Jc. Ter Maaten et al., Renal sodium handling and haemodynamics are equally affected by hyperinsulinaemia in salt-sensitive and salt-resistant hypertensives, J HYPERTENS, 19(9), 2001, pp. 1633-1641
Citations number
49
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Objective It is well-known that insulin induces renal sodium retention. It
is not yet known whether insulin's renal effects are involved in the develo
pment of salt-sensitive hypertension. We assessed the effects of insulin on
renal sodium handling and haemodynamics in 10 salt-sensitive (SS) and 10 s
alt-resistant (SR) essential hypertensives.
Design After a baseline period of 90 min, all subjects underwent a euglycae
mic clamp with sequential infusion of a physiological and supraphysiologica
l dose of insulin (50 and 150 mU/kg per h) during 90 min periods each. Time
-control studies were performed in the same subjects. Clearances of I-131-h
ippuran, I-125-iothalamate, sodium and lithium were used to evaluate renal
plasma flow (RPF), C-Na/glomerular filtration rate (GFR) and fractional pro
ximal and distal sodium reabsorption.
Results Plasma insulin levels and insulin-mediated glucose uptake did not d
iffer between both groups. RPF and GFR showed similar increases during both
insulin infusions in both groups. During physiological hyperinsulinaemia,
fractional sodium excretion decreased 38% (P = 0.009) in the SS group and 3
6% (P = 0.002) in the SR group. During supraphysiological hyperinsulinaemia
, fractional sodium excretion decreased 49% (P = 0.01) in the SS group and
19% (P = 0.2) in the SR group, not statistically different between both gro
ups. Fractional proximal sodium reabsorption was unaffected and fractional
distal sodium reabsorption increased to a similar magnitude in both groups.
Conclusion The comparable renal effects of acute exogenous hyperinsulinaemi
a in SS and SR hypertensives do not support a role for insulin in the devel
opment of salt-sensitive hypertension. However, the results do not yet excl
ude a role for chronic hyperinsulinaemia. (C) 2001 Lippincott Williams & Wi
lkins.