These data indicate that the recognized role of resistance exercise in lowering the BP in hypertensive individuals [32] may work through a different mechanism and that ANP would be primarily involved in physical activities that were performed in the water. In Selleckchem Erastin fact, these data show that the recognized role of predominantly aerobic exercise in lowering blood pressure in hypertensive individuals [32] may work through different mechanisms, in which the ANP would be primarily involved in physical activities that were performed in the water. In a study conducted by Melo et al.,

ANP-knockout animals developed severe hypertension. A blockage of the autonomic nervous system with hexamethonium caused a decrease in blood pressure to levels that were similar to those of the control animals [23]. Another study that used an animal model that was characterized by high basal sympathetic tones, such as SHR, showed that the infusion of ANP promotes Rapamycin chemical structure a considerable hypotensive effect when compared to the control animals, with no change in cardiac output, intravascular volume, sodium, or water excretion [18]. These data show that ANP is an important mediator in the attenuation of cardiovascular sympathetic tone and, if tonically active, may be involved in the chronic

vasodilation mechanism. Thus, it becomes the most likely factor to explain the decrease in blood pressure induced by ANP in chronic conditions. This is an important finding because, to date, there is no evidence of the efficiency of the hormone on other mechanisms that regulate blood pressure, such as electrolyte balance [24]. Another hypothesis that can be considered is the role of ANG II in the secretion ANP. Exercise training decreases the sympathetic drive [4] and [35] to the heart and consequently decreases the local ANG II synthesis [31]. An earlier study

showed that ANG II produced in the heart decreases the secretion of ANP by the atria [27]. However, this hypothesis is unlikely because both modalities decrease the sympathetic drive and there was an increase in ANP levels in the SW group only. Finally, there is evidence that increased ID-8 cardiac and plasma BNP levels result in elevated plasma ANP levels in mice with deletion of NPR-A in the heart [15]. However, these alterations by BNP due to transient myocardial ischemia, like that which occurs during acute exercise, are inconclusive [10] and [47] and might not explain our data because we analyzed chronic conditions. Physiological behavior is different in an aquatic environment than in a terrestrial environment; thus, chronic swimming training decreased NPR-C expression in the kidney and mesenteric adipose tissue, resulting in increased plasma levels of its hormone, findings which were not found in chronic running training.