Biventricular Autocrine/Paracrine Systems in Monocrotaline Induced Pulmonary Hypertension.

• Type: Summary of Presentation in an International Conference
• Date: 2004

Authors

Lourenço AP (Author) FMUP; Wieland J (Author) Other; Roncon-Albuquerque R Jr (Author) FMUP; Henriques-Coelho T (Author) FMUP; Correia-Pinto J (Author) FMUP; Leite-Moreira AF (Author) FMUP

Conference proceedings International

Title: Journal of the American College of Cardiology

Pages: 456A-457A

54th Annual Scientific Session of the American-College-of-Cardiology

New Orleans, LA, 07 a 10 de março 2004

Indexing

ISI Web of Science

Scientific classification

FOS: Medical and Health sciences > Other medical sciences

Other information

Resumo (PT): Increasing evidence suggests occurrence of LV contractile dysfunction in pulmonary hypertension (PH) in the absence of LV overload. The role of autocrine/paracrine mechanisms on the development of such dysfunction remains largely unknown. RV and LV hemodynamic and morphometric measurements along with evaluation of mRNA expression (RT real time PCR, normalized for GAPDH) of angiotensinogen (Agtg), ACE, aldosterone synthase (A-synt), chymase, ET-1, IGF-1 and BNP were carried in Wistar rats 4 (M4, n=7) and 6 (M6, n=7) weeks after monocrotaline injection (MCT, 60mg/Kg, sc) and compared with sham (S, n=7), Results presented as mean±SEM; p<0.05: * vs S, † vs M4, with mRNA data reported in Arbitrary Units of ratios. MCT increased systolic RV pressure (S=21±1; M4=39±2*; M6=51±4*† mmHg) and RV/ LV weight ratio (S=0.23±0.02; M4=0.37±0.03*; M6=0.58±0.03*†), whilst end-diastolic LV dimensions decreased (S=8.2±0.6; M4=6.9±0.7; M6=5.4±0.9* mm). LV function was impaired only in the M6 group: dP/dtmax (S=4953±550; M4=5263±393; M6=2205±272*† mmHg/s), time constant τ (S=22±2; M4=19±2; M6=27±2*† ms). MCT significantly changed gene expression of RV-ACE (S=1.0±0.1; M4=1.7±0.3; M6=9.8±1.4*†), LV-ACE (S=1.0±0.1; M4=1.9±0.1; M6=4.5±1.1*), RV-ET-1 (S=1.0±0.1; M4=0.7±0.1*; M6=3.2±0.8*†), LV-ET-1 (S=1.0±0.2; M4=0.9±0.1; M6=6.8±2.0*†), RV-BNP (S=1.0±0.3; M4=8.2±2.3*; M6=11.6±1.9*†), but not of LV-BNP or RV and LV Agtg, A-synt, chymase and IGF-1. RV mRNA levels were linearly related (p<0.01) with those of the LV, both for ACE (r=+0.88) and ET-1 (r=+0.71). The present study showed that LV dysfunction in a model of selective RV overload is accompanied by biventricular activation of regulatory (ACE and ET-1) systems, while counter-regulatory BNP is selectively activated in the RV. These findings might add to the understanding of the relative importance of load and autocrine/paracrine activation in the progression to heart failure.

Language: English

Type (Professor's evaluation): Scientific

Notes: 54th Annual Scientific Session of the American-College-of-Cardiology, published in Journal, American College of Cardiology. 2004; Vol.43(Suppl.A):456A-457A.