Exercise training improves ambulatory blood pressure but not arterial stiffness in heart transplant recipients

BACKGROUND: Hypertension is the most prevalent comorbidity after heart transplantation (HT). Exercise training (ET) is widely recommended as a key non-pharmacologic intervention for the prevention and management of hypertension, but its effects on ambulatory blood pressure (ABP) and some mechanisms involved in the pathophysiology of hypertension have not been studied in this population. The primary purpose of this study was to investigate the effects of ET on ABP and arterial stiffness of HT recipients.METHODS: 40 HT patients, randomized to ET (n = 31) or a control group (n = 9) underwent a maximal graded exercise test, 24-hour ABP monitoring, and carotid-femoral pulse wave velocity (PWV) assessment before the intervention and at a 12-week follow-up assessment. The ET program was performed thrice-weekly and consisted primarily of endurance exercise (40 minutes) at similar to 70% of maximum oxygen uptake (Vo(2MAX))RESULTS: The ET group had reduced 24-hour (4.0 +/- 1.4 mm Hg, p < 0.01) and daytime (4.8 +/- 1.6 mm Hg, p < 0.01) systolic ABP, and 24-hour (7.0 +/- 1.4 mm Hg, p < 0.001) daytime (7.5 +/- 1.6 mm Hg, p < 0.001) and nighttime (5.9 +/- 1.5 mm Hg, p < 0.001) diastolic ABP after the intervention. The ET group also had improved Vo(2MAX) (9.7% +/- 2.6%, p < 0.001) after the intervention. However, PWV did not change after ET. No variable was changed in the control group after the intervention.CONCLUSIONS: The 12-week ET program was effective for reducing ABP but not PWV in heart transplant recipients. This result suggesfs that endurance ET may be a tool to counteract hypertension in this high-risk population. (C) 2015 International Society for Heart and Lung Transplantation. All rights reserved.

Disfunção arterial como possível mecanismo de agressão cardíaca em pacientes com diabetes mellitus tipo II. Estudo Doppler-ecocardiográfico

OBJETIVO: Avaliar a estrutura e função do ventrículo esquerdo (VE) e a rigidez arterial em portadores de diabetes mellitus tipo II. MÉTODOS: Foram estudados 13 doentes diabéticos de ambos os sexos (55±8 anos) sem outras doenças. A estrutura e função do VE foram avaliadas por meio de ecodopplercardiografia associada à monitorização não invasiva da pressão arterial (PA). Os resultados foram comparados aos obtidos em grupo de indivíduos normais de mesma idade (n=12). RESULTADOS: Não houve diferenças entre os grupos quanto a PA diastólica, dimensões das câmaras esquerdas e índices de função sistólica e diastólica. Os pacientes diabéticos apresentaram índice de massa do VE (101±10 vs 80±14g/m²; p<0,001) e índice de rigidez arterial sistêmica (0,86±0,26 vs 0,69±0,19mmHg/mL; p<0,05) significantemente maiores que os controles. CONCLUSÃO: O diabetes mellitus está associado a aumento da rigidez arterial sistêmica e esse fator poderia contribuir para seus efeitos adversos sobre o VE.

Associação entre o condicionamento físico e rigidez arterial em pacientes com doença renal crônica

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Inflammation, Diabetes, and Chronic Kidney Disease: Role of Aerobic Capacity

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Vascular effects of long-term propranolol administration after chronic nitric oxide blockade

