Non-modulating hypertension (NMHT) is a high renin subtype of salt sensitive
hypertension, which fails to achieve renal vasodilatation and a correct Na+ handling during
We investigate, in MHT and NMHT, the role of ANP, the renin-angiotensin system and PgI2, in
the renal sodium handling mechanisms.
After 10 days of low (20mmol.L) or after 72hs of high (250mmol.L) sodium intake, 13 NMHT
(34±5y; 9 male) and 13 MHT (32±4y; 10male) were studied. Pro-ANP (1-30) PgI2, PRA and total exchangeable
Na+24 (ENa+) were measured.
Under low sodium intake, PRA (4.2±0.5ng.ml.h; p<0.05) and Pro-ANP (78.6±2pg/ml, p<0.05) were higher than in
NMHT under (3.1±0.4ng.ml.h and 69.8±3 pg/ml).
After 72h of high Na+ intake, Pro-ANP (1-30) increased significantly only in MHT (82.1±3pg/ml, p<0.05).
PgI2, under low sodium intake (1.83±0.2pg/24h), increased in MHT after 72h under high sodium (2.58±0.5pg/
24h, p<0.02). Under low sodium diet, PgI2 (2.16±0.11pg/24h) was as higher in NMHT, as in MHT. After 72h under
high Na+ intake, it failed to show any change (2.61±0.36 pg/24h; p=ns).
A significant correlation between variations in ENa+ and mean blood pressure (r=0.50, p<0.01), variations in
Pro-ANP (1-30) values and ENa+ in MHT (r=0.95; p<0.001) while a negative correlation between ENa+ variations
and ENa+ (r=0.81, p<0.05) was observed in NMHT. ENa+ variations were only significantly related to variations in
FF in MHT.
Thus, in NMHT, there is an unbalanced relationship between vasonstrictor and vasodilator mediators. From these, as
an extrarenal homeostatic mediator, ANP seems to play an important role to compensate the altered renal sodium