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Albeit hypertension is a leading risk factor for an initial stroke, the role of blood pressure (BP) lowering to prevent a subsequent stroke is controversial. The present systematic review searched randomized trials published from January 1990 to January 2014 with the aim to assess antihypertensive treatment effects on recurrent stroke prevention. Seven randomized placebo-controlled trials enrolling 49,518 patients, two randomized trials not placebo controlled comparing antihypertensive drugs, and one randomized trial that compared the effects of intensive systolic BP lowering with a more conservative systolic BP management, were identified. The placebo-controlled trials had substantial methodological differences, explaining the difficulties to compare their results. An important obstacle arises from the large dispersion in the window's time between the qualifying stroke and randomization. Another barrier is the variation among studies in the recruited patient's stroke subtypes. Differences between trials could not be attributed to disparity in lowering BP or to different degrees of no adherence. The American Heart Association/American Stroke Association stated that although an absolute target of BP level has not been clearly defined, a reduction in recurrent stroke has been associated with an average lowering of 10/5 mm Hg. It should be taken into account that it is not advisable to reduce BP levels to <120/80 mm Hg. It should carry out an individualized selection, based on demographic characteristics and comorbidities (cardiovascular disease, diabetes mellitus, and chronic disease) among diuretics, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, or calcium channel blockers., (Copyright © 2014 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Hypertension is the leading risk factor for ischemic and intracerebral hemorrhagic subtypes of stroke. Additionally, high blood pressure (BP) in the acute cerebrovascular event is associated with poor outcome, and a high percentage of stroke survivors have inadequate control of hypertension. The present is a systematic review of prospective, randomized, and controlled trials carried out on safety and efficacy of antihypertensive treatment of both subtypes of acute stroke. Six trials involving 7512 patients were included, which revealed controversies on the speed and the goals of treatment. These controversies could be due at least in part, from the fact that some studies analyzed the results of antihypertensive treatment in ischemic and intracerebral hemorrhagic subtypes of acute stroke together, and from a different prevalence of past-stroke in the randomized groups. Further research is necessary to establish whether standard antihypertensive treatment provides greater benefit than simple observation in patients with ischemic acute stroke and Stage 2 hypertension of JNC 7, albeit they were not candidates for acute reperfusion. In that case, the target reduction in BP could be 10% to 15% within 24 hours. The recently published INTERACT 2 has provided evidence that patients with hemorrhagic stroke may receive intensive antihypertensive treatment safely with the goal of reducing systolic BP to levels no lower than 130 mm Hg. It is important to take into account that marked BP lowering in acute stroke increases the risk of poor outcome by worsening cerebral ischemia from deterioration of cerebral blood flow autoregulation., (Copyright © 2014 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Nocturia is a risk factor for morbidity and mortality but is frequently overlooked and underreported by patients and unrecognized by physicians. Epidemiologic studies reported that nocturnal voiding is associated not only with aging and benign prostatic hyperplasia, but also with many other clinical conditions. The majority of epidemiologic studies reported a significant relationship between nocturia and hypertension. However, the cause-and-effect relationship between them has not been established. Some physiopathological changes in hypertension are conducive to result in nocturia. These include the effects of hypertension on glomerular filtration and tubular transport, resetting of the kidney pressure-natriuresis relationship, atrial stretch and release of atrial natriuretic peptide when congestive heart failure complicates hypertension, and peripheral edema. Another link between hypertension and nocturia is obstructive sleep apnea. Furthermore, some evidence supports the relationship between nondipping behavior of blood pressure and an increased prevalence of nocturia. The use of some classes of antihypertensive agents may result in nocturia. The present review aims to provide a comprehensive evaluation of the epidemiologic evidence and physiopathological links that correlate hypertension and nocturia. Emphasis is placed on the need to take a pro-active attitude to detect and treat this hazardous condition., (Copyright © 2013 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)