NT-proBNP and the risk of incident hypertension

Abstract

See original paper on page 966 I n many different areas of cardiovascular physiology [1], cardiac biomarkers have been shown to be very useful tools in evaluating cardiac (dys)function [2], assessing diagnosis [3,4], guiding subsequent management [5], stratifying prognosis [6], as well as assessing total cardiovascular risk [7]. Moreover, they significantly contribute to our knowledge of mechanisms of disease genesis and progression. In this area, the release of natriuretic peptides has been extensively studied in the past decades, and B-type natriuretic peptide (BNP) has been defined as a 'window' to the cardiovascular system [8], able to help clinicians in diagnosis, follow-up, and prognostication [9][10][11]. This is the case not only for heart failure [12,13] but also for specific cardiac diseases, such as amyloid cardiomyopathy [14][15][16][17], congenital heart disease [18], hypertrophic cardiomyopathy [19], pulmonary embolism [20], and many other conditions [21].In the setting of arterial hypertension, the role of natriuretic peptides is complex. On the one hand, a higher serum concentration of BNP is a rather robust marker of pressureinduced cardiac damage [22], on the one hand a reduced risk of hypertension has been associated with genetically elevated concentrations of either BNP or the N-terminal fragment of proBNP (NT-proBNP) [23,24]. Among many others, the main effects of BNP are vasodilation as well as natriuresis, both representing key mechanisms in arterial pressure control and in the cardio-renal cross-talk. Opposite effects are exerted by the renin-angiotensin-aldosterone system, and it has been recently shown that natriuretic peptides buffer renal vascular hypertension via reninindependent effects [25]. BNP is released by ventricular cardiomyocytes as a result of 'spontaneous' and 'inducible' production, the former being largely under genetic control and the latter being stimulated by mechanical stretch, as well as by direct or indirect toxic effects. The final serum concentration results from the net balance between production, degradation, and renal clearance. The many modifications of cardiac, arterial, as well as kidney function that are associated with hypertension may therefore affect BNP serum concentration, being concomitantly possible targets of BNP-mediated effects. A possible role of diminished vasodilation and natriuresis in the pathogenesis of hypertension has been very recently suggested by Seven et al. [26], showing that lower 'baseline' NT-proBNP concentrations were associated with a higher risk of developing hypertension during the 5-year follow-up of a cohort of 5307 participants. However, they did not report 'changes' of serum levels of natriuretic peptides over time in patients who did develop hypertension as compared with patients whose blood pressure remained in the normotensive range. The hypothesis that NT-proBNP changes (DNT-proBNP) are associated with the subsequent incidence of hypertension was evaluated in a study published in the current issue of the Journal of Hype...

Levels of Plasma N-terminal Pro-brain Natriuretic Peptide and D‑dimer on the Prognosis of Patients with Acute Cerebral Infarction

“… 11 Studies have found that NT-pro BNP has important significance in cerebrovascular diseases. 12 , 13 In this study, the level of NT-pro BNP of the observation group was significantly higher than that of the control group, which was consistent with the results of the current studies. BNP can promote natriuresis, inhibit secretion of antidiuretic hormone and sympathetic nerve impulse, and regulate baroreceptor.…”

Assessment of glomerular and tubulointerstitial apparatus state depending on the level of the natriuretic peptide in hypertension patients

“…Аргументация полученных данных может быть обеспечена тем, что в почках BNP увеличивает СКФ, расслабляя мезангиальные клетки, и ингибирует фракционную реабсорбцию натрия в канальцах, тем самым усиливая натрийурез и снижая АД, а также уменьшает сосудистое сопротивление, расслабляя гладкомышечные клетки артерий. Поэтому многие исследователи отмечают, что более низкие "исходные" концентрации BNP и NT-proBNP у пациентов с ГБ были связаны с более высоким риском развития как ХСН, так и поражения органов-мишеней [10,11]. Тем не менее, не вызывает сомнения и тот факт, что в патогенезе поражения органов-мишеней большую роль играют и другие системы: ренин-ангиотензин-альдостероновая система (РААС) и симпато-адреналовая система (СНС).…”