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Acute and chronic effects of human urocortin-2 therapy on intracellular calcium homeostasis in right heart failure induced by pulmonary artery hypertension
Session:
CO - Prémio Jovem Investigador (Investigação Básica)
Speaker:
Rui Adão
Congress:
CPC 2019
Topic:
O. Basic Science
Theme:
36. Basic Science
Subtheme:
36.2 Basic Science - Cardiac Biology and Physiology
Session Type:
Comunicações Orais
FP Number:
---
Authors:
Rui Adão; Simon C. Kraler; Mahmoud Abdellatif; Senka Ljubojevic-Holzer; Adelino Leite-Moreira; Simon Sedej; Carmen Brás-Silva
Abstract
<p>Background: Disturbances in intracellular Ca2+ homeostasis contribute to the right ventricular dysfunction in pulmonary arterial hypertension. Human urocortin-2 (hUcn-2) therapy attenuates pulmonary arterial hypertension and right ventricular dysfunction in rats with monocrotaline-induced pulmonary arterial hypertension.</p> <p>Purpose: Here we tested whether beneficial effects of hUcn-2 are associated with improved cellular Ca2+ handling in the pulmonary arterial hypertension-induced right ventricular failure.</p> <p>Methods: Wistar rats were injected with monocrotaline (60mg/kg) or saline (control) and after 14 days they were subjected to hUcn-2 treatment (5µg/kg, bi-daily, i.p.) or vehicle for 10 days. After the treatment, intracellular Ca2+ transients were recorded in isolated right ventricle cardiomyocytes using confocal Ca2+ imaging (Fluo-4/AM, 1Hz). In acute experiments, cells were perfused for 15 min with hUcn-2 (100nM) in the absence or presence of the PKA inhibitor H89 (2µM) or CaMKII inhibitor KN93 (1µM) and transients were acquired in 5 min intervals. Sarcoplasmatic reticulum Ca2+ load was assessed upon rapid caffeine surge (30mM). In another set of experiments, right ventricle was dissected and immediately frozen in liquid nitrogen and stored at -80°C until mechanical measurements on isolated skinned cardiomyocytes were performed.</p> <p>Results: We found that acute administration of hUcn-2 transiently and incompletely improved intracellular Ca2+ mishandling in right ventricular myocytes from monocrotaline-treated rats via stimulating both protein kinase A and Ca2+/calmodulin-dependent kinase II. However, chronic treatment with hUcn-2 failed to rescue intracellular Ca2+ handling defects, but reduced the active tension development and myofilament sensitivity to Ca2+ in isolated skinned right ventricular myocytes from rats with monocrotaline-induced pulmonary arterial hypertension.</p> <p>Conclusions: Our study suggests that hUcn-2 chronic therapy attenuates right ventricular systolic and diastolic dysfunction in monocrotaline-induced pulmonary arterial hypertension, at least in part, through improving cardiomyocyte-autonomous Ca2+ modulation.</p>
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