PMID- 9453315
OWN - NLM
STAT- MEDLINE
DCOM- 19980220
LR  - 20190722
IS  - 0194-911X (Print)
IS  - 0194-911X (Linking)
VI  - 31
IP  - 1 Pt 2
DP  - 1998 Jan
TI  - Protective effect of angiotensin II-induced increase in nitric oxide in the renal 
      medullary circulation.
PG  - 271-6
AB  - This study examined the effect of intravenous infusion of subpressor doses of 
      angiotensin (Ang II) on renal medullary blood flow (MBF), medullary partial 
      oxygen pressure (PO2), and nitric oxide (NO) concentration under normal 
      conditions and during reduction of the medullary nitric oxide synthase (NOS) 
      activity in anesthetized rats. With laser Doppler flowmetry and polarographic 
      measurement of PO2 with microelectrodes, Ang II (5 ng/kg per minute) did not 
      alter renal cortical and medullary blood flows or medullary PO2. 
      N(omega)-nitro-L-arginine methyl ester (L-NAME) was infused into the renal 
      medullary interstitial space at a dose of 1.4 microg/kg per minute, a dose that 
      did not significantly alter basal levels of MBF or PO2. Intravenous infusion of 
      Ang II at the same dose in the presence of L-NAME decreased MBF by 23% and 
      medullary PO2 by 28%, but it had no effect on cortical blood flow or arterial 
      blood pressure. An in vivo microdialysis-oxyhemoglobin NO trapping technique was 
      used in other rats to determine tissue NO concentrations using the same protocol. 
      Ang II infusion increased tissue NO concentrations by 85% in the renal cortex and 
      150% in the renal medulla. Renal medullary interstitial infusion of L-NAME (1.4 
      microg/kg per minute) reduced medullary NO concentrations and substantially 
      blocked Ang II-induced increases in NO concentrations in the renal medulla, but 
      not in the renal cortex. Tissue slices of the renal cortex and medulla were 
      studied to determine the effects of Ang II and L-NAME on the nitrite/nitrate 
      production. Ang II stimulated the nitrite/nitrate production predominately in the 
      renal medulla, which was significantly attenuated by L-NAME. We conclude that 
      small elevations of circulating Ang II levels increase medullary NO production 
      and concentrations, which plays an important role in buffering the 
      vasoconstrictor effects of this peptide and in maintaining a constancy of MBF.
FAU - Zou, A P
AU  - Zou AP
AD  - Department of Physiology, Medical College of Wisconsin, Milwaukee 53226, USA. 
      azou@post.its.mcw.edu
FAU - Wu, F
AU  - Wu F
FAU - Cowley, A W Jr
AU  - Cowley AW Jr
LA  - eng
GR  - DK-52112/DK/NIDDK NIH HHS/United States
GR  - HL-29587/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Hypertension
JT  - Hypertension (Dallas, Tex. : 1979)
JID - 7906255
RN  - 0 (Nitrates)
RN  - 0 (Nitrites)
RN  - 11128-99-7 (Angiotensin II)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
SB  - IM
MH  - Angiotensin II/*pharmacology
MH  - Animals
MH  - In Vitro Techniques
MH  - Kidney Cortex/drug effects/metabolism
MH  - Kidney Medulla/*blood supply/drug effects/*enzymology
MH  - Male
MH  - Microdialysis
MH  - NG-Nitroarginine Methyl Ester/*pharmacology
MH  - Nitrates/metabolism
MH  - Nitric Oxide/*metabolism
MH  - Nitric Oxide Synthase/*metabolism
MH  - Nitrites/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Regional Blood Flow/drug effects
MH  - Renal Circulation/*drug effects/physiology
EDAT- 1998/02/07 08:44
MHDA- 2001/03/28 10:01
CRDT- 1998/02/07 08:44
PHST- 1998/02/07 08:44 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1998/02/07 08:44 [entrez]
AID - 10.1161/01.hyp.31.1.271 [doi]
PST - ppublish
SO  - Hypertension. 1998 Jan;31(1 Pt 2):271-6. doi: 10.1161/01.hyp.31.1.271.