Manuel Varas

Enalapril Attenuates Downregulation of Angiotensin-Converting Enzyme 2 in the Late Phase of Ventricular Dysfunction in Myocardial Infarcted Rat

The early and long-term effects of coronary artery ligation on the plasma and left ventricular angiotensin-converting enzyme (ACE and ACE2) activities, ACE and ACE2 mRNA levels, circulating angiotensin (Ang) levels [Ang I, Ang-(1-7), Ang-(1-9), and Ang II], and cardiac function were evaluated 1 and 8 weeks after experimental myocardial infarction in adult Sprague Dawley rats. Sham-operated rats were used as controls. Coronary artery ligation caused myocardial infarction, hypertrophy, and dysfunction 8 weeks after surgery. At week 1, circulating Ang II and Ang-(1-9) levels as well as left ventricular and plasma ACE and ACE2 activities increased in myocardial-infarcted rats as compared with controls. At 8 weeks post-myocardial infarction, circulating ACE activity, ACE mRNA levels, and Ang II levels remained higher, but plasma and left ventricular ACE2 activities and mRNA levels and circulating levels of Ang-(1-9) were lower than in controls. No changes in plasma Ang-(1-7) levels were observed at any time. Enalapril prevented cardiac hypertrophy and dysfunction as well as the changes in left ventricular ACE, left ventricular and plasmatic ACE2, and circulating levels of Ang II and Ang-(1-9) after 8 weeks postinfarction. Thus, the decrease in ACE2 expression and activity and circulating Ang-(1-9) levels in late ventricular dysfunction post-myocardial infarction were prevented with enalapril. These findings suggest that in this second arm of the renin-angiotensin system, ACE2 may act through Ang-(1-9), rather than Ang-(1-7), as a counterregulator of the first arm, where ACE catalyzes the formation of Ang II.

Copper, copper mine tailings and their effect on marine algae in Northern Chile

Results are presented of a long-term research programme on the effect of copper contamination on biota in Chilean coastal waters. In spite of the magnitude of the copper mining tailings that affected Caleta Palito and surroundings in northern Chile, the effects on the intertidal assemblages remain restricted to a small geographic area. Even within the affected area, the effects are not homogeneous and there is evidence of active recovery in biological diversity in recent few years. Experimental evidence suggests that the current low algal diversity and abundance is strongly influenced by herbivory, although chronic effects of the discharges cannot be ruled out. Cellular changes in Enteromorpha compressa from the impacted area were characterised by abnormal granules in the cytoplasm, though these granules did not contain detectable levels of copper or other heavy metals.

The rocky intertidal plankton trap RIPT2: A modified device

Abstract The paper describes a modification (RIPT2) of an earlier described, passive Rocky Intertidal Plankton Trap (RIPT1) to be used in exposed rocky shores. The trap is light, simple to build, easy to install, and inexpensive. It aims to evaluate and integrate over time the mero- and holoplankton arriving to the rocky shore. A set of 3 RIPT2 and 3 RIPT1 traps were tested, over a period of 3 days, on an exposed horizontal rocky platform at El Eden, Antofagasta, Chile. RIPT-flowmeters permitted an approximation of the rate of water filtering, which was about 3 times greater (ranging from 1.48 to 1.69 m3 24 h−1) through the RIPT2 trap than the RIPT1 trap. Maximum water velocities on the intertidal platforms, determined with the use of an intertidal dynamometer, ranged between 1.64 and 3.28 m s−1. The RIPTs collected a total of 21–22 major plankton items belonging to 7–8 phyla. The individuals ranged between approximately 100 µm (bivalve larvae) and 2720 µm (Isopoda). The cumulative (over 72 h) number of planktonic organisms collected by RIPT2 was significantly greater than those collected by RIPT1 traps.

