Arginine vasopressin increases renal sodium excretion in the anesthetized rat through V1 receptors.
We have previously suggested that the increase in renal Na+ excretion in response to physiological doses of arginine vasopressin (AVP) is not directly linked to the V2-mediated antidiuretic effect. In the present study we investigated the possible involvement of AVP V1 receptors in this natriuresis using a specific AVP V1 antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid), 2-O-methyltyrosine arginine vasopressin, d(CH2)5[Tyr(Me)2]AVP, infused at a rate of 15 ng.min-1. Male anesthetized Sprague-Dawley rats were placed on a continuous jugular infusion of 0.077 M NaCl at 150 microL.min-1. After a 3-h equilibration period, samples were collected at 20-min intervals for 4 h for the determination of urine flow, and Na+ and K+ excretion rates. In those animals in which the effects of AVP were studied, a 1-h control period was allowed following which AVP was infused at 0.02-0.08 pmol.min-1 for 1 h 20 min in separate groups of animals and then returned to the infusate alone for the last part of the experiment. In other groups the AVP V1 antagonist d(CH2)5[Tyr(Me)2]AVP (15 ng.min-1) alone or in combination with AVP (at various dose rates) was also administered for 1 h 20 min. All dose rates of AVP produced an antidiuresis which was associated significantly to increased Na+ excretion rate. However, AVP administration at the median dose rate (0.04 pmol.min-1) significantly (p < 0.01) decreased the amount of urine voided by comparison with control animals (6.34 +/- 1.05 ml vs. 11.892 +/- 0.03 mL, n = 7) although the urinary Na+ was elevated (967 +/- 18 mumol, vs. 742 +/- 81 mumol, n = 7). This AVP-induced increase in urinary Na+ loss was abolished in animals receiving combined AVP (0.04 pmol.min-1) and AVP V1 antagonist (674 +/- 47 mumol, n = 7) although the antidiuretic effect persisted. Urine flow and Na+ excretion rates remained unchanged in groups of animals administered AVP V1 antagonist alone. In all groups, the K+ excretion rates did not significantly differ. It is concluded that the V1 receptor mediates the natriuretic effect of AVP.
Musabayane
C T
CT
Department of Physiology, University of Zimbabwe, Harare, Zimbabwe.
Forsling
M L
ML
Balment
R J
RJ
D000758:Anesthesia; D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001127:Arginine Vasopressin / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005919:Glomerular Filtration Rate; D007262:Infusions, Intravenous; D007668:Kidney / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009318:Natriuresis / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000652:urine; D051381:Rats; D017207:Rats, Sprague-Dawley; D017483:Receptors, Vasopressin / Q000502:physiology*; D012076:Renal Agents / Q000008:administration & dosage / Q000494:pharmacology*; D012964:Sodium / Q000652:urine; D014563:Urodynamics / Q000187:drug effects
D065092:Antidiuretic Hormone Receptor Antagonists; D017483:Receptors, Vasopressin; D012076:Renal Agents; D001127:Arginine Vasopressin; C025044:argipressin, beta-mercapto-beta,beta cyclopentamethylenepropionic acid(1)-; D012964:Sodium; D011188:Potassium