Vol. 274, Issue 6, R1619-R1625, June 1998
Mechanism of vasopressin natriuresis in the dog: role of
vasopressin receptors and prostaglandins
Elzbieta
Kompanowska-Jezierska,
Claus
Emmeluth,
Lisbeth
Grove,
Poul
Christensen,
Janusz
Sadowski, and
Peter
Bie
Department of Medical Physiology, The Panum Institute, University of
Copenhagen, 2200 Copenhagen, Denmark; and Laboratory of Renal and
Body Fluid Physiology, Medical Research Centre, Polish Academy of
Sciences, 02-106 Warsaw, Poland
Renal effects of
physiological amounts of vasopressin were studied in conscious dogs
during servocontrolled overhydration (2% body wt). During infusion of
vasopressin (50 pg · min
1 · kg
body wt1), plasma
vasopressin concentration increased to 2.30 ± 0.20 pg/ml compared
with 0.12 ± 0.03 pg/ml during control (water diuresis). With
vasopressin infusion, urine flow was significantly lower (0.30 ± 0.10 ml/min) and sodium excretion
(UNaV) was significantly higher
(58.0 ± 15.8 µmol/min) than without vasopressin (4.6 ± 0.4 ml/min and 14.4 ± 4.1 µmol/min, respectively).
Deamino-[Cys1,D-Arg8]vasopressin,
a V2 receptor agonist (4 pg · min1 · kg1),
mimicked the antidiuretic response (0.20 ± 0.03 ml/min) without changing UNaV (9.7 ± 4.4 µmol/min). Indomethacin given during arginine vasopressin (AVP)
infusion suppressed prostaglandin
E2 excretion, intensified the
antidiuresis (0.10 ± 0.02 ml/min), and abolished the natriuresis
(13.4 ± 3.7 µmol/min). During AVP infusion,
UNaV was highly correlated
(r = 0.85) with prostaglandin E2 excretion. Blood pressure,
glomerular filtration rate, plasma atrial natriuretic peptide
concentration, and the rate of proximal tubule reabsorption (derived
from lithium clearance) were similar in all series. The data indicate
that, in the dog, physiological amounts of vasopressin can induce
natriuresis, probably through activation of
non-V2 receptors and the
intrarenal synthesis of prostaglandins.
sodium excretion; indomethacin; deamino-[Cys1,D-Arg8]vasopressin; urinary concentration; lithium clearance
