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 sev eral different physiological effects that might be mediated through di fferent alpha(1)-AR subtypes. Two alpha(1)-AR subtypes have been clone d from the rat, the alpha(1B) and the alpha 1D; both are present in ad ult 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 fou nd 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 i n 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)-subty pe mRNAs were each present in isolated adult and neonatal cardiac myoc ytes 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 cardia c fibroblasts. In addition, alpha(1)-ARs were absent in fibroblasts by prazosin binding and norepinephrine-stimulated [H-3]inositol phosphat e production. The absence of alpha(1)-ARs in cardiac fibroblasts diffe rs from beta-adrenergic and angiotensin II receptors, which are presen t in both cardiac fibroblasts and cardiac myocytes. Three alpha(1)-AR subtypes in cardiac myocytes will need to be considered in future stud ies of the physiological effects of alpha(1)-BR activation in cardiac muscle.