Arginine vasopressin-mediated stimulation of nitric oxide within the rat renal medulla

Frank Park, Ai Ping Zou, Allen W. Cowley

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

The present study was designed to determine whether arginine vasopressin (AVP) can stimulate nitric oxide (NO) production within the renal medulla and thereby modulate renal medullary blood flow. An in vivo microdialysis/NO trapping technique was used to determine changes in medullary interstitial [NO]. AVP (2 ng/kg per minute) was delivered into the renal medullary interstitium and resulted in a significant increase in renal medullary [NO] of 35%, which was blocked by pretreatment with nitro-L-arginine methyl ester (L-NAME) (1.3 μg/kg per minute) administered into the renal medullary interstitium. The vasopressin V2 receptor agonist 1-desamino-8-D-arginine vasopressin (dDAVP) resulted in a significant increase of 32% in renal medullary interstitial [NO]. No change in renal medullary interstitial [NO] was observed after selective vasopressin V1 receptor stimulation. Laser- Doppler flowmetry with implanted optical fibers was performed to measure cortical and medullary blood flow changes within the kidney. Renal interstitial infusion of dDAVP in rats pretreated with a vasopressin V1 receptor antagonist resulted in a 15% increase (P<0.05) in medullary blood flow, which was completely blocked by pretreatment with L-NAME (1.3 μg/kg per minute). This study demonstrates that AVP increases renal medullary interstitial [NO] through vasopressin V2 receptor stimulation, which in turn elevates blood flow to the renal medulla.

Original languageEnglish (US)
Pages (from-to)896-901
Number of pages6
JournalHypertension
Volume32
Issue number5
DOIs
StatePublished - Jan 1 1998

Fingerprint

Arginine Vasopressin
Nitric Oxide
Vasopressin Receptors
Kidney
Deamino Arginine Vasopressin
Renal Circulation
NG-Nitroarginine Methyl Ester
Optical Fibers
Laser-Doppler Flowmetry
Microdialysis

All Science Journal Classification (ASJC) codes

  • Internal Medicine

Cite this

Arginine vasopressin-mediated stimulation of nitric oxide within the rat renal medulla. / Park, Frank; Zou, Ai Ping; Cowley, Allen W.

In: Hypertension, Vol. 32, No. 5, 01.01.1998, p. 896-901.

Research output: Contribution to journalArticle

Park, Frank ; Zou, Ai Ping ; Cowley, Allen W. / Arginine vasopressin-mediated stimulation of nitric oxide within the rat renal medulla. In: Hypertension. 1998 ; Vol. 32, No. 5. pp. 896-901.
@article{3bbce72afbbf4c23bbb161499bf9291b,
title = "Arginine vasopressin-mediated stimulation of nitric oxide within the rat renal medulla",
abstract = "The present study was designed to determine whether arginine vasopressin (AVP) can stimulate nitric oxide (NO) production within the renal medulla and thereby modulate renal medullary blood flow. An in vivo microdialysis/NO trapping technique was used to determine changes in medullary interstitial [NO]. AVP (2 ng/kg per minute) was delivered into the renal medullary interstitium and resulted in a significant increase in renal medullary [NO] of 35{\%}, which was blocked by pretreatment with nitro-L-arginine methyl ester (L-NAME) (1.3 μg/kg per minute) administered into the renal medullary interstitium. The vasopressin V2 receptor agonist 1-desamino-8-D-arginine vasopressin (dDAVP) resulted in a significant increase of 32{\%} in renal medullary interstitial [NO]. No change in renal medullary interstitial [NO] was observed after selective vasopressin V1 receptor stimulation. Laser- Doppler flowmetry with implanted optical fibers was performed to measure cortical and medullary blood flow changes within the kidney. Renal interstitial infusion of dDAVP in rats pretreated with a vasopressin V1 receptor antagonist resulted in a 15{\%} increase (P<0.05) in medullary blood flow, which was completely blocked by pretreatment with L-NAME (1.3 μg/kg per minute). This study demonstrates that AVP increases renal medullary interstitial [NO] through vasopressin V2 receptor stimulation, which in turn elevates blood flow to the renal medulla.",
author = "Frank Park and Zou, {Ai Ping} and Cowley, {Allen W.}",
year = "1998",
month = "1",
day = "1",
doi = "10.1161/01.HYP.32.5.896",
language = "English (US)",
volume = "32",
pages = "896--901",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Arginine vasopressin-mediated stimulation of nitric oxide within the rat renal medulla

AU - Park, Frank

AU - Zou, Ai Ping

AU - Cowley, Allen W.

PY - 1998/1/1

Y1 - 1998/1/1

N2 - The present study was designed to determine whether arginine vasopressin (AVP) can stimulate nitric oxide (NO) production within the renal medulla and thereby modulate renal medullary blood flow. An in vivo microdialysis/NO trapping technique was used to determine changes in medullary interstitial [NO]. AVP (2 ng/kg per minute) was delivered into the renal medullary interstitium and resulted in a significant increase in renal medullary [NO] of 35%, which was blocked by pretreatment with nitro-L-arginine methyl ester (L-NAME) (1.3 μg/kg per minute) administered into the renal medullary interstitium. The vasopressin V2 receptor agonist 1-desamino-8-D-arginine vasopressin (dDAVP) resulted in a significant increase of 32% in renal medullary interstitial [NO]. No change in renal medullary interstitial [NO] was observed after selective vasopressin V1 receptor stimulation. Laser- Doppler flowmetry with implanted optical fibers was performed to measure cortical and medullary blood flow changes within the kidney. Renal interstitial infusion of dDAVP in rats pretreated with a vasopressin V1 receptor antagonist resulted in a 15% increase (P<0.05) in medullary blood flow, which was completely blocked by pretreatment with L-NAME (1.3 μg/kg per minute). This study demonstrates that AVP increases renal medullary interstitial [NO] through vasopressin V2 receptor stimulation, which in turn elevates blood flow to the renal medulla.

AB - The present study was designed to determine whether arginine vasopressin (AVP) can stimulate nitric oxide (NO) production within the renal medulla and thereby modulate renal medullary blood flow. An in vivo microdialysis/NO trapping technique was used to determine changes in medullary interstitial [NO]. AVP (2 ng/kg per minute) was delivered into the renal medullary interstitium and resulted in a significant increase in renal medullary [NO] of 35%, which was blocked by pretreatment with nitro-L-arginine methyl ester (L-NAME) (1.3 μg/kg per minute) administered into the renal medullary interstitium. The vasopressin V2 receptor agonist 1-desamino-8-D-arginine vasopressin (dDAVP) resulted in a significant increase of 32% in renal medullary interstitial [NO]. No change in renal medullary interstitial [NO] was observed after selective vasopressin V1 receptor stimulation. Laser- Doppler flowmetry with implanted optical fibers was performed to measure cortical and medullary blood flow changes within the kidney. Renal interstitial infusion of dDAVP in rats pretreated with a vasopressin V1 receptor antagonist resulted in a 15% increase (P<0.05) in medullary blood flow, which was completely blocked by pretreatment with L-NAME (1.3 μg/kg per minute). This study demonstrates that AVP increases renal medullary interstitial [NO] through vasopressin V2 receptor stimulation, which in turn elevates blood flow to the renal medulla.

UR - http://www.scopus.com/inward/record.url?scp=0031738947&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031738947&partnerID=8YFLogxK

U2 - 10.1161/01.HYP.32.5.896

DO - 10.1161/01.HYP.32.5.896

M3 - Article

VL - 32

SP - 896

EP - 901

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 5

ER -