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Am J Physiol Heart Circ Physiol 278: H2076-H2083, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 6, H2076-H2083, June 2000

Changes of beta -adrenergic signaling in compensated human cardiac hypertrophy depend on the underlying disease

Ulrich Schotten1, Karsten Filzmaier1, Britta Borghardt1, Simone Kulka1, Friedrich Schoendube2, Carlos Schumacher1, and Peter Hanrath1

1 Department of Cardiology and 2 Department of Thoracic and Cardiovascular Surgery, University Hospital Aachen, D-52057 Aachen, Germany

In human heart failure, desensitization of the beta -adrenergic signal transduction has been reported to be one of the main pathophysiological alterations. However, data on the beta -adrenergic system in human compensated cardiac hypertrophy are very limited. Therefore, we studied the myocardial beta -adrenergic signaling in patients suffering from hypertrophic obstructive cardiomyopathy (HOCM, n = 9) or from aortic valve stenosis (AoSt, n = 8). beta -Adrenoceptor density determined by [125I]iodocyanopindolol binding was reduced in HOCM and AoSt compared with nonhypertrophied, nonfailing myocardium (NF) of seven organ donors. In HOCM the protein expression of stimulatory G protein alpha -subunit (Gsalpha ) measured by immunoblotting was unchanged, whereas the inhibitory G protein alpha -subunit (Galpha i-2) was increased. In contrast, in AoSt, Galpha i-2 protein was unchanged, but Gsalpha protein was increased. Adenylyl cyclase stimulation by isoproterenol was reduced in HOCM but not in AoSt. Plasma catecholamine levels were normal in all patients. In conclusion, both forms of hypertrophy are associated with beta -adrenoceptor downregulation but with different changes at the G protein level that occur before symptomatic heart failure due to progressive dilatation of the left ventricle develops and are not due to elevated plasma catecholamine levels.

aortic valve stenosis; G proteins; hypertrophic obstructive cardiomyopathy; beta -adrenoceptors; signal transduction


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