Suênia Karla Pacheco Porpino

Quercetin Improves Baroreflex Sensitivity in Spontaneously Hypertensive Rats

Quercetin is a well-known antioxidant. Here, we investigated the effects of treatment with quercetin on mean arterial pressure (MAP), heart rate (HR) and baroreflex sensitivity (BRS) in spontaneously hypertensive rats (SHR). SHR and their controls (WKY) were orally treated with quercetin (2, 10 or 25 mg/kg/day) or saline for seven days. On the 8th day, MAP and HR were recorded. BRS was tested using phenylephrine (8 mg/kg, i.v.) and sodium nitroprusside (25 mg/kg, i.v.). Oxidative stress was measured by tiobarbituric acid reactive species assay. The doses of 10 (n = 8) and 25 mg/kg (n = 8) were able to decrease the MAP in SHR (n = 9) (163 ± 4 and 156 ± 5 vs. 173 ± 6, respectively, p < 0.05) but not in WKY (117 ± 1 and 118 ± 2 vs. 113 ± 1, respectively, p < 0.05). The dose of 25 mg/kg/day increased the sensitivity of parasympathetic component of the baroreflex (−2.47 ± 0.31 vs. −1.25 ± 0.8 bpm/mmHg) and decreased serum oxidative stress in SHR (2.04 ± 0.17 vs. 3.22 ± 0.37 nmol/mL, n = 6). Our data suggest that treatment with quercetin reduces hypertension and improves BRS in SHR via reduction in oxidative stress.

Coconut oil supplementation and physical exercise improves baroreflex sensitivity and oxidative stress in hypertensive rats

The hypothesis that oral supplementation with virgin coconut oil (Cocos nucifera L.) and exercise training would improve impaired baroreflex sensitivity (BRS) and reduce oxidative stress in spontaneously hypertensive rats (SHR) was tested. Adult male SHR and Wistar Kyoto rats (WKY) were divided into 5 groups: WKY + saline (n = 8); SHR + saline (n = 8); SHR + coconut oil (2 mL·day(-1), n = 8); SHR + trained (n = 8); and SHR + trained + coconut oil (n = 8). Mean arterial pressure (MAP) was recorded and BRS was tested using phenylephrine (8 μg/kg, intravenous) and sodium nitroprusside (25 μg·kg(-1), intravenous). Oxidative stress was measured using dihydroethidium in heart and aorta. SHR + saline, SHR + coconut oil, and SHR + trained group showed higher MAP compared with WKY + saline (175 ± 6, 148 ± 6, 147 ± 7 vs. 113 ± 2 mm Hg; p < 0.05). SHR + coconut oil, SHR + trained group, and SHR + trained + coconut oil groups presented lower MAP compared with SHR + saline group (148 ± 6, 147 ± 7, 134 ± 8 vs. 175 ± 6 mm Hg; p < 0.05). Coconut oil combined with exercise training improved BRS in SHR compared with SHR + saline group (-2.47 ± 0.3 vs. -1.39 ± 0.09 beats·min(-1)·mm Hg(-1); p < 0.05). SHR + saline group showed higher superoxide levels when compared with WKY + saline (774 ± 31 vs. 634 ± 19 arbitrary units (AU), respectively; p < 0.05). SHR + trained + coconut oil group presented reduced oxidative stress compared with SHR + saline in heart (622 ± 16 vs. 774 ± 31 AU, p < 0.05). In aorta, coconut oil reduced oxidative stress in SHR compared with SHR + saline group (454 ± 33 vs. 689 ± 29 AU, p < 0.05). Oral supplementation with coconut oil combined with exercise training improved impaired BRS and reduced oxidative stress in SHR.

Nitric oxide generation by the organic nitrate NDBP attenuates oxidative stress and angiotensin II-mediated hypertension.

NO deficiency and oxidative stress are crucially involved in the development or progression of cardiovascular disease, including hypertension and stroke. We have previously demonstrated that acute treatment with the newly discovered organic nitrate, 2‐nitrate‐1,3‐dibuthoxypropan (NDBP), is associated with NO‐like effects in the vasculature. This study aimed to further characterize the mechanism(s) and to elucidate the therapeutic potential in a model of hypertension and oxidative stress.

Brain Angiotensin-II-derived Reactive Oxygen Species: Implications for High Blood Pressure

Hypertension and its relation to free radicals have been matter of continuous research worldwide. This review is based on the premise that some forms of neurogenic hypertension is, in part, caused by the formation of Angiotensin- II (Ang II)-derived reactive oxygen species within the brain, especially in areas along the Subfornical Organ- Paraventricular Nucleus of the Hypothalamus-Rostral Ventrolateral Medulla pathway (SFO-PVN-RVLM pathway). Here we will discuss the recent contribution of our laboratory and others regarding the mechanisms by which neurons in the Rostral Ventrolateral Medulla (RVLM) are activated by Ang II, how they communicate with the SFO and PVN and more importantly, how Ang II-derived Reactive Oxygen Species (ROS) participate along the SFO-PVN-RVLM pathway in the pathogenesis of neurogenic hypertension.

Developing New Organic Nitrates for Treating Hypertension: A Review

Nitric oxide (NO) is one of the most important vasodilator molecules produced by endothelium and presents plenty of cardiovascular actions. It has already been established that deficiency in NO/cGMP signaling pathway is involved in pathophysiological mechanisms of many cardiovascular diseases. In this context, the use of NOreleasing drugs appears to be an effective alternative to replace the deficient endogenous NO and mimic the role of this molecule in the body. Organic nitrates represent the oldest class of NO donors that have been clinically applied. Considering that tolerance can occur when these drugs are used chronically, the search for new compounds of this class with lower tolerance potential is increasing. Here we briefly discuss the mechanisms involved in nitrate tolerance and highlight some achievements from our group in the development of new organic nitrates and their preclinical application in cardiovascular disorders.

A OBESIDADE LIMITA OS BENEFÍCIOS DO EXERCÍCIO NA REDUÇÃO DA PRESSÃO ARTERIAL EM HIPERTENSOS

Was investigated the influence of obesity on post-exercise hypotension (PEH) in hypertensive subjects. Sixteen mild aged women underwent an anthropometric evaluation and blood sampling for analysis of lipoproteins levels. Then held a session of aerobic exercise lasting 40 minutes and moderate intensity between. Blood pressure was measured before exercise, immediately at the end and at 10, 20 and 30 minutes of recovery. Was observed systolic PEH of -15.2, -9.5 and -1.7mmHg and diastolic PEH of -3.6, -1.5 and -3.4mmHg for the eutrophic, overweight and obese, respectively. Subjects with lower waist circumference had higher values of HPE (-17.2 and -7.2 mmhh) that subjects with larger circunferences (-0.3 and -1.8 mmHg) for systolic and diastolic PEH, respectively. We observed systolic and diastolic PEH of -16.5 and -4.7mmHg and -3.5 and -3.2 for normocholesterolemic and hypercholesterolemic subjects, respectively. There was a significant difference in systolic HPE between groups with waist circumferences to 88cm and above 88cm, but the magnitude of the hypotensive differences in other variables are considered clinically important. Therefore, these data show that obesity and hypercholesterolemia, in addition to being a risk factor for hypertension, also limits the benefits of exercise in the hypotensive response in hypertensive. Abdominal fat is the main factor in this limitation.