Patrick Wander Endlich

Effects of Chronic Swimming Training and Oestrogen Therapy on Coronary Vascular Reactivity and Expression of Antioxidant Enzymes in Ovariectomized Rats

The aim of this study was to evaluate the effects of swimming training (SW) and oestrogen replacement therapy (ERT) on coronary vascular reactivity and the expression of antioxidant enzymes in ovariectomized rats. Animals were randomly assigned to one of five groups: sham (SH), ovariectomized (OVX), ovariectomized with E2 (OE2), ovariectomized with exercise (OSW), and ovariectomized with E2 plus exercise (OE2+SW). The SW protocol (5×/week, 60 min/day) and/or ERT were conducted for 8 weeks; the vasodilator response to bradykinin was analysed (Langendorff Method), and the expression of antioxidant enzymes (SOD-1 and 2, catalase) and eNOS and iNOS were evaluated by Western blotting. SW and ERT improved the vasodilator response to the highest dose of bradykinin (1000 ng). However, in the OSW group, this response was improved at 100, 300 and 1000 ng when compared to OVX (p<0,05). The SOD-1 expression was increased in all treated/trained groups compared to the OVX group (p<0,05), and catalase expression increased in the OSW group only. In the trained group, eNOS increased vs. OE2, and iNOS decreased vs. SHAM (p<0,05). SW may represent an alternative to ERT by improving coronary vasodilation, most likely by increasing antioxidant enzyme and eNOS expression and augmenting NO bioavailability.

Efeitos agudos do alongamento estático no desempenho da força dinâmica em homens jovens

BACKGROUND: Muscular stretching is frequently used in sports practice with the aim to increase muscular flexibility and joint range of motion as well as to reduce injury risks and to improve athletic performance. AIM: To analyze the acute effect of stretching with different times in the dynamic strength performance of lower and upper extremities in young men. METHODS: The sample was composed by 14 healthy male volunteers aged 23 ± 2 years, weight of 84 ± 10 Kg , height of 178 ± 7 cm, BMI of 26 ± 2 Kg/m2 and body fat of 11 ± 3 %. They were evaluated in a 10-maximum repetition test (10-RM) in three situations: no stretching (NS); after an 8-minute session of static stretching followed by specific warm-up (SS-8); and after 16-minute and specific warm-up before 10 RM test (SS-16). Tests were performed in bench press and 45o leg press exercises, and stretching was selected as to reach the musculature required in these exercises. RESULTS: There was significant reduction (p<0.001) of dynamic muscular strength of upper extremities in comparison to NS with SS-16 (9.2%) and between SS-8 (4.2%) and SS-16 (14.3%) to lower extremities. This difference was found in all tested conditions. CONCLUSION: Static stretching sessions before activities involving dynamic strength are able to negatively change performance in longer stretching periods.

Involvement of the atrial natriuretic peptide in the reduction of arterial pressure induced by swimming but not by running training in hypertensive rats.

The aim of this study was to compare, under resting conditions, the influence of chronic training in swimming or running on mean arterial pressure (MAP) and the involvement of the natriuretic peptide system in this response. Two-month-old male spontaneously hypertensive rats (SHR) were divided into three groups-sedentary (SD), swimming (SW) and running (RN)-and were trained for eight weeks under regimens of similar intensities. Atria tissue and plasma atrial natriuretic peptide (ANP) concentrations were measured by radioimmunoassay. ANP mRNA levels in the right and left atria as well as the natriuretic peptide receptors (NPR), NPR-A and NPR-C, mRNA levels in the kidney were determined by real-time PCR. Autoradiography was used to quantify NPR-A and NPR-C in mesenteric adipose tissue. Both training modalities, swimming and running, reduced the mean arterial pressure (MAP) of SHR. Swimming, but not running, training increased plasma levels of ANP compared to the sedentary group (P<0.05). Expression of ANP mRNA in the left atrium was reduced in the RN compared to the SD group (P<0.05). Expression of NPR-A and NPR-C in the kidneys of the SW group decreased significantly (P<0.05) compared to the SD group. Although swimming increased (125)I-ANP binding to mesenteric adipose tissue, displacement by c-ANF was reduced, indicating a reduction of NPR-C. These results suggest that the MAP reduction induced by exercise in SHR differs in its mechanisms between the training modalities, as evidenced by the finding that increased levels of ANP were only observed after the swimming regimen.

