This Article Abstract Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Neri Serneri, G. G. Articles by Modesti, P. A. Search for Related Content PubMed PubMed Citation Articles by Neri Serneri, G. G. Articles by Modesti, P. A.

Activation of cardiac renin-angiotensin system in unstable angina

Gian Gastone Neri Serneri, MD^*, Maria Boddi, MD, PhD^*, Loredana Poggesi, MD^*, Ignazio Simonetti, MD^*, Mirella Coppo, BSc^*, Maria Letizia Papa, BSc^*, Gian Franco Lisi, MD, Massimo Maccherini, MD, Roberto Becherini, MD^*, Andrea Boncompagni, MD^*, Thomas Toscano, MD and Pietro Amedeo Modesti, MD, PhD^*

^* Clinica Medica Generale e Cardiologia, University of Florence, Florence, Italy
Institute of Thoracic and Cardiovascular Surgery, University of Siena, Siena, Italy

View larger version (44K): [in a new window]   Figure 1 Black circles indicate the patients and the controls who performed 125I-Ang I kinetics study. (A) Aortic (A) and coronary sinus (CS) plasma concentrations of Angiotensin (Ang) I and II in anginal patients and in controls. (B) Relationship between cardiac Ang II formation and overall duration of ischemia in the five days of Holter monitoring preceding the study of cardiac RAS. (C) The amount of Ang II formed was not related to the time elapsed since the last ischemic episode or anginal attack (F = 1.8). Ang = angiotensin; RAS = renin-angiotensin system; SA = stable effort angina; UA = unstable angina.

View larger version (41K): [in a new window]   Figure 2 (A) Reverse-transcriptase polymerase chain reaction (RT-PCR) products of angiotensinogen (AGTN), angiotensin-converting enzyme (ACE), AT1, AT2 and chymase from the myocardium of the control hearts (CH) and from the hearts of patients with stable effort angina (SA) and unstable angina (UA). (B) Densitometric quantification of RT-PCR products of AGTN, ACE and AT1 from human myocardium in a nonfailing heart, SA and UA hearts. In UA hearts, the levels for AGTN, ACE and AT1 messenger RNA were significantly increased versus control hearts and SA hearts (for both p < 0.01). Data are reported as mean ± SD.

View larger version (165K): [in a new window]   Figure 3 In situ hybridization for angiotensinogen (AGTN) (A,D,G), angiotensin-converting enzyme (ACE) (B,E,H), Glyceraldeyde-3-phosphate dehydrogenase (C,I) and plasmid vector pB322 (F) in controls (A,B,C) and in patients with unstable (D,E,F) and stable (G,H,I) angina. Magnification x 400. Positive messenger RNA (mRNA) signal for AGTN (D) and ACE mRNA (E) was detectable in the interstitial and endothelial cells of patients with unstable angina. On the contrary, mRNA for AGTN (G) and for ACE (H) was not expressed in myocardial biopsy specimens from patients with stable effort angina.