As usual, this short editorial introduction tries to provide the readers with a lead by which to get through the content of the current issue of the Journal of Hypertension.
An important topic, upon which an initial group of articles are focused, is that of the factors influencing blood pressure levels. The issue opens with a Consensus Document produced by the Working Group on Obesity, Diabetes and the High Risk Patient of the European Society of Hypertension regarding the pathogenesis of obesity-induced hypertension (Kotsis et al., pp. 1499–1508). Although obesity is clearly associated with an increased prevalence of hypertension, it is also known that many obese individuals do not develop hypertension. The expert Consensus Document clearly discusses a number of protective and promoting factors for hypertension in obesity, and highlights gaps in our current knowledge. Within the same area of the influences of obesity on blood pressure, a large population study in China by Wang et al. (pp. 1555–1562) shows that measurements of the visceral fat index (VFI) or of the VFI to percentage body fat ratio (VFI/PBF) may provide a better understanding of adiposity-related risks for hypertension and prehypertension.
Another important factor influencing blood pressure is reviewed by Binia et al. (pp. 1509–1520), who publish a meta-analysis of randomized controlled trials of potassium supplementation, showing that this is associated with a reduction of blood pressure in individuals who are not on antihypertensive medication, and the effect is significant in hypertensive individuals. A meta-regression analysis shows that the reduction in blood pressure significantly correlates with decreased daily urinary sodium-to-potassium ratio and increased urinary potassium.
A large study from Finland (Laine et al., pp. 1549–1554) has explored the hypothesis that vigorous physical activity during young adulthood protects against hypertension later in life and reports that former elite athletes (2037 versus 1403 matched controls) had lower age-adjusted prevalence of hypertension than controls, the protective effect of past exercise being particularly marked in former endurance athletes. The authors conclude that a former career as an elite athlete not only seems to be associated with a lower prevalence of hypertension in later life, but also the current volume of leisure-time physical activity is inversely related to the presence of hypertension.
Stress being another factor often associated with blood pressure elevation, Schoen et al. (pp. 1571–1579) have measured copeptin, a vasopressin-related stress hormone, in a large cohort of over 2000 healthy young adult individuals, and found plasma levels of copeptin were significantly associated with an increased blood pressure variability in both sexes and an elevated night-time blood pressure among men. In an accompanying editorial, Schillaci et al. (pp. 1524–1527) remark that the findings of Schoen et al. suggest circulating copeptin may be considered as an integrated marker of the stressful events associated with sleep apnoea and a harbinger of future cardiovascular complications. Finally, the often reported associations of either foetal growth restriction or prematurity with elevated blood pressure in adult life has been further investigated by Juonala et al. (pp. 1542–1548) in the context of the Cardiovascular Risk in Young Finns Study, who suggest that both factors are likely to play a role, their 31-year long follow-up of 1756 individuals showing that elevated blood pressure levels associated with prematurity are more likely to be present in those with foetal growth restriction.
Two other articles focus on the influences exerted by blood pressure levels, specifically on organ damage. Satoh et al. (pp. 1536–1541) report that blood pressure variability is associated with a known cardiovascular risk predictor, N-terminal proB-type natriuretic peptide (NT-proBNP), and suggest that the association of blood pressure variability with NT-proBNP levels may be taken to indicate that blood pressure variability is associated with organ damage or complications. In an accompanying editorial, Bilo et al. (pp. 1521–1523) point out that, although the results reported by Satoh et al. do not have an immediate clinical applicability, they generate stimulating hypotheses on early cardiac alterations related to cardiovascular dynamics. Obviously, testing these hypotheses will require further research. The role of organ damage in predicting cardiovascular risk is also enlightened by a study in which Greve et al. (pp. 1563–1570) have found that both an elevated urinary albumin to creatinine ratio and presence of atherosclerotic plaques in the carotid artery (but not an elevated pulse wave velocity) can identify individuals with actual high cardiovascular risk (cardiovascular event incidence during follow-up) despite being classified at moderate/intermediate risk with SCORE or Framingham risk algorithms.