Long-term propranolol treatment reduces arterial blood pressure in hypertensive individuals mainly by reducing peripheral vascular resistance, but mechanisms underlying their vasodilatory effect remain poorly investigated. This study aimed to investigate whether long-term propranolol administration ameliorates the impairment of relaxing responses of aorta and mesenteric artery from rats made hypertensive by chronic nitric oxide (NO) deficiency, and underlying mechanisms mediating this phenomenon. Male Wistar rats were treated with N-omega-Nitro-L-arginine methyl ester (L-NAME; 20 mg/rat/day) for four weeks. DL-Propranolol (30 mg/rat/day) was given concomitantly to L-NAME in the drinking water. Treatment with L-NAME markedly increased blood pressure, an effect largely attenuated by DL-propranolol. In phenylephrine-precontracted aortic rings, the reduction of relaxing responses for acetylcholine (0.001-10 mu M) in L-NAME group was not modified by DL-propranolol, whereas in mesenteric rings the impairment of acetylcholine-induced relaxation by L-NAME was significantly attenuated by DL-propranolol. In mesenteric rings precontracted with KCl (80 MM), DL-propranolol failed to attenuate the impairment of acetylcholine-induced relaxation by L-NAME. The contractile responses to extracellular CaCl2 (1-10 mM) were increased in L-NAME group, and co-treatment with DL-propranolol reduced this response in both preparations in most Ca2+ concentrations used. The NO2/NO3 plasma levels and superoxide dismutase (SOD) activity were reduced in L-NAME-treated rats, both of which were significantly prevented by DL-propranolol. In conclusion, propranolol-induced amplification of the relaxation to acetylcholine in mesenteric arteries from L-NAME-treated rats is sensitive to depolarization. Additional mechanisms involving blockade of Ca2+ entry in the vascular smooth muscle and increase in NO bioavailability contributes to beneficial effects of long-term propranolol treatment. (C) 2007 Elsevier B.V. All rights reserved.

Morphologic and biomechanical changes of thoracic and abdominal aorta in a rat model of cigarette smoke exposure

Background: Smoking is the most relevant environmental factor that affects the development of aortic aneurysm. Smokers have elevated levels of elastase activity in the arterial wall, which leads to weakening of the aorta. The aim of this study was to verify whether cigarette smoke exposure itself is capable of altering the aortic wall. Methods: Forty-eight Wistar rats were divided into 2-, 4-, and 6-month experimental periods and into 2 groups: smokers (submitted to smoke exposure at a rate of 40 cigarettes/day) and nonsmokers. At the end of the experimental periods, the aortas were removed and cross-sectioned to obtain histologic specimens for light microscopic and morphometric analyses. The remaining longitudinal segments were stretched to rupture and mechanical parameters were determined. Results: A degenerative process (i.e., a reduction in elastic fibers, the loss of lamellar arrangement, and a reduction of smooth muscle cells) was observed, and this effect was proportional in intensity to the period of tobacco exposure. We observed a progressive reduction in the yield point of the thoracic aorta over time (P < 0.05). There was a decrease in stiffness (P < 0.05) and in failure load (P < 0.05) at 6 months in the abdominal aorta of rats in the smoking group. Conclusions: Chronic exposure to tobacco smoke can affect the mechanical properties of the aorta and can also provoke substantial structural changes of the arterial wall. © 2013 Elsevier Inc. All rights reserved.

Avaliação vascular não invasiva (NIVA) em gestantes com diabete gestacional e com hiperglicemia leve utilizando o SphygmoCor

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Efeito do treinamento físico na qualidade de vida, capacidade funcional e fatores de risco cardiovascular nos portadores de doença renal crônica em tratamento conservador

Pós-graduação em Fisiopatologia em Clínica Médica - FMB

Rastreamento e detecção precose de doença aterosclerítica em pacientes com HIV positivo

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

High-intensity interval training and hypertension: Maximizing the benefits of exercise?

Essential arterial hypertension is the most common risk factor for cardiovascular morbidity and mortality. Regular exercise is a well-established intervention for the prevention and treatment of hypertension. Continuous moderate-intensity exercise training (CMT) that can be sustained for 30 min or more has been traditionally recommended for hypertension prevention and treatment. On the other hand, several studies have shown that high-intensity interval training (HIT), which consists of several bouts of high-intensity exercise (~85% to 95% of HRMAX and/or VO2MAX lasting 1 to 4 min interspersed with intervals of rest or active recovery, is superior to CMT for improving cardiorespiratory fitness, endothelial function and its markers, insulin sensitivity, markers of sympathetic activity and arterial stiffness in hypertensive and normotensive at high familial risk for hypertension subjects. This compelling evidence suggesting larger beneficial effects of HIT for several factors involved in the pathophysiology of hypertension raises the hypothesis that HIT may be more effective for preventing and controlling hypertension.

