Dietary and metabolic aspects of hypertension and hypertension-related organ damage are two topics largely approached by studies published in the current issue of the Journal of Hypertension.
A systematic review by Serban et al. (pp. 1119–1127) has investigated whether the asserted antihypertensive action of black tea – Hibiscus sabdariffa – is substantiated by a meta-analysis of available randomized controlled trials, and concludes for a significant effect of black tea beverages in lowering both SBP and DBP. Only five small trials (with 390 participants) were available, however, and the authors advise further well designed trials are necessary. Jiang et al. (pp. 1193–1200) report the results of a longitudinal study of the blood pressure effects of different dietary patterns in a low-income country, such as Bangladesh, showing that higher intake of fruits and vegetables is associated with a lower annual rate of change in SBP and pulse pressure, whereas higher meat intake is related to a more rapid annual increase in pulse pressure. A study by Farajian et al. (pp. 1174–1181) has investigated possible associations of dietary patterns with high blood pressure in a nation-wide sample of Greek school children and found that a dietary pattern characterized by high cheese and red processed meat (and probably high sodium intake) consumption increases the likelihood of having high blood pressure in children. According to another study in children (Pieruzzi et al., pp. 1182–1192), obesity and waist circumference, but not hypertension, are associated with a worsening of diastolic function, whereas hypertension is associated with a high prevalence of concentric cardiac remodeling. In a cross-sectional investigation of a large Brazilian cohort, Aneni et al. (pp. 1207–1214) found that nonalcoholic fatty liver disease, although prevalent among individuals with elevated BMI, is also more prevalent in individuals with prehypertension and hypertension, and among nonobese hypertensive patients good blood pressure control is associated with lower odds of nonalcoholic fatty liver disease. Bonfils et al. (pp. 1215–1225) report the ambulatory blood pressure results of gastric bypass surgery in a group of obese patients, half with and half without hypertension. Gastric bypass resulted in a significant ambulatory blood pressure decrease or reduction in antihypertensive medications, accompanied by an increase of cardiac natriuretic peptides in hypertensive obese patients, but not in the normotensive obese individuals. These observations are commented by Jordan and Grassi (pp. 1139–1141), who call attention to the possibility that the tight link between cardiovascular and metabolic disease through natriuretic peptides may have therapeutic implications. A mechanistic study in rats (do Carmo et al., pp. 1201–1206) shows that melanocortin 3/4 receptor activity in the hindbrain, although contributing to regulation of food intake and body weight, does not play a major role in mediating the elevated blood pressure in spontaneously hypertensive rats.
Studies on hypertension-related organ damage cover alterations in a number of different organs. A comprehensive review by Li et al. (pp. 1128–1136) is focused on molecular mechanisms of reduced nitric oxide bioavailability to the endothelium in hypertension and discusses potential novel therapeutic strategies to restore eNOS function in hypertension. In an accompanying editorial, Taddei and Bruno (pp. 1137–1138) underline the role endothelial dysfunction may play in the development of vascular organ damage rather than in raising blood pressure.
Michael O’Rourke's group (Kim et al., pp. 1233–1241) presents experimental data on the effects of intracranial pressure on brain hemodynamics, and Gonzalez et al. (pp. 1242–1248) show that, among participants from the Baltimore Longitudinal Study of Ageing, those being hypertensive have increased rates of cortical brain thinning compared to normotensive individuals, and suggest inter-visit blood pressure variability and mid-life blood pressure contribute to these longitudinal differences.
In the Lewis polycystic kidney rat model of chronic kidney disease, blockade of angiotensin AT1 receptors was found to selectively improve baroreceptor control of splanchnic sympathetic activity and peripheral chemoreflex control of all sympathetic outflows, suggesting these anomalies in reflex function are driven, at least in part, by angiotensin II (Yao et al., pp. 1249–1260). Ott et al. (pp. 1261–1266), in a pilot study on patients with chronic kidney disease stages 3 and 4 and uncontrolled hypertension, report that renal denervation decreased blood pressure and slowed down the rate of decline of renal function.
Naito et al. (pp. 1267–1275) have investigated the mechanism of cardiac remodeling following chronic iron deficiency and report remodeling is associated with cardiac erythropoietin receptor (EpoR) signaling as it is absent in EpoR-/--restricted mice. Trachsel et al. (pp. 1276–1283) have found that a relevant proportion of middle-aged athletes have masked hypertension associated with a lower diastolic function and a higher left ventricular mass/volume ratio. In the longitudinal Health 2000 Study, a large national general population survey in Finland, Porthan et al. (pp. 1284–1290) have found that electrocardiographic left ventricular hypertrophy has a higher prognostic value in women than in men, and suggest the use of the composite of Sokolow–Lyon voltage and Cornell voltage criteria. A multicentre Italian study (Moreo et al. pp. 1291–1300) indicates that three integrated cardiovascular ultrasound parameters may have incremental predictive value for diagnosing obstructive coronary artery disease.
Other topics are also covered by articles published in the current issue of the Journal. Chittani et al. (pp. 1301–1309) have conducted an exploratory pharmacogenomic study of blood pressure responsiveness to hydrochlorothiazide identifying two plausible loci: TET2, an aldosterone-responsive mediator of αENaC gene transcriptor, and CSMD1, previously described as associated with hypertension. In an accompanying commentary Menni (pp. 1142–1143) raises the question whether pharmacogenetic genome-wide association studies (GWAS) SNPs are useful at an individual level, given the low predictive value of GWAS SNPs in general across all other traits studied.
Systemic hypertension is a frequent side effect of antiangiogenic drugs used in the treatment of cancer. Alivon et al. (pp. 1310–1317) report that large arteries stiffen during antiangiogenic drug treatment partly independent of blood pressure changes, and that arterial stiffening is related with the drug effects on cancer progression and thus may help monitor the success of antiangiogenic therapy in cancer patients. An additional clinical study focuses on targeted screening of hypertension in children, showing that, although children with hypertensive parents are at a higher risk of hypertension, nevertheless parental history of hypertension only marginally helps to identify hypertension in offsprings (Bloetzer et al., pp. 1167–1173); and another study reports the results of a retrospective study of a large case series of primary aldosteronism, suggesting normokaliemic and hypokaliemic cases may represent the same disease at different evolution stages (Martell-Claros et al., pp. 1226–1232). An epidemiological study has found positive associations of pulse pressure and SBP with short-term exposure to particulate matters in two Swiss populations (Tsai et al., pp. 1144–1152), and two longitudinal cohort studies have investigated the relationship of blood pressure phenotypes with incident cardiovascular disease and mortality. Lotfaliany et al. (pp. 1153–1161), in a large Iranian cohort, report that isolated systolic hypertension, systolic/diastolic hypertension, and uncontrolled blood pressure increase the risk of incident cardiovascular disease; however, control of blood pressure to less than 140/90 mmHg decreases the risk of mortality among middle-aged individuals, whereas it significantly increases mortality in the elderly. In a cohort of elderly patients with type 2 diabetes, van Hateren et al. (pp. 1162–1166) have found that fraility, rather than old age, modifies the relationship between blood pressure and mortality: higher blood pressure was related to increased cardiovascular mortality in nonfrail patients, even in the oldest elderly, but was found to lower all-cause mortality in frail patients.
Conflicts of interest
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