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Cardiovascular Research 1998 38(2):340-347; doi:10.1016/S0008-6363(98)00015-7
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Angiotensin II receptor subtype AT1 and AT2 expression after heart transplantation

Lars Gullestada,1,1, Guy Haywooda, Halfdan Aassb, Heather Rossa, Gail Yeea, Thor Uelandb, Odd Geiranb, John Kjekshusb, Svein Simonsenb, Nanette Bishoprica and Michael Fowlera,*

aFalk Cardiovascular Research Center, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305-5246, USA
bRikshospitalet University Hospital, Oslo, Norway

* Corresponding author. Tel.: +1 (415) 723 7846; Fax: +1 (415) 725 1599.

Objective: Cardiac hypertrophy appears early after heart transplantation, and may represent a myocardial response to injury. Recent evidence suggests that angiotensin II (Ang II) may promote growth through the AT1 and inhibit growth through the AT2 receptor subtypes. We therefore asked whether hypertrophy after heart transplantation is characterized by alterations in Ang II receptor gene expression. Methods: The expression of Ang II receptor subtypes, AT1 and AT2, was analyzed in right ventricular endomyocardial biopsies taken from 10 human donor hearts prior to implantation (controls) and from 17 heart transplant recipients, 11 studied during annual evaluation (>1 year after transplantation) and 6 one week after transplantation. Competitive reverse transcription polymerase chain reaction (RT-PCR) was performed using synthetic RNA internal standards for both receptor subtypes. Results: AT1 and AT2 receptor mRNAs were detected in all samples. AT1 receptor mRNA decreased 4.5 fold (p<0.01) and AT2 receptor mRNA 4.2 fold (p<0.001) in transplant patients compared with controls. In the subgroup of patients examined one week after surgery AT1 was reduced relative to AT2 receptor mRNA, resulting in an altered ratio of AT1 to AT2 early after transplantation. There was no correlation between Ang II receptor levels and left ventricular wall thickness, and the decrease in receptor level did not correlate with any hemodynamic parameters, cyclosporine blood levels, or plasma renin, Ang II or pANP, except for a negative correlation between AT2 mRNA and plasma renin (r=–0.49,p=0.05). Conclusions: Contrary to our expectations, mRNA for both Ang II receptors was downregulated after heart transplantation. The cause of myocardial hypertrophy after heart transplantation is still unclear, but the hypertrophy does not appear to be driven by increased transcription of the AT1 receptor.

KEYWORDS Clinical; Heart; Molecular biology; Human; Angiotensin; Gene expression; Receptors; Transplantation

1 Medical Department B, Rikshospitalet, 0027 Oslo, Norway. Tel.: +47 22 867010, Fax: +47 22 868357.


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