CLONING OF THE RAT ALPHA(1C)-ADRENERGIC RECEPTOR FROM CARDIAC MYOCYTES - ALPHA(1C), ALPHA(1B) AND ALPHA(1D) MESSENGER-RNAS ARE PRESENT IN CARDIAC MYOCYTES BUT NOT IN CARDIAC FIBROBLASTS

alpha(1)-Adrenergic receptor (AR) activation in cardiac muscle has several different physiological effects that might be mediated through different alpha(1)-AR subtypes. Two alpha(1)-AR subtypes have been cloned from the rat, the alpha(1B) and the alpha 1D; both are present in adult rat heart. A third subtype, the alpha(1C), cloned from the cow and human, was reported to be absent in the rat. However, we recently found alpha(1C) mRNA in adult rat heart by using a partial alpha(1C) cDNA. Thus, all three cloned alpha(1)-AR subtypes are present in the heart, but it is unknown whether each is expressed in cardiac myocytes or in cardiac fibroblasts. In the present study, the full-length rat alpha(1C)-AR was cloned from cultured neonatal cardiac myocytes. alpha(1C) mRNA transcripts of 3, 9.5, and 11 kb were present in adult rat heart by Northern blot analysis. alpha(1B)-, alpha(1C)-, and alpha(1D)-subtype mRNAs were each present in isolated adult and neonatal cardiac myocytes by RNase protection assay. In addition, cultured neonatal cardiac myocytes expressed the three alpha(1)-AR subtype mRNAs. In contrast, none of the alpha(1)-AR mRNAs was detected in cultured neonatal cardiac fibroblasts. In addition, alpha(1)-ARs were absent in fibroblasts by prazosin binding and norepinephrine-stimulated [H-3]inositol phosphate production. The absence of alpha(1)-ARs in cardiac fibroblasts differs from beta-adrenergic and angiotensin II receptors, which are present in both cardiac fibroblasts and cardiac myocytes. Three alpha(1)-AR subtypes in cardiac myocytes will need to be considered in future studies of the physiological effects of alpha(1)-BR activation in cardiac muscle.