In this issue of the Journal, a large body of research is devoted to blood vessel functional and structural changes. Vascular fibrosis is the focus of two articles: Fedorova et al. (pp. 1602–1610) report that aortic fibrosis induced by marinobufagenin, an endogenous cardiotonic steroid, is responsive to the mineralocorticoid antagonist, canrenone. In a mechanistic article, Xu et al. (pp. 1611–1623) find that in high fat fed obese mice made knockout for the BK (large conductance Ca2+-activated K+) channel ß1-subunits have higher norepinephrine reactivity, greater wall thickness and collagen accumulation in the mesenteric arteries than wild-type mice. The authors suggest that BK channel deficiency promotes sympathetic activity and vascular remodelling and fibrosis. Endothelial dysfunction is the object of two articles: Gu et al. (pp. 1624–1632) report that chemerin, a recently discovered adipokine elevated in obesity and metabolic syndrome, is an independent predictor of impaired endothelial function and increased stiffness in hypertension. Fontes-Guerra et al. (pp. 1666–1675) find that nitroglycerin-mediated, but not flow-mediated, vasodilatation is independently associated with higher night-time blood pressure and nondipping patterns in patients with resistant hypertension, and suggest that it may be a better cardiovascular risk marker in this type of patients. This article is commented by Palatini and Grassi (pp. 1533–1535), who remark that the cross-sectional nature of the study by Fontes-Guerra et al. does not allow us to understand whether the endothelial/vascular dysfunction is the causative factor or the consequence of the high nocturnal blood pressure.
Two articles from the Maastricht study focus on the role of serum uric acid on vascular function: neither stiffness of large arteries nor skin microvascular function was found correlated with serum uric acid after suitable adjustments (Wijnands et al., pp. 1642–1650). These findings are commented by Virdis and Grassi (pp. 1531–1532), who point out that the authors are the first to have utilized a high-quality methodology for exploring the relationship between uric acid and skin microvascular function, but the problem whether skin microcirculation can be regarded as a model of microvascular function in all vascular beds remains open.
In elderly hypertensive patients from Korea, Cho et al. (pp. 1633–1641) report that heavy aortic calcification is associated with arterial stiffening and suggest that this association may underlie the left ventricular hypertrophy often occurring in elderly hypertensive individuals. Another mechanistic experimental study deals with cardiac hypertrophy (Lu et al., pp. 1676–1687), showing that in rats with abdominal aortic constriction, the ensuing cardiac hypertrophy can be prevented by administration of intermedin (IMD), a novel member of the calcitonin/calcitonin gene-related peptide family. The authors suggest that IMD may exert its effect on cardiac hypertrophy by inhibiting endoplasmic reticulum stress and apoptosis, possibly via activation of AMP-activated protein kinase (AMPK) signalling.
Other mechanistic articles, though in different areas of hypertension research, are focused on mechanisms of the increased cardiovascular risk of orthostatic hypotension (Isma et al., pp. 1594–1601, suggest that one mechanism may be an increased concentration of von Willebrand factor) and on mechanisms of preeclampsia [Li et al., pp. 1658–1665, show that trophoblast cells respond to cell-free foetal DNA through the interferon (IFN)-inducible protein 16 (IFI16) receptor, resulting in the production of preeclampsia-related antiangiogenic factors].
Two methodological articles refer to blood pressure measurement procedures. Kang et al. (pp. 1580–1587) have compared the accuracy of home blood pressure monitoring in the diagnosis of white-coat and masked hypertension in comparison with ambulatory blood pressure, and report home measurements have a high diagnostic specificity but low sensitivity. In an accompanying editorial, Stergiou et al. (pp. 1528–1530) remark these findings support the position of the European Society of Hypertension, that recommends home blood pressure measurement as a reliable alternative to ambulatory monitoring. Young et al. (pp. 1588–1593) have investigated the reliability of oscillometric central blood pressure and augmentation index calculations, and conclude that the highest reliability is obtained when participants are supine and fasted.
As usual, therapeutic aspects are also covered in the current issue of the Journal. On the basis of the longitudinal data of the China Health and Nutrition Survey, Guo et al. (pp. 1688–1696) report that between 1991 and 2001, blood pressure and hypertension prevalence have increased among Chinese adults. Although the levels of awareness, treatment and control of hypertension have increased, they have remained at quite low levels. Two studies concern long-term chronic baroreflex activation therapy in resistant hypertension: Halbach et al. (pp. 1697–1703) have investigated acute blood pressure increases and decreases after device deactivation and reactivation (on/off effects) in patients on chronic unilateral baroreflex stimulation and found that there is a significant on/off effect on blood pressure supporting the continuing efficacy of the stimulation. Persistent efficacy of chronic baroreflex stimulation is also reported by Gronda et al. (pp. 1704–1708) in patients with heart failure, in whom improvements observed after 6 months were found maintained at 12 months after initiation of stimulation, the improvements including reduced sympathetic activity and hospitalization rates.
Finally, the current issue also includes a case report of an interesting case of reninoma, which has allowed a detailed study of tumoral cells in culture (Vidal-Petiot et al., pp. 1709–1715).
Conflicts of interest
There are no conflicts of interest.