Abstract
OBJECTIVES: Myocardial adenosine is increased in pressure-overload hypertrophy (POH) and exerts important cardioprotective effects that delay transition to left ventricular failure. Adenosine-mediated signaling is attenuated in POH, but whether this depends on receptor or postreceptor defects is unknown. We therefore examined left ventricular adenosine A1-receptor gene and protein expression in experimental POH. METHODS: Six week-old Sprague-Dawley rats were subjected to abdominal aortic banding (group B) or sham operation (group S). Echocardiography and left ventricular catheterization were performed 10 weeks later under ketamine anesthesia. Left ventricular and lung weight indices were obtained postmortem. A1-Receptor mRNA and protein expression were measured in samples from left ventricular, right ventricular and aortic arch tissue. Group B rats were subgrouped as having compensated or decompensated hypertrophy according to the absence or presence of lung congestion (lung weight index below or above mean ± 2SD compared with group S rats). RESULTS: Both mRNA and protein A1-receptor expression were significantly increased in compensated group B versus group S rats (by, respectively, 37 and 77%; both P <0.01). This was not observed in decompensated group B rats. No consistent gene or receptor expression changes were observed in right ventricular or aortic tissues. CONCLUSIONS: In compensated POH, increased interstitial adenosine concentrations are accompanied by increased expression of the specific receptor mediating the major cardioprotective effects of this autacoid. Such overexpression is no longer detectable once the transition from POH to left ventricular failure has occurred. These observations may have pathophysiological and, in perspective, therapeutic relevance to the course of hypertensive heart disease.
| Original language | English |
|---|---|
| Pages (from-to) | 449-454 |
| Number of pages | 6 |
| Journal | Journal of Hypertension |
| Volume | 25 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Feb 2007 |
Fingerprint
Keywords
- Adenosine
- Adenosine receptors
- Cardioprotection
- Gene expression
- Heart failure
- Hypertrophy
ASJC Scopus subject areas
- Endocrinology
- Internal Medicine
Cite this
Adenosine A1 receptor expression during the transition from compensated pressure overload hypertrophy to heart failure. / Perlini, Stefano; Arosio, Beatrice; Parmeggiani, Luciano; Santambrogio, Daniela; Palladini, Giuseppina; Tozzi, Rossana; Gatti, Chiara; Annoni, Giorgio; Meyer, Theo E.; Ferrari, Alberto U.
In: Journal of Hypertension, Vol. 25, No. 2, 02.2007, p. 449-454.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Adenosine A1 receptor expression during the transition from compensated pressure overload hypertrophy to heart failure
AU - Perlini, Stefano
AU - Arosio, Beatrice
AU - Parmeggiani, Luciano
AU - Santambrogio, Daniela
AU - Palladini, Giuseppina
AU - Tozzi, Rossana
AU - Gatti, Chiara
AU - Annoni, Giorgio
AU - Meyer, Theo E.
AU - Ferrari, Alberto U.
PY - 2007/2
Y1 - 2007/2
N2 - OBJECTIVES: Myocardial adenosine is increased in pressure-overload hypertrophy (POH) and exerts important cardioprotective effects that delay transition to left ventricular failure. Adenosine-mediated signaling is attenuated in POH, but whether this depends on receptor or postreceptor defects is unknown. We therefore examined left ventricular adenosine A1-receptor gene and protein expression in experimental POH. METHODS: Six week-old Sprague-Dawley rats were subjected to abdominal aortic banding (group B) or sham operation (group S). Echocardiography and left ventricular catheterization were performed 10 weeks later under ketamine anesthesia. Left ventricular and lung weight indices were obtained postmortem. A1-Receptor mRNA and protein expression were measured in samples from left ventricular, right ventricular and aortic arch tissue. Group B rats were subgrouped as having compensated or decompensated hypertrophy according to the absence or presence of lung congestion (lung weight index below or above mean ± 2SD compared with group S rats). RESULTS: Both mRNA and protein A1-receptor expression were significantly increased in compensated group B versus group S rats (by, respectively, 37 and 77%; both P <0.01). This was not observed in decompensated group B rats. No consistent gene or receptor expression changes were observed in right ventricular or aortic tissues. CONCLUSIONS: In compensated POH, increased interstitial adenosine concentrations are accompanied by increased expression of the specific receptor mediating the major cardioprotective effects of this autacoid. Such overexpression is no longer detectable once the transition from POH to left ventricular failure has occurred. These observations may have pathophysiological and, in perspective, therapeutic relevance to the course of hypertensive heart disease.
AB - OBJECTIVES: Myocardial adenosine is increased in pressure-overload hypertrophy (POH) and exerts important cardioprotective effects that delay transition to left ventricular failure. Adenosine-mediated signaling is attenuated in POH, but whether this depends on receptor or postreceptor defects is unknown. We therefore examined left ventricular adenosine A1-receptor gene and protein expression in experimental POH. METHODS: Six week-old Sprague-Dawley rats were subjected to abdominal aortic banding (group B) or sham operation (group S). Echocardiography and left ventricular catheterization were performed 10 weeks later under ketamine anesthesia. Left ventricular and lung weight indices were obtained postmortem. A1-Receptor mRNA and protein expression were measured in samples from left ventricular, right ventricular and aortic arch tissue. Group B rats were subgrouped as having compensated or decompensated hypertrophy according to the absence or presence of lung congestion (lung weight index below or above mean ± 2SD compared with group S rats). RESULTS: Both mRNA and protein A1-receptor expression were significantly increased in compensated group B versus group S rats (by, respectively, 37 and 77%; both P <0.01). This was not observed in decompensated group B rats. No consistent gene or receptor expression changes were observed in right ventricular or aortic tissues. CONCLUSIONS: In compensated POH, increased interstitial adenosine concentrations are accompanied by increased expression of the specific receptor mediating the major cardioprotective effects of this autacoid. Such overexpression is no longer detectable once the transition from POH to left ventricular failure has occurred. These observations may have pathophysiological and, in perspective, therapeutic relevance to the course of hypertensive heart disease.
KW - Adenosine
KW - Adenosine receptors
KW - Cardioprotection
KW - Gene expression
KW - Heart failure
KW - Hypertrophy
UR - http://www.scopus.com/inward/record.url?scp=33846051456&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33846051456&partnerID=8YFLogxK
U2 - 10.1097/HJH.0b013e3280110de3
DO - 10.1097/HJH.0b013e3280110de3
M3 - Article
C2 - 17211253
AN - SCOPUS:33846051456
VL - 25
SP - 449
EP - 454
JO - Journal of Hypertension
JF - Journal of Hypertension
SN - 0263-6352
IS - 2
ER -