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Altered Beta-2 Adrenergic Receptor Gene Expression in Human Clinical Hypertension

Duke University School of Nursing, Durham, North Carolina, jennifer.dungan{at}duke.edu

Yvette P. Conley, PhD

Department of Health Promotion & Development, University of Pittsburgh School of Nursing, Pittsburgh, Pennsylvania

Taimour Y. Langaee, MSPH, PhD

Department of Pharmacy Practice, University of Florida College of Pharmacy, Gainesville, Florida

Julie A. Johnson, PharmD, FCCP, BCPS

Department of Pharmacy Practice and Cardiology, University of Florida Colleges of Pharmacy and Medicine, Gainesville, Florida

Shawn M. Kneipp, PhD, ARNP

Health Care Environments and Systems Department, University of Florida College of Nursing, Gainesville, Florida

Philip J. Hess, MD

Department of Thoracic and Cardiovascular Surgery, University of Florida College of Medicine and Shands Hospital, Gainesville, Florida

Carolyn B. Yucha, PhD, RN, FAAN

Department of Physiological Nursing, School of Nursing, University of Nevada, Las Vegas, Nevada

Objectives: The beta-2 adrenergic receptor is involved in mediating vasodilatation via neurohumoral and sympathetic nervous system pathways. Alterations in beta-2 adrenergic receptor gene expression (mRNA transcription) may contribute to the hypertensive phenotype. Human gene expression in clinical phenotypes remains largely unexplored due to ethical constraints involved in obtaining human tissue. We devised a method to obtain normally discarded internal mammary artery tissue from coronary artery bypass graft patients. We then investigated differences in hypertensive and normotensive participants' beta-2 adrenergic receptor gene expression in this tissue. Methods: We collected arterial tissue samples from 46 coronary artery bypass patients in a surgical setting. Using 41 of the samples, we performed TaqMan real-time polymerase chain reaction (RT-PCR) and used the delta delta cycle threshold (Ct) relative quantitation method for determination of fold-differences in gene expression between normotensive and hypertensive participants. The beta-2 adrenergic receptor target was normalized to glyceraldehyde-phosphate dehydrogenase. Results: Participants with hypertension had significantly less-expressed beta-2 adrenoceptor gene (2.76-fold, p < .05) compared to normotensive participants. After Bonferroni correction, gene expression did not differ by race, gender, type/dose of β-blocker prescribed, positive family history of hypertension, or diagnosis of diabetes mellitus type 2. Conclusions: These data support the possibility of a molecular basis for impaired adrenoceptor-mediated vascular tone in hypertension. Modification and extension of this research is required.

Key Words: Beta-2 adrenergic receptor • gene expression • transcription • hypertension • coronary artery

This version was published on July 1, 2009

Biological Research For Nursing, Vol. 11, No. 1, 17-26 (2009)
DOI: 10.1177/1099800409332538


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