Influência do treinamento aeróbico intradialítico no fluxo sanguíneo cerebral e o reflexo sobre a função cognitiva e qualidade de vida em pacientes renais crônicos

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Central blockade of nitric oxide synthesis reduces moxonidine-induced hypotension

1 Nitric oxide (NO) and alpha(2)-adrenoceptor and imidazoline agonists such as moxonidine may act centrally to inhibit sympathetic activity and decrease arterial pressure.2 In the present study, we investigated the effects of pretreatment with L-NAME ( NO synthesis inhibitor), injected into the 4th ventricle (4th V) or intravenously (i.v.), on the hypotension, bradycardia and vasodilatation induced by moxonidine injected into the 4th V in normotensive rats.3 Male Wistar rats with a stainless steel cannula implanted into the 4th V and anaesthetized with urethane were used. Blood flows were recorded by use of miniature pulsed Doppler flow probes implanted around the renal, superior mesenteric and low abdominal aorta.4 Moxonidine (20 nmol), injected into the 4th V, reduced the mean arterial pressure (-42+/-3 mmHg), heart rate (-22+/-7 bpm) and renal (-62+/-15%), mesenteric (-41+/-8%) and hindquarter (-50+/-8%) vascular resistances.5 Pretreatment with L-NAME (10 nmol into the 4th V) almost abolished central moxonidine-induced hypotension (-10+/-3 mmHg) and renal (-10+/-4%), mesenteric (-11+/-4%) and hindquarter (-13+/-6%) vascular resistance reduction, but did not affect the bradycardia (-18+/-8 bpm).6 the results indicate that central NO mechanisms are involved in the vasodilatation and hypotension, but not in the bradycardia, induced by central moxonidine in normotensive rats. British Journal of Pharmacology (2004).

Lateral hypothalamus lesions influences water and salt intake, and sodium and urine excretion, and arterial blood pressure induced by L-NAME and FK 409 injections into median preoptic nucleus in conscious rats

Male Holtzman rats weighting 200-250 g were anesthetized with zoletil 50 mg/Kg (tiletamine chloridrate 125,0 mg and zolazepan chloridrate 125,0 mg) into quadriceps muscle and submitted an electrolytic lesion of the lateral hypothalamus (LH) and a stainless steel cannula was implanted into their median preoptic nucleus (MnPO). We investigated the effects of the injection into the (MnPO) of FK 409 (20 mug/0.5 mul), a nitric oxide (NO) donor, and N-W-nitro-L-arginine methyl ester (L-NAME) 40 mug/0.5 mul, a nitric oxide synthase inhibitor (NOSI), on the water and sodium appetite and the natriuretic, diuretic and cardiovascular effects induced by injection of L-NAME and FK 409 injected into MnPO in rats with LH lesions. Controls were injected with a similar volume of 0.15 M NaCl. L-NAME injected into MnPO produced an increase in water and sodium intake and in sodium and urine excretion and increase de mean arterial pressure (MAP). FK 409 injected into MnPO did not produce any change in the hydro electrolytic and cardiovascular parameters in LH-sham and lesioned rats. FK 409 injected before L-NAME attenuated its effects. These data show that electrolytic lesion of the LH reduces fluid and sodium intake as well as sodium and urine excretion, and the pressor effect induced by L-NAME. LH involvement with NO of the MnPO excitatory and inhibitory mechanisms related to water and sodium intake, sodium excretion and cardiovascular control is suggested. (C) 2004 Elsevier B.V. All rights reserved.