Lack of RAAS inhibition by high-salt intake is associated with arterial stiffness in hypertensive patients

Abstract

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.

A higher baseline plasma uric acid level is an independent predictor of arterial stiffness

“…The biological behaviors of smooth muscle cells above-mentioned are triggered by the activated renin-angiotensin system and reactive oxygen species. [ 30 – 32 ] Secondly, studies have also indicated that the essential role of UA in arterial stiffness before the development of hypertension may be attributed to the activation of inflammatory pathways (increased levels of C-reactive protein and other proinflammatory factors). [ 33 ] Thirdly, UA has also been implicated in endothelial cell dysfunction, which plays a crucial role in arterial stiffening.…”

Current Data on Dietary Sodium, Arterial Structure and Function in Humans: A Systematic Review

“…In a single study, Kotliar et al indicate a significant positive association between Na and PWV only in the group of participants who had high RAAS activity. However, the group with high Na and low RAAS activity did not show a significant association with PWV [24]. One of the studies suggested that only middle-aged and not young participants presented increased PWV after a high-salt diet [43].…”

“…Moreover, one out of the 11 studies showed that high Na excretion (mean: 2898 mg/day, range 2035.5-3588) is associated with cfPWV only when high Na excretion was combined with high renin-angiotensin-aldosterone system (RAAS) activity but not in the other groups (i.e., those with high Na and low RAAS, low Na and low RAAS, as well as low Na and high RAAS) [24].…”

“…Indeed, the majority of the studies (observational 11/14 and interventional 7/17) do imply the presence of a harmful effect of high Na intake [15,[17][18][19][20][28][29][30][32][33][34]38,44,46] or even benefits of low Na intake on arterial stiffening parameters [34,36,44,48] (18 out of 31, 11 observational and seven interventional), in various populations [22,26,29,34,44], involving several different segments of the arterial tree [22,29,30,33,45,48], independently of the applied methodology, technology used [22,29,33,34]. However, most of these positive studies do not take into consideration the well-known effect of Na on BP increase [15,24,28,29,36,37,44]. Overall only 1/3 of the studies included in our analysis, and only 10 out of the 17 positive studies adjusted their findings for BP levels [17][18][19][20]…”

Association of ambulatory arterial stiffness index with sEPCR in newly diagnosed hypertensive patients

“…30 Other studies have demonstrated that a pro-thrombotic state can be induced by the activation of the renin-angiotensin system (RAS), which is associated with arterial stiffness in hypertensive patients. 31,32 Remková et al reported that hypertensive patients have a significant increase in sEPCR levels versus the healthy controls. The sEPCR level decreases in response to the treatment with an angiotensin II type 1 receptor blocker (ARB).…”