Hypothesis/introduction:The relationship between salt intake, blood pressure and RAAS activation is still controversial, being that both high-and low-salt intakes are associated with cardiovascular events in a J-shaped curve pattern. We hypothesized that different patterns of RAAS response to dietary salt intake among hypertensives could be identified, while vascular damage would be related to high-salt intake plus absence of expected RAAS inhibition. Objective: We aim to assess the relationship between sodium intake, RAAS and vascular stiffness in hypertension. Materials and methods: We screened 681 hypertensive patients for urinary/plasma electrolytes, renin, aldosterone and pulse wave velocity (PWV) under their usual salt intake level. Results: After applying exclusion criteria, an inverse relation between urinary sodium and RAAS was observed in the 300 remaining subjects. Additionally, four types of response were identified: 1) Low (L) sodium (S)-Low RAAS, 2) LS-High (H) SRAAS, 3) HS-Low RAAS, 4) HS-High RAAS. We found no differences in age/BP among groups, but type 4 response individuals included more females and a higher pulse wave velocity. Conclusions: We showed a) an inverse salt-RAAS relation, b) an association between HS plus high RAAS with increased PWV that could identify a higher-risk hypertensive condition.

de Cavanagh EM, González SA, Inserra F, Forcada P, Castellaro C, Chiabaut-Svane J, Obregón S, Casarini MJ, Kempny P, Kotliar C. Sympathetic predominance is associated with impaired endothelial progenitor cells and tunneling nanotubes in controlled-hypertensive patients. Am J Physiol Heart Circ Physiol 307: H207-H215, 2014. First published May 23, 2014; doi:10.1152/ajpheart.00955.2013.-Early endothelial progenitor cells (early EPC) and late EPC are involved in endothelial repair and can rescue damaged endothelial cells by transferring organelles through tunneling nanotubes (TNT). In rodents, EPC mobilization from the bone marrow depends on sympathetic nervous system activity. Indirect evidence suggests a relation between autonomic derangements and human EPC mobilization. We aimed at testing whether hypertension-related autonomic imbalances are associated with EPC impairment. Thirty controlled-essential hypertensive patients [systolic blood pressure/diastolic blood pressure ϭ 130(120 -137)/85(61-88) mmHg; 81.8% male] and 20 healthy normotensive subjects [114(107-119)/75(64 -79) mmHg; 80% male] were studied. Mononuclear cells were cultured on fibronectin-and collagen-coated dishes for early EPC and late EPC, respectively. Low (LF)-and high (HF)-frequency components of short-term heart rate variability were analyzed during a 5-min rest, an expiration/inspiration maneuver, and a Stroop color-word test. Modulations of cardiac sympathetic and parasympathetic activities were evaluated by LF/HF (%) and HF power (ms 2 ), respectively. In controlled-hypertensive patients, the numbers of early EPC, early EPC that emitted TNT, late EPC, and late EPC that emitted TNT were 41, 77, 50, and 88% lower than in normotensive subjects (P Ͻ 0.008), respectively. In controlled-hypertensive patients, late EPC number was positively associated with cardiac parasympathetic reserve during the expiration/inspiration maneuver (rho ϭ 0.45, P ϭ 0.031) and early EPC with brachial flow-mediated dilation (rho ϭ 0.655; P ϭ 0.049); also, late TNT number was inversely related to cardiac sympathetic response during the stress test (rho ϭ Ϫ0.426, P ϭ 0.045). EPC exposure to epinephrine or norepinephrine showed negative dose-response relationships on cell adhesion to fibronectin and collagen; both catecholamines stimulated early EPC growth, but epinephrine inhibited late EPC growth. In controlled-hypertensive patients, sympathetic overactivity/ parasympathetic underactivity were negatively associated with EPC, suggesting that reducing sympathetic/increasing parasympathetic activation might favor endothelial repair. endothelial regeneration; autonomic balance; parasympathetic CURRENT EVIDENCE SUPPORTS the concept that circulating bone marrow-derived endothelial progenitor cells (EPCs) contribute to the repair and regeneration of the injured endothelium (15).Tissue ischemia and/or endothelial damage promote EPC mobilization from the bone marrow and EPC recruitment and incorporation at sites of vascular damage (15). Two distinct types of EPC have been ide...

Patients presenting classical cardiovascular risk factors within acceptable or average value ranges often develop cardiovascular disease, suggesting that other risk factors need to be considered. Considering that endothelial progenitor cells (EPC) contribute to endothelial repair, we investigated whether EPC might be such a factor. We compared the ability of peripheral blood EPC to attach to extracellular matrix proteins, and to grow and function in culture, between controlled-hypertensive patients exhibiting Framingham scores (FS)<10% while displaying severe vascular impairment (intima-media thickness/diameter, carotid-femoral pulse wave velocity, brachial artery flow-mediated dilation, carotid and femoral atherosclerotic plaque presence) (Vulnerable group, N=30), and those with FS≥10% and scarce vascular changes (Protected group, N=30). In Protected patients early- and late-EPC, and early- and late-tunneling nanotube (TNT) numbers were significantly higher versus Vulnerable patients. Significant negative associations were found between vascular damage severity and early-EPC, late-EPC, or late-TNT numbers, whereas EPC or TNT numbers and patient´s characteristics or cardiovascular risk factors were not associated. Except for Protected patients, in all controlled-hypertensive patients early- and late-EPC and early- and late-TNT counts were significantly lower than in the Normotensive subjects studied (N=30). We found that the disparity in vascular status between patients presenting both FS≥10%/scarce vascular changes and those displaying both FS<10%/severe vascular impairment, is related to differences in peripheral blood EPC and TNT numbers. These observations support the role of EPC as contributors to vascular injury repair, and suggest that EPC numbers may be a potential cardiovascular risk factor to be included in FS calculation.

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