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[Alteration of cardiac alpha 1-adrenergic receptor subtypes in cardiac insufficient rat].

The cardiac insufficiency was produced by simultaneous constriction of abdominal aortae and renal artery in rat. Radioligand binding and reverse transcription-polymerase chain reaction (RT-PCR) were used respectively to determine the alterations of cardiac alpha 1-adrenergic receptor (alpha 1-AR) subtypes at protein level and gene transcription level. The Scatchard analysis of 125I-BE 2254 saturation curves showed that in cardiac insufficient rat hearts the KD values (229 +/- 32 vs 195 +/- 15 pmol/L) and the Bmax values (102 +/- 12 vs 96 +/- 17 fmol/mg) were not significantly different from those of control hearts. In the insufficient rat hearts, the inhibition of alpha 1-AR specific binding by WB 4101 showed that the high affinity sites (alpha 1A + alpha 1D) were increased from the 22 +/- 5% of the control to 51 +/- 7% (P < 0.01). The alpha 1A-AR mRNA level was increased, alpha 1B-AR mRNA level decreased while alpha 1D-AR unchanged. The results suggest that in cardiac insufficient rat hearts the subtype composition is altered as shown by increased alpha 1A-AR, decreased alpha 1B-AR and unchanged alpha 1D-AR, although the total amount of alpha 1-AR is unchanged.