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


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.
Centre of Hypertension, Cardiology Service, Hospital Universitario Austral, Argentina ckotliar@cas.austral.edu.ar.
Carol
C
Kotliar
Centre of Hypertension, Cardiology Service, Hospital Universitario Austral, Argentina.
Pablo
P
Kempny
Centre of Hypertension, Cardiology Service, Hospital Universitario Austral, Argentina.
Sergio
S
Gonzalez
Centre of Hypertension, Cardiology Service, Hospital Universitario Austral, Argentina.
Carlos
C
Castellaro
Centre of Hypertension, Cardiology Service, Hospital Universitario Austral, Argentina.
Pedro
P
Forcada
Centre of Hypertension, Cardiology Service, Hospital Universitario Austral, Argentina.
Sebastián
S
Obregon
Biomedical School of Medicine, Universidad Austral, Argentina.
Elena
E
Cavanagh
Centre of Hypertension, Cardiology Service, Hospital Universitario Austral, Argentina.
Jorge
J
Chiabaut Svane
Centre of Hypertension, Cardiology Service, Hospital Universitario Austral, Argentina.
Maria Jesus
MJ
Casarini
Biochemical Central Laboratory, Hospital Universitario Austral, Argentina.
Mercedes
M
Rojas
Biomedical School of Medicine, Universidad Austral, Argentina.
Felipe
F
Inserra
D000450:Aldosterone / Q000097:blood; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000503:physiopathology* / Q000652:urine; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects*; D012964:Sodium / Q000652:urine; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*; D059289:Vascular Stiffness / Q000187:drug effects*
D017673:Sodium Chloride, Dietary; D000450:Aldosterone; D012964:Sodium; D012083:Renin
Sodium intake; aldosterone; hypertensive; renin; vascular stiffness