Prostanoids counterbalance the synergism between endothelin-1 and angiotensin II in mesenteric veins of trained rats

Abstract

Exercise-induced adaptations of the modulating mechanisms that influence the angiotensin (Ang II) responses assume different features depending on the venous bed. In femoral veins, exercise mobilizes vasodilator prostanoids to cooperate with NO in order to maintain reduced Ang II responses. On the other hand, exercise's influence on the Ang II responses in veins that drain blood from the mesenteric region has been poorly described. Therefore, the present study aimed to identify the effects of a single bout of exercise, as well as exercise training, on the Ang II responses in mesenteric veins. The present study also aimed to investigate the involvement of prostanoids, NO and ET-1 in eventual exercise-induced modifications in these veins. To this end, mesenteric veins taken from resting-sedentary, exercised-sedentary, resting-trained and exercised-trained animals were studied in organ baths. In addition, the mRNA expression of prepro-endothelin-1 (ppET-1), as well as that of the ET and ET receptors, were quantified by real-time PCR in these veins. The results show that, either in absence or in presence of L-NAME, the Ang II responses were not different between groups. In the presence of indomethacin, higher Ang II responses were observed in the resting-trained animals than in the resting-sedentary animals. This difference, however, disappeared when L-NAME, BQ-123 or BQ-788 were added during incubation. In addition, no differences in ppET-1, ET or ET mRNA expression were observed between groups. Furthermore, in the presence of PD123,319, the Ang II responses in the exercised-sedentary animals were higher than those in the resting-sedentary animals. In conclusion, exercise training mobilizes endothelin-1 (ET-1) to reinforce the Ang II-induced responses mainly through ET activation. On the other hand, vasodilator prostanoids are mobilized to act in parallel with NO in order to counterbalance the Ang II responses that have been potentiated by ET-1 in these trained animals.

Exercise training attenuates angiotensin II‐induced vasoconstriction in the aorta of normotensive but not hypertensive rats

“…These adaptations generally involve improved endothelial function (de Moraes, Davel, Rossoni, Antunes, & Zanesco, 2008; Guizoni et al., 2016; Husain et al., 2006). Other studies found that the actions of the effector peptides of RAAS on blood vessels can also be modulated as a consequence of exercise (Chies et al., 2003, 2017; Maeda, Iemitsu, Jesmin, & Miyauchi, 2005; Park et al., 2012). Nevertheless, studies examining the effects of exercise on Ang II‐induced vasoconstriction in aortas of 2K1C animals are scarce in the literature, although this is one of the most used experimental models employed to evaluate the endothelial mechanisms that modulate vascular tonus.…”

“…On the other hand, Ang II‐induced vasoconstriction is strictly modulated by endothelium‐derived mediators. Nitric oxide (NO), prostanoids and hyperpolarizing substances produced by the endothelium may act in isolation or in combination to modulate the vascular responses to Ang II (Chies et al., 2017; Chies, Rossignoli, Baptista, de Lábio, & Payão, 2013; da Silva, de Souza Rossignoli, Carrillo‐Sepúlveda, Barreto‐Chaves, & Chies, 2011; Tirapelli et al., 2005). Thus, modifications in the endothelial functioning, accompanied or not by changes in the smooth muscle cells or the extracellular matrix, may lead to hypertension and/or contribute to its maintenance.…”

“…In addition, most of the studies addressing exercise‐induced modifications in vasoconstrictor responses to Ang II in normotensive animals employ exercise training protocols (Chies et al., 2003; Park et al., 2012). However, Ang II‐induced vasoconstrictor responses may also be influenced by acute exercise (Chies et al., 2013, 2017; Izawa et al., 1995).…”