Navegando por Palavras-chave "Hipertensão Arterial Sistêmica"

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    Estudo da associação da vitamina D e do inibidor da 3- hidroximetilglutaril coa redutase na função endotelial em portadores de hipertensão arterial: um estudo duplo-cego, placebo-controlado
    (Universidade Federal de São Paulo (UNIFESP), 2020-01-30) Kohatsu, Anderson Simabuco [UNIFESP]; Batista, Marcelo Costa [UNIFESP]; http://lattes.cnpq.br/0614350233628814; http://lattes.cnpq.br/6572506670639242; Universidade Federal de São Paulo
    Hypertension is considered a substantial trouble in public health. Because it is an easily diagnosed disease, but difficult to control and follow up, it needs special attention especially due to its association with cardiovascular outcomes and the great impact on morbidity and mortality of the population. The biological vulnerability of an inflammatory vascular environment can lead to impaired vascular regulation linked to a process of endothelial dysfunction and, consequently, a higher risk of developing hypertension. In this scenario, there is growing evidence of the benefits of Vitamin D and the 3- Hydroxymethylglutaryl CoA Reductase Inhibitor (Statin) in reducing inflammation and improving endothelial function through pleiotropic effects. However, the number of intervention studies is limited and raises questions about causal relationship, long-term interaction and benefits of these drugs in blood pressure control. The present double-blind, placebo-controlled study using a 2x2 factorial design proposals to evaluate the effect of the association between Vitamin D and Statin, compared with their respective placebos, on blood pressure, mensuration of dimethyl arginine-asymmetric endothelial function (ADMA) and inflammatory profile in patients with hypertension. Sixty eligible subjects were randomized to 4 groups of 15 patients at a 1: 1: 1: 1 ratio to receive simvastatin 40mg/day or vitamin D 200,000Ui starting dose followed by 100,000Ui/month (4 doses) alone or simvastatin with vitamin D or placebos treatment over 22 weeks. Throughout the period, monthly consultations were performed with monitoring of clinical parameters including blood pressure and antihypertensive adjustments in a stepwise manner according to protocol. Additionally before the intervention and at the end of the study, blood pressure was also measured by ambulatory blood pressure monitoring (ABPM) and laboratory tests including serum ADMA and C-reactive protein measurements from all participants. The results obtained with the intervention did not determine changes in systemic blood pressure levels at the end of follow-up, either by ABPM or office blood pressure, nor did it change the values of asymmetric dimethylarginine and C-reactive protein. Thus, we demonstrated that vitamin D supplementation and simvastatin treatment, alone or in combination, over 22 weeks in hypertensive patients with low cardiovascular risk did not lead to a reduction in blood pressure or changes in variables related to endothelial function and inflammation.
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    Estudo Dos Efeitos Agudos E Crônicos De Um Modelo De Apneia Obstrutiva Do Sono Em Ratos
    (Universidade Federal de São Paulo (UNIFESP), 2017-11-30) Ferreira, Caroline Borges [UNIFESP]; Cravo, Sergio Luiz Domingues [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The obstructive sleep apnea (OSA) is the most common respiratory disturbance of sleep in humans and it seems to be linked with genesis and/or worsening of several cardiovascular diseases. Each event of apnea can evoke respiratory effort and intense muscle SNA activation, but the mechanisms involved in these adjustments are no clear yet. To investigate the acute and chronic effects of OSA the present was divided in two parts. The purposes of the part I were a) to investigate regional changes in SNA during apnea, b) to study the contribution of carotid chemoreceptors and c) neurotransmission in the nucleus tractus solitarious (NTS) in the cardiovascular, respiratory and sympathetic responses induced by obstructive acute apnea. Acute apneas were induced in anesthetized male rats by clamping a tracheal tube for 20 s. Apnea promptly increased arterial blood pressure (ABP) and phrenic nerve activity (PNA). In addition, the magnitude of sympathoexcitation across lumbar, renal and splanchnic SNA was similar. Inactivation of chemoreceptors by hyperoxia (100% O2) attenuated the changes in ABP and SNA. Surgical denervation of carotid chemoreceptors abolished cardiovascular, respiratory and sympathetic responses to NaCN. In contrast, it only attenuated cardiovascular, PNA and sympathetic responses to apnea. To test the contribution of carotid and extra carotid afferents we tested apnea-induced responses after interruption of neurotransmission in the NTS. Injections of NMDA and non-NMDA antagonist cocktail attenuated PNA and SNA responses induced by acute apnea. In addition, NTS injection of the GABAA receptor agonist muscimol had a similar effect. In addition, the NTS injections did significantly attenuate responses to chemoreflex and baroreflex. Collectively, these findings suggest that sympathoexcitation and PNA activation induced by obstructive acute apnea depends in part of chemoreceptors afferents and glutamatergic neurotransmission of NTS. Otherwise, other mechanisms, for example activation of central chemoreceptors by hypercapnia and/or respiratory central generators, might be important to evoke sympathetic and respiratory responses induced by apnea. The part II of our study was developed to study the effect of chronic OSA and the role of sleep fragmentation on cardiovascular, sympathetic, and respiratory characteristics, and on expression of several genes in the rat brains. Male Wistar rats were anaesthetized and submitted to implant of a tracheal balloon and EEG/EMG electrodes. After 1 week to recovery, rats were assigned to control, OSA or arousal treatments. OSA rats were subjected to obstructive apnea, each time they entered sleep, up to 60 times per hour, for 15 days, 8 h per day. Rats from arousal group were similarly awake, same frequency and duration of OSA, using a vibration system with a small vibratory motor, mounted on the ECG/EMG wires, close to the rat’s head. One day after the last apnea or arousal, rats were anesthetized and prepared for recording ABP, phrenic nerve activity (PNA) and splanchnic sympathetic nerve activity (SSNA). Baseline ABP was higher after OSA than after other treatments. OSA did not alter baseline total voltage for SSNA. In contrast, SSNA was lower in arousal rats. OSA and arousal potentiated the sympathetic excitation induced by chemoreceptor activation. Expression of tyrosine hydroxylase were increased in the brainstems of rats exposed to OSA and arousal by vibration motor. However, expression of genes involved in oxidative stress and choline acetiltransferase biosynthesis were increased only in animals submitted to OSA. These data suggest that the hypertension induced by OSA depend of several mechanisms that include, potentiation of SNA responses, increase of oxidative stress and biosynthesis of tyrosine hydroxylase and choline acetiltransferase biosynthesis. In addition, chronic fragmentation of sleep seems to direct contribute with changes in SNA responses and gene expression of tyrosine hydroxylase. Furthermore, our findings indicate that future studies aimed to investigate the pathophysiology of OSA should consider multiple approaches or models to better understand cardiorespiratory physiology.