Alteration of messenger RNA and protein levels of cardiac alpha(1)-adrenergic receptor and angiotensin II receptor subtypes during aging in rats.
BACKGROUND
Structural and functional alterations in the senescent heart have been associated with an activated sympathetic nervous system and a regional cardiac renin-angiotensin system. To date, however, limited information related to their expression alteration during the whole procress of growth and development has been reported.


OBJECTIVE
To examine the expression of alpha(1)-adrenergic receptor (alpha(1)-AR) and angiotensin II receptor (ATR) subtypes in the left ventricle of hearts from young adult, middle-aged, presenescent and senescent rats.


METHODS
Semiquantitative reverse transcriptase polymerase chain reaction and Western blot were used to quantitate the messenger RNA and protein of alpha(1)-AR and ATR subtypes, respectively, in the left ventricles of three- (young adult), 12- (middle age), 18- (presenescent) and 24-month-old (senescent) Wistar rats.


CONCLUSIONS
alpha(1A)-AR expression decreased gradually with age, and alpha(1D)-AR expression was repressed in middle age and presenescence, while the expression of alpha(1B)-AR remained unchanged during senescence. AT(1)R expression was unaffected by aging from young adulthood to presenescence, but exhibited a remarkable upregulation in senescence. There were no significant discrepancies of cardiac AT(2)R expression among the four age groups, but both messenger RNA and protein had a tendency to upregulate during aging. The results suggest that there are considerable changes of expression of cardiac alpha(1)-AR and ATR subtypes during growth and development. The change of cardiac alpha(1)-AR and ATR expression during aging is a protective response to senescence by keeping normal myocardial contractility, while the upregulation of AT(1)R and AT(2)R promotes age-related myocardium hypertrophy and cardiac remodelling.
Cao
Xiao-jing
XJ
The Cardiology Department, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Li
Yan-fang
YF
D000367:Age Factors; D000375:Aging / Q000378:metabolism*; D000818:Animals; D018507:Gene Expression Regulation, Developmental; D006352:Heart Ventricles / Q000378:metabolism*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology; D009206:Myocardium / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics* / Q000378:metabolism; D018340:Receptors, Adrenergic, alpha-1 / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D020257:Ventricular Remodeling / Q000502:physiology
D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D018340:Receptors, Adrenergic, alpha-1