypertrophy (in stroke-prone spontaneously hypertensive rats). Adrenalectomy, angiotensin II, ACE inhibition, and spironolactone vs. Wistar-Kyoto control rats / untreated controls was evaluated on Cardiac aldosterone production, aldosterone synthase activity, CYP11B2 mRNA expression, and myocardial hypertrophy. 2- and 4-week-old SHRSP rats had significantly higher cardiac aldosterone synthesis and CYP11B2 mRNA than Wistar-Kyoto controls, and spironolactone prevented cardiac hypertrophy.
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