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Vol. 284, Issue 1, 323-336, 1998
Department of Histochemistry (J.W., K.M., R.A.D.R., J.M.P.),
Imperial College School of Medicine, The Hammersmith Hospital, London
W12 ONN, UK;
Vascular Biology Centre (J.D.C.), Medical College of
Georgia, Augusta, Georgia;
Heart Science Centre (A.C., M.H.Y.),
Harefield Hospital, Harefield, Middlesex UB9 6JH, UK; and
Cardiothoracic Unit (B.F.W., M.R.DeL.), Great Ormond Street Hospital
for Children, London WC1 3JH, UK
Cardiac expression of angiotensin II (Ang II) AT1 and
AT2 receptor subtypes is species dependent, and changes in
their relative proportion may influence myocardial hypertrophy and
fibrosis. Regional differences in the distribution of Ang II receptors
in the normal and failing human heart were assessed using
125I-(Sar1,Ile8)Ang II binding and
quantitative autoradiography. Receptor subtypes were distinguished by
their affinity for selective nonpeptide antagonists (losartan and
PD123319) and sensitivity to dithiothreitol. Ventricular and atrial
tissues displayed a heterogeneous distribution of ligand binding sites.
AT2 receptors predominated, representing 70% to 77% of
the sites in normal and noninfarcted myocardium. Endocardial,
interstitial, perivascular and infarcted regions in the ventricles of
patients with end-stage ischemic heart disease or dilated
cardiomyopathy exhibited a significantly greater density (P < .001) of high affinity AT2 binding sites
(Kd = 0.57 nmol/liter) compared
with adjacent noninfarcted myocardium. Regions displaying the relative
increase in AT2 binding sites corresponded to areas of
fibroblast proliferation and collagen deposition, shown by picrosirius
red staining. AT1 binding sites were localized to nerves,
occurred at relatively low density in coronary vessels and represented
only 23% to 29% of myocardial
125I-(Sar1,Ile8)Ang II binding
sites. The border zone between infarcted and noninfarcted myocardium
characteristically contained numerous microvessels, exhibiting
perivascular AT2 receptors and endothelial angiotensin converting enzyme activity, as demonstrated by binding of
125I-351A. Specific myocardial AT2 receptor
mRNA transcripts (
3 kb) were identified and exhibited alternative
splicing of untranslated 5
exons. The differential distribution of
cardiac Ang II receptor subtypes and selective increase in binding to
AT2 sites in the diseased heart suggest that cells bearing
the AT2 receptor represent a significant target for Ang II,
possibly contributing to its growth-related actions.
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