Exercise modulates the aortic renin-angiotensin system independently of estrogen therapy in ovariectomized hypertensive rats.

HIGHLIGHTSSome components of the renin‐angiotensin system (RAS) are altered under conditions of estrogen deficiency and hypertension.Exercise training reverses the detrimental effects of ovariectomy on the aortic reactivity to ANG II and ANG‐(1–7) in hypertensive rats.Exercise training modulates RAS independently of estrogen therapy, protecting the hypertensive postmenopausal women against CVD. ABSTRACT The renin‐angiotensin‐system is an important component of cardiovascular control and is up‐regulated under various conditions, including hypertension and menopause. The aim of this study was to evaluate the effects of swimming training and estrogen therapy (ET) on angiotensin‐II (ANG II)‐induced vasoconstriction and angiotensin‐(1–7) [ANG‐(1–7)]‐induced vasorelaxation in aortic rings from ovariectomized spontaneously hypertensive rats. Animals were divided into Sham (SH), Ovariectomized (OVX), Ovariectomized treated with E2 (OE2), Ovariectomized plus swimming (OSW) and Ovariectomized treated with E2 plus swimming (OE2 + SW) groups. ET entailed the administration of 5 &mgr;g of 17&bgr;‐Estradiol three times per week. Swimming was undertaken for sixty minutes each day, five times per week. Both, training and ET were initiated seven days following ovariectomy. Forty‐eight hours after the last treatment or training session, the animals’ systolic blood pressures were measured, and blood samples were collected to measure plasma ANG II and ANG‐(1–7) levels via radioimmunoassay. In aortic rings, the vascular reactivity to ANG II and ANG‐(1–7) was assessed. Expression of ANG‐(1–7) in aortic wall was analyzed by immunohistochemistry. The results showed that both exercise and ET increased plasma ANG II levels despite attenuating systolic blood pressure. Ovariectomy increased constrictor responses to ANG II and decreased dilatory responses to ANG‐(1–7), which were reversed by swimming independently of ET. Moreover, it was observed an apparent increase in ANG‐(1–7) content in the aorta of the groups subjected to training and ET. Exercise training may play a cardioprotective role independently of ET and may be an alternative to ET in hypertensive postmenopausal women.

Swimming training prevents fat deposition and decreases angiotensin II-induced coronary vasoconstriction in ovariectomized rats.

We investigated the effects of chronic swimming training (ST) on the deposition of abdominal fat and vasoconstriction in response to angiotensin II (ANG II) in the coronary arterial bed of estrogen deficient rats. Twenty-eight 3-month old Wistar female rats were divided into 4 groups: sedentary sham (SS), sedentary-ovariectomized (SO), swimming-trained sham (STS) and swimming-trained ovariectomized (STO). ST protocol consisted of a continuous 60-min session, with a 5% BW load attached to the tail, completed 5 days/week for 8-weeks. The retroperitoneal, parametrial, perirenal and inguinal fat pads were measured. The intrinsic heart rate (IHR), coronary perfusion pressure (CPP) and a concentration-response curve to ANG II in the coronary bed was constructed using the Langendorff preparation. Ovariectomy (OVX) significantly reduced 17-β-estradiol plasma levels in SO and STO groups (p<0.05). The STO group had a significantly reduced retroperitoneal and parametrial fat pad compared with the SO group (p<0.05). IHR values were similar in all groups; however, baseline CPP was significantly reduced in the SO, STS and STO groups compared with the SS group (p<0.05). ANG II caused vasoconstriction in the coronary bed in a concentration-dependent manner. The SO group had an increased response to ANG II when compared with all other experimental groups (p<0.05), which was prevented by 8-weeks of ST in the STO group (p<0.05). OVX increased ANG II-induced vasoconstriction in the coronary vascular bed and abdominal fat pad deposition. Eight weeks of swimming training improved these vasoconstrictor effects and decreased abdominal fat deposition in ovariectomized rats.

