Hypertension research : official journal of the Japanese Society of Hypertension
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Effective treatment with nasal continuous positive airway pressure (nCPAP) lowers blood pressure (BP) in patients with obstructive sleep apnea (OSA). It was reported that OSA might influence BP in middle-aged but not in elderly patients. However, effects of nCPAP treatment in elderly hypertensive OSA patients are not well known. ⋯ There were no significant changes in systolic BP, BMI or usage time of nCPAP. With a daily average of 3 h or more of nCPAP treatment, diastolic BP decreased significantly in subject groups ≥ 60 and <60 years of age. Even in the elderly, a daily average use of nCPAP for 3 h would lower diastolic BP in OSA patients.
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There is growing recognition of cardiovascular consequences of obstructive sleep apnea (OSA). Recurrent episodes of airway obstructions result in hypoxia and hypercapnia increasing sympathetic neural tone, which in turn causes vasoconstriction and marked increases in blood pressure (BP). BP response to OSA may be important in understanding the absence of nocturnal BP fall in the subgroup of hypertensive patients termed 'non-dippers'. ⋯ Effective treatment of sleep apnea may attenuate neurohumoral and metabolic abnormalities, improve diurnal BP control and conceivably reduce cardiovascular risk. This review examines the evidence linking OSA to non-dipping pattern of hypertension, and discusses potential mechanisms underlying this link. We will review first, prognostic value of nighttime BP; second, the cardiovascular consequences of sleep apnea; third, the evidence for altered diurnal BP profile in sleep apnea; fourth, the mechanisms contributing to both nocturnal and daytime hypertension in sleep apnea; fifth, the benefits of sleep apnea treatment and finally implications for hypertension management.
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Isolated office hypertension (IOH) has been associated with structural cardiac abnormalities; however, its relation to worse cardiovascular prognosis remains uncertain. Less is known regarding the consequences of uncontrolled IOH in treated hypertensives. The aim was to investigate whether uncontrolled IOH was independently associated with two subclinical markers of cardiovascular disease, aortic stiffness and left ventricular hypertrophy (LVH). ⋯ On logistic regression, the presence of uncontrolled IOH was independently associated with 2.7-fold (95% CI: 1.3-5.5) and 2.1-fold (95% CI: 1.1-4.0) higher risks of having increased aortic stiffness and LVH, respectively. In conclusion, uncontrolled IOH is associated with increased aortic stiffness and LVH in hypertensive type 2 diabetic patients. This may be a link to augmented cardiovascular risk.
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Blood flow reduction induces inward remodeling of resistance arteries (RAs). This remodeling occurs in ischemic diseases, diabetes and hypertension. Nonetheless, the effect of flow reduction per se, independent of the effect of pressure or metabolic influences, is not well understood in RA. ⋯ ERK1/2 inhibition in vivo (U0126) prevented LF-induced diameter reduction. Thus, inward remodeling because of blood flow reduction in mesenteric RA depends on unopposed angiotensin II-induced contraction and ERK1/2 activation, independent of superoxide production. These findings might be of importance in the treatment of vascular disorders.
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Recent genetic studies have uncovered a link between familial and idiopathic pulmonary arterial hypertension (PAH) and germline mutations in the bone morphogenetic protein type-II receptor (BMPRII). The pathology of PAH is characterized by remodeling of the pulmonary arteries due to pulmonary artery smooth muscle cell (PASMC) hyperproliferation. Although increased endothelial injury and impaired suppression of PASMC proliferation are both critical for the cellular pathogenesis of PAH, a detailed molecular mechanism underlying PAH has yet to be elucidated. ⋯ Inhibition of extracellular signal-regulated kinase 1 (ERK1)/ERK2 signaling suppressed basal-, ET1- and aldosterone-induced PASMC mitosis more potently than that of stress-activated protein kinase/c-Jun NH2-terminal kinase inhibition. Given the fact that BMP-2 and BMP-7 upregulated ETA/BR and MR expression and that BMP-2 decreased 11betaHSD2 (11beta-hydroxysteroid dehydrogenase type 2) levels in PASMCs isolated from idiopathic PAH, BMPR-Smad signaling may have a key role in amplifying the ETA/BR and/or MR-ERK signaling in PASMCs of the PAH lung. Collectively, the functional link between BMP and ET and/or the MR system may be involved in the progress of PASMC mitosis, ultimately leading to the development of clinical PAH.