| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
RENIN-MINERALCORTICOIDS-ANF-ADH |
Institut National de la Santé et de la Recherche Médicale, Unité-367 (S.F., N.B.) and Unité-430 (P.B., D.H.); and Hôpital Necker-Enfants Malades (A.H., S.G.), Paris, France
Address all correspondence and requests for reprints to: Dr. Nadine Bouby, Institut National de la Santé et de la Recherche Médicale, Unité-367, 17 rue du Fer à Moulin, 75005 Paris, France. E-mail: . bouby{at}ifm.inserm.fr
The present study was intended to determine whether the long-term V2 receptor-mediated effects of vasopressin on sodium reabsorption in the renal collecting duct is an aggravating factor in salt-sensitive hypertension. Deoxycorticosterone acetate (DOCA)-salt hypertension was induced in uninephrectomized rats that had been chronically pretreated with a V2 agonist (dDAVP; 1-deamino-8D-arginine vasopressin; 0.6 µg/kg·d) or a V2 antagonist (SR121463, 3 mg/kg·d) or were untreated. Plasma osmolality and natremia were not significantly different in the groups. Blood pressure was significantly increased by dDAVP pretreatment (+11 mm Hg; P = 0.006), and this effect was exacerbated after DOCA-salt-induced hypertension (+17 mm Hg; P = 0.042). The dDAVP-treated rats had a lower hematocrit (40 ± 2% vs. 47 ± 1% and 45 ± 2%) and markedly higher albuminuria (91 ± 9 vs. 17 ± 8 and 15 ± 8 mg/d), mortality rate (50% vs. 0% and 0%), and cardiac and renal hypertrophy than the control and SR121463 groups. Histological renal lesions were worsened by V2 agonism and prevented by V2 antagonism. Renal mRNA expression of ß- and 
-subunits of the epithelial sodium channel was significantly increased by dDAVP treatment (P < 0.05). These findings provide evidence that chronic stimulation of vasopressin V2 receptor raises basal blood pressure in rats and exacerbates the development of DOCA-salt hypertension, organ damage, and mortality. These effects could be due at least in part to the sustained stimulation of sodium reabsorption by epithelial sodium channel in the distal part of the nephron, which promotes sodium retention.
This article has been cited by other articles:
 |
|
 |
|
  J. Perucca, D. G. Bichet, P. Bardoux, N. Bouby, and L. Bankir Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists J. Am. Soc. Nephrol., September 1, 2008; 19(9): 1721 - 1731. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. E. Torres Role of Vasopressin Antagonists Clin. J. Am. Soc. Nephrol., July 1, 2008; 3(4): 1212 - 1218. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Bankir, J. Perucca, and M. H. Weinberger Ethnic Differences in Urine Concentration: Possible Relationship to Blood Pressure Clin. J. Am. Soc. Nephrol., March 1, 2007; 2(2): 304 - 312. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. C. Luft Vasopressin, Urine Concentration, and Hypertension: A New Perspective on an Old Story Clin. J. Am. Soc. Nephrol., March 1, 2007; 2(2): 196 - 197. [Full Text] [PDF]
|
|
|
|
 |
|
 J. Perucca, N. Bouby, P. Valeix, and L. Bankir Sex difference in urine concentration across differing ages, sodium intake, and level of kidney disease Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2007; 292(2): R700 - R705. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. L. O'Donaughy, Y. Qi, and V. L. Brooks Central Action of Increased Osmolality to Support Blood Pressure in Deoxycorticosterone Acetate-Salt Rats Hypertension, October 1, 2006; 48(4): 658 - 663. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Bankir, S. Fernandes, P. Bardoux, N. Bouby, and D. G. Bichet Vasopressin-V2 Receptor Stimulation Reduces Sodium Excretion in Healthy Humans J. Am. Soc. Nephrol., July 1, 2005; 16(7): 1920 - 1928. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
