BackgroundMetabolic syndrome is characterized by the association of 3 or more risk factors, including: abdominal obesity associated with an excess of abdominal fat, insulin resistance, type 2 diabetes, dyslipidemia and hypertension. Moreover, the prevalence of hypertension and metabolic dysfunctions sharply increases after the menopause. However, the mechanisms involved in these changes are not well understood. Thus, the aim of this study was to assess the effects of fructose overload on cardiovascular autonomic modulation, inflammation and cardiac oxidative stress in an experimental model of hypertension and menopause.MethodsFemale SHR rats were divided into (n = 8/group): hypertensive (H), hypertensive ovariectomized (HO) and hypertensive ovariectomized undergoing fructose overload (100 g/L in drinking water) (FHO). Arterial pressure (AP) signals were directly recorded. Cardiac autonomic modulation was evaluated by spectral analysis. Oxidative stress was evaluated in cardiac tissue.ResultsAP was higher in the FHO group when compared to the other groups. Fructose overload promoted an increase in body and fat weight, triglyceride concentration and a reduction in insulin sensitivity. IL-10 was reduced in the FHO group when compared to the H group. TNF-α was higher in the FHO when compared to all other groups. Lipoperoxidation was higher and glutathione redox balance was reduced in the FHO group when compared to other groups, an indication of increased oxidative stress. A negative correlation was found between IL-10 and adipose tissue.ConclusionFructose overload promoted an impairment in cardiac autonomic modulation associated with inflammation and oxidative stress in hypertensive rats undergoing ovarian hormone deprivation.

Diabetes mellitus (DM) is characterised by alterations in the intrarenal renin-angiotensin system (RAS). Insulin treatment may reverse these changes by an unknown mechanism.We aimed to verify the association between somatic ACE with 136 kDa (sACE) and N-domain ACE with 69 kDa (nACE) from Wistar (W) rat tissue with DM.Three groups were studied: control (CT), insulin treated diabetic (DT) and untreated (D). ACE activity was determined using Hippuryl-His-Leu and Z-Phe-His-Leu as substrates. In D group, urine ACE activity increased for both substrates when compared with CT and DT, despite the decreased activity of renal tissues. Immunostaining of renal tissue demonstrated that ACE is more strongly expressed in the proximaltubule of D than in the same nephron portion in the other groups.Angiotensin (Ang) 1-7 and Ang II are less expressed in DT group when compared with CT and D. Ang II levels decreased in the D and DT groups showed when compared to the control. Ang 1-7 was detected in all studied groups with low levels in DT.The modulation of angiotensin peptides suggests that sACE, nACE,ACE 2 and NEP could have important functions in renal RAS regulation through a counter-regulatory mechanism to protect the kidney in diabetes mellitus.

The cardiovascular autonomic imbalance in patients after myocardial infarction (MI) provides a significant increase in mortality rate, and seems to precede metabolic, hormonal, and immunological changes. Moreover, the reduction in the parasympathetic function has been associated with inflammatory response in different pathological conditions. Over the years, most of the studies have indicated the exercise training (ET) as an important nonpharmacological tool in the management of autonomic dysfunction and reduction in inflammatory profile after a myocardial infarction. In this work, we reviewed the effects of ET on autonomic imbalance after MI, and its consequences, particularly, in the post-MI inflammatory profile. Clinical and experimental evidence regarding relationship between alterations in autonomic regulation and local or systemic inflammation response after MI were also discussed.

These results indicate that exercise training in ovariectomized rats submitted to myocardial infarction improves resting hemodynamic status and reflex control of the circulation, which may be due to an increase in the vagal component. This suggests a homeostatic role for exercise training in reducing the autonomic impairment of myocardial infarction in postmenopausal women.

In 2016, cardiovascular disease remains the first cause of mortality worldwide [1]. Coronary artery disease, which is the most important precursor of myocardial infarction (MI), is the main component of total cardiovascular mortality, being responsible for approximately seven million of deaths [1]. In approximately 20% of infarcted patients, MI is recurrent in the first year after the event [2]. Moreover, among cardiovascular disease, coronary artery disease accounts for the most increased index of life years lost due to morbidity and/or mortality [1]. Sedentarism highly contributes to cardiovascular disease burden, especially for coronary artery disease, and is also one of the MI risk factors [3]. For many years, it was recommended to avoid physical activity after a cardiovascular event; nowadays, it is a consensus that exercise training (ET) should be part of cardiac rehabilitation programs. There is increasing evidence confirming that, when adequately prescribed and supervised, ET after MI can prevent future complications and increase the quality of life and longevity of infarcted patients [4, 5]. ET after MI follows international specialized guidelines; however, there are different protocols adopted by several societies worldwide in cardiac rehabilitation [6], and there is still lack of information on which type and regimen of exercise may be the ideal after MI, as well as how these exercises act to promote beneficial effects to cardiovascular and other organic systems. Thus, experimental studies are important contributors to elicit mechanisms behind clinical results, and to test and compare different ET protocols. Therefore, exercise prescription can be optimized, individualized, and safely practiced by patients. In this chapter, we present a brief review of MI pathophysiology followed by an updated discussion of the most relevant discoveries regarding ET and MI in basic science.