Key result
Bosentan blocked pressure overload-induced increases in BNP mRNA levels in atrial myocytes but not in ventricular myocytes, demonstrating ET-1 differentially regulates BNP expression.
Why the study?
Does endothelin-1 or angiotensin II receptor antagonism reduce stretch-induced BNP gene expression in atrial and ventricular myocytes in spontaneously hypertensive rats?
Does endothelin-1 or angiotensin II receptor antagonism reduce stretch-induced BNP gene expression in atrial and ventricular myocytes in spontaneously hypertensive rats?
Endogenous endothelin-1 is required for stretch-induced BNP gene expression in atrial myocytes, but not in ventricular myocytes.
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ET-1 antagonism selectively attenuates atrial BNP induction in pressure overload; leaves open chamber-specific roles in human hypertension or HF.
Magga et al. (1997) studied Acute pressure overload. Bosentan vs. Vehicle, Losartan, and CV-11974 was evaluated on BNP mRNA levels. Bosentan blocked pressure overload-induced increases in BNP mRNA levels in atrial myocytes but not in ventricular myocytes, demonstrating ET-1 differentially regulates BNP expression.
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