Distribution of α1-Adrenergic Receptor mRNA Species in Rat Heart

Abstract

Radioligand binding studies have detected alpha1A- and alpha1B-adrenergic receptors (AR) in rat heart, but the ligands available for these studies lack the sensitivity and specificity needed to map possible differences in alpha1-AR subtype expression. We therefore used competitive reverse transcriptase-polymerase chain reaction (RT-PCR) techniques to measure steady-state amounts of alpha1-AR messenger RNA (mRNA) subtypes in tissue dissected from several regions of rat heart. We detected mRNA for alpha1A-, alpha1B-, and alpha1D-AR in each region. Irrespective of the alphaAR subtype, the total number of alpha1-AR transcripts has the following regional rank order: left ventricular papillary muscle > left ventricle > left atrium > apex > right ventricle > ventricular septum > right atria. Among the regions, the fractional contribution of alpha1A-, alpha1B-, and alpha1D-AR mRNA to the total amount of alpha1-AR displays considerable variability. The alpha1B-AR mRNA accounts for >50% of the total alpha1-AR mRNA in all regions except the ventricular septum. There are also significant percentages of alpha1A-AR in each region, especially in the papillary muscle (48%) and ventricular septum (48%). The alpha1D-AR mRNA transcripts are found in comparatively low numbers; their highest levels (18% of total) were found in the right ventricle. These differences in alpha1-AR mRNA expression may contribute to the observed regional differences in myocardial responses to alpha1-AR agonists and antagonists.

Distribution of mRNA and binding sites of adrenoceptors and muscarinic receptors in the rat heart

“…In general, our data also agree with those of Wolff et al (1998) about the distribution of α 1 -adrenoceptor mRNA in different parts of the heart although we do not find the differences in the distribution of α 1A -adrenoceptor mRNA. Moreover, we were able to identify not only the differences in the distribution of mRNA, but also in the density of binding sites for α 1B -adrenergic receptors.…”

The Mechanism of Increasing Ca2+ Responsiveness by .ALPHA.1-Adrenoceptor Stimulation in Rat Ventricular Myocytes.

“…After Langendorff perfusion for 3-4 min at 37°C with Ca 2ϩ -free Tyrode solution containing 0.2 mg/ml collagenase (Nitta Zerachin, Tokyo, Japan) and 0.04 mg/ml protease (type XIV, Sigma Chemical, St. Louis, MO, USA), the enzymes were washed out with 0.2 mM Ca 2ϩ -Tyrode solution, and cells were dispersed from the ventricular tissue into a dish. We obtained myocytes from the left ventricle or septum, because ␣ 1 -adrenoceptor could be localized in the left ventricle or septum [12]. The isolated cells were stored in 1 mM Ca 2ϩ -Tyrode solution at 4°C until use (up to 8 h).…”

Noradrenaline-induced increase in protein synthesis in adult rat cardiomyocytes: involvement of only α 1A -adrenoceptors

“…While there seems to be agreement in the literature that in neonatal rat cardiomyocytes α 1 -AR-stimulated cardiac hypertrophy is brought about by α 1A -AR stimulation (Knowlton et al 1993;Autelitano and Woodcock 1998;Rohde et al 2000), it is not known which α 1 -AR subtype might mediate α 1 -ARevoked hypertrophic response in adult rat ventricular cardiomyocytes. In the adult rat heart (Price et al 1994;Scofield et al 1995;Wolff et al 1998) and in adult rat cardiomyocytes (Rokosh et al 1996) at the mRNA-level all three α 1 -AR subtypes have been demonstrated with α 1B -AR having the greatest abundance (Price et al 1994;Wolff et al 1998). Similarly, binding studies in the rat heart have revealed an α 1A :α 1B -AR ratio of 20%:80% (Michel et al 1994a) while it is still a matter of debate whether or not α 1D -AR can be demonstrated in the rat heart on a protein level (Deng et al 1996;Yang et al 1997).…”