Rocky Intertidal Zonation Pattern in Antofagasta, Chile: Invasive Species and Shellfish Gathering

Background Biological invasions affecting rocky intertidal zonation patterns, yield information on species interactions. In the Bay of Antofagasta, northern Chile, the non-indigenous tunicate Pyura praeputialis, originally from Australia, has invaded (in the past century or so) and monopolized a major portion of the mid-intertidal rocky shore, displacing upshore the native mussel Perumytilus purpuratus. In Antofagasta the tunicate is subjected to intensive exploitation. Monitoring protocols show that in the past 10 years Antofagastas tunicate population has experienced a drastic decline, affecting the intertidal zonation pattern. Methodology/Principal Findings A 12.5 km of coastline, on the southern eastern shore of the Bay of Antofagasta, was studied. Eight sites were systematically (1993–1994) or sporadically (2003–2014) monitored for the seaward-shoreward expansion or reduction of the tunicate Pyura praeputialis, and native mussel and barnacle bands. A notable reduction in the mid-intertidal band of P. praeputialis and a seaward expansion of the mussel, Perumytilus purpuratus, and barnacle bands was observed. We suggest that the major cause for the decline in the tunicate is due to its intensive exploitation by rocky shore Pyura-gathers. The rate of extraction of tunicates by professional Pyura-gathers ranged between 256–740 tunicates hour−1. Between 2009–2014 the density of professional Pyura-gather ranged between 0.5–4.5 km−1 per low tide. Hence, 10 professional Pyura-gathers working 1 h for 10 low tides per month, during 6 months, will remove between 307–888 m2 of tunicates. A drastic decline in tunicate recruitment was observed and several P. praeputialis ecosystems services have been lost. Conclusion and Significance In Antofagasta, the continuous and intensive intertidal gathering of the invasive tunicate Pyura praeputialis, has caused a drastic reduction of its population modifying the zonation pattern. Thereby, native mussel Perumytilus purpuratus has regained its ecological center in the intertidal zone. We recorded a Pyura recruitment failure and loss of ecosystem services.

Menores niveles tisulares de la enzima convertidora de angiotensina I homologa (ECA-2) y angiotensina-(1-9) están asociados a mayor remodelamiento de la pared aórtica de ratas hipertensas

Antecedentes: Recientemente hemos propuesto en un modelo experimental de infarto al miocardio una significativa interregulacion entre los niveles de la enzima convertidora de angiotensina I (ECA) y su homologa (ECA-2), junto con que angiotensina (Ang)-(1-9) mas que Ang-(1-7) actuaria como un contrarregulador de Ang II. Sin embargo tal relacion no se ha investigado en el remodelado aortico hipertensivo. Objetivo: Determinar la expresion de ECA y ECA-2, los niveles de Angs I, II, (1-7) y (1-9) y los parametros de remodelado de la pared aortica de ratas hipertensas. Metodos: Ratas normotensas Lewis (n=18) fueron randomizadas a hipertension (HTA) por sobrecarga de presion (modelo Goldblatt, GB, 2 rinones-1 pinzado, n=9). Ratas pseudo-operadas se usaron como controles (S, n=9). A las 6 semanas post cirugia, se determino la masa cardiaca relativa (MCR) y la presion arterial sistolica (PAS). En la aorta toracica se determino el grosor de la tunica media (GTM), area de la TM (ATM), niveles de mRNA de ECA y ECA-2, factor de crecimiento transformante tipo s (TGF-s), inhibidor del activador de plasminogeno (PAI-1) y de la proteina quimioatractante de monocitos (MCP-1) por RT-PCR. La actividad y niveles proteicos de ECA y ECA-2 por fluorimetria y Western blot y los niveles de Angs I, II, (1-7) y (1-9) por HPLC y radioinmunoensayo. Resultados: La MCR y la PAS aumentaron significativamente (p ), MCP-1 (53%,) junto con mayor actividad (89%,), niveles proteicos de ECA (130%,) y Ang II (48%,). Esos efectos se asociaron a una significativa disminucion del mRNA, los niveles proteicos y actividad de ECA-2 (- 55%, -41%, y 54%, respectivamente) y a menores niveles aorticos (-25%,) de Ang- (1-9), sin diferencias en los niveles de ang-(1-7). Conclusion: Estos resultados fuertemente sugieren que en la hipertension arterial experimental, el remodelado de la pared aortica esta asociado a una interaccion entre ECA y ECA-2 y los niveles de Ang II y Ang-(1-9), pero no de Ang-(1-7).