Adenosine A1 receptor expression during the transition from compensated pressure overload hypertrophy to heart failure

Stefano Perlini, Beatrice Arosio, Luciano Parmeggiani, Daniela Santambrogio, Giuseppina Palladini, Rossana Tozzi, Chiara Gatti, Giorgio Annoni, Theo E. Meyer, Alberto U. Ferrari

Research output: Contribution to journalArticle

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 languageEnglish
Pages (from-to)449-454
Number of pages6
JournalJournal of Hypertension
Volume25
Issue number2
DOIs
Publication statusPublished - Feb 2007

Fingerprint

Adenosine A1 Receptors
Hypertrophy
Heart Failure
Pressure
Adenosine
Lung
Autacoids
Weights and Measures
Messenger RNA
Proteins
Ketamine
Left Ventricular Hypertrophy
Thoracic Aorta
Catheterization
Sprague Dawley Rats
Echocardiography
Heart Diseases
Anesthesia
Gene Expression
Genes

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 journalArticle

Perlini, S, Arosio, B, Parmeggiani, L, Santambrogio, D, Palladini, G, Tozzi, R, Gatti, C, Annoni, G, Meyer, TE & Ferrari, AU 2007, 'Adenosine A1 receptor expression during the transition from compensated pressure overload hypertrophy to heart failure', Journal of Hypertension, vol. 25, no. 2, pp. 449-454. https://doi.org/10.1097/HJH.0b013e3280110de3
Perlini, Stefano ; Arosio, Beatrice ; Parmeggiani, Luciano ; Santambrogio, Daniela ; Palladini, Giuseppina ; Tozzi, Rossana ; Gatti, Chiara ; Annoni, Giorgio ; Meyer, Theo E. ; Ferrari, Alberto U. / Adenosine A1 receptor expression during the transition from compensated pressure overload hypertrophy to heart failure. In: Journal of Hypertension. 2007 ; Vol. 25, No. 2. pp. 449-454.
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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.",
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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.

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KW - Cardioprotection

KW - Gene expression

KW - Heart failure

KW - Hypertrophy

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