Uso crônico de decanoato de nandrolona como fator de risco para hipertensão arterial pulmonar em ratos Wistar

INTRODUCTION: The unsystematic use of anabolic steroids, synthetic analogs of testosterone, implies enhanced cardiovascular risk and cardiac hypertrophy. Thus, increased right ventricular mass corrected by the body weight (e.g.right ventricular hypertrophy -RVH) could raise the risk for development of pulmonary arterial hypertension (PAH). OBJECTIVES: to examine the effects of long-term chronic treatment with nandrolone decanoate on the RVH and its relationship with PAH in rats. METHODS: 16 three-month Wistar male rats were treated with nandrolone decanoate (6.0 mg/kg-1 body weight; DECA, n=8) or control vehicle (CONT, n=8). The drug and vehicle were administered by a single injection in the femoral muscle once a week for 4 weeks. After the treatment, rats were anesthetized with chloral hydrate (4.0mL/kg-1, ip), and catheterized in the femoral artery. Twenty-four hours later, mean arterial pressure (MAP) and heart ratio were measured. The heart, kidneys and liver were removed, weighed and the rates of hypertrophy (RH) were measured, which were calculated by the ratio of the weight of the organs by the body weight (mg.g-1). RESULTS: DECA treatment increased body weight (338 ± 6g; p <0.01) vs. CONT (315 ± 5g). This treatment had no effect on the MAP (CONT, 110±4mmHg, DECA, 113 ± 4mmHg). However, the bradycardia of animals treated with DECA (321 ± 13bpm, p<0.01) was significantly lower than that of CONT (368 ±11bpm). RH increased (p <0.01) the cardiac ventricles and the kidneys, but not in the liver. The correlation between the RVH and MAP in DECA showed positive and higher Pearsons coefficient (r2 = 0.4013) vs CONT (r2 = 0.0003). CONCLUSIONS: It was concluded that chronic nandrolone decanoate treatment induced bradycardia and RVH, which suggests increased risk for PAH.

Neuronal nitric oxide synthase-derived hydrogen peroxide effect in grafts used in human coronary bypass surgery

Recently, H2O2 has been identified as the endothelium-dependent hyperpolarizing factor (EDHF), which mediates flow-induced dilation in human coronary arteries. Neuronal nitric oxide synthase (nNOS) is expressed in the cardiovascular system and, besides NO, generates H2O2 The role of nNOS-derived H2O2 in human vessels is so far unknown. The present study was aimed at investigating the relevance of nNOS/H2O2 signaling in the human internal mammary artery (IMA) and saphenous vein (SV), the major conduits used in coronary artery bypass grafting. In the IMA, but not in the SV, ACh (acetylcholine)-induced vasodilatation was decreased by selective nNOS inhibition with TRIM or Inhibitor 1, and by catalase, which specifically decomposes H2O2 Superoxide dismutase (SOD), which generates H2O2 from superoxide, decreased the vasodilator effect of ACh on SV. In the IMA, SOD diminished phenylephrine-induced contraction in endothelium-containing, but not in endothelium-denuded vessels. Importantly, while exogenous H2O2 produced vasodilatation in IMA, it constricted SV. ACh increased H2O2 production in both sets of vessels. In the IMA, the increase in H2O2 was inhibited by catalase and nNOS blockade. In SV, H2O2 production was abolished by catalase and reduced by nNOS inhibition. Immunofluorescence experiments showed the presence of nNOS in the vascular endothelium and smooth muscle cells of both the IMA and SV. Together, our results clearly show that H2O2 induced endothelium-dependent vascular relaxation in the IMA, whereas, in the SV, H2O2 was a vasoconstrictor. Thus, H2O2 produced in the coronary circulation may contribute to the susceptibility to accelerated atherosclerosis and progressive failure of the SV used as autogenous graft in coronary bypass surgery.