PMID- 8821827
OWN - NLM
STAT- MEDLINE
DCOM- 19961115
LR  - 20190725
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 49
IP  - 2
DP  - 1996 Feb
TI  - Macula densa derived nitric oxide in regulation of glomerular capillary pressure.
PG  - 430-6
AB  - Nitric oxide (NO) is produced by enzymes called nitric oxide synthases (NOS). At 
      least three different isoforms of NOS have been identified in the kidney. This 
      study examines the effects of selective inhibition of the inducible isoform 
      (iNOS) and the neuronal isoform (bNOS) on the glomerular capillary pressure 
      (PGC), through studies of the tubuloglomerular feedback (TGF) mechanism in 
      anaesthetized rats. The proximal tubular stop-flow pressure (PSF) was measured to 
      estimate changes in PGC obtained after activation of the TGF system by varying 
      the loop of Henle perfusion rate with artificial ultrafiltrate including vehicle, 
      NOS inhibition or L-arginine. Infusion of nonspecific NOS inhibition (N 
      omega-Nitro-L-arginine) increased maximal TGF responses (delta PSF) by 84% and 
      L-arginine decreased delta PSF by 37%. Aminoguanidine, a selective 
      iNOS-inhibitor, failed to increase delta PSF, whereas the nonspecific NOS 
      inhibitor methylguanidine increased delta PSF by 64%. 7-Nitro indazole (7-NI), a 
      selective bNOS inhibitor, increased delta PSF by 57% when infused intratubularly, 
      and intraperitoneal administration of 7-NI increased delta PSF by 78%, without 
      any change in blood pressure. Since bNOS is exclusively located in the macula 
      densa (MD) cells, these results confirm and strengthen the obligatory role of 
      MD-produced NO in regulation of TGF and PGC, which has been suggested earlier. 
      iNOS, widely expressed in the kidney, does not seem to play any important role in 
      regulation of PGC.
FAU - Thorup, C
AU  - Thorup C
AD  - Department of Physiology, Lund University, Sweden.
FAU - Erik, A
AU  - Erik A
FAU - Persson, G
AU  - Persson G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Guanidines)
RN  - 0 (Indazoles)
RN  - 2149-70-4 (Nitroarginine)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 5L0H5Q9VAG (Methylguanidine)
RN  - 94ZLA3W45F (Arginine)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - SCQ4EZQ113 (pimagedine)
RN  - UX0N37CMVH (7-nitroindazole)
SB  - IM
MH  - Animals
MH  - Arginine/pharmacology
MH  - Capillary Resistance/physiology
MH  - Enzyme Inhibitors/pharmacology
MH  - Guanidines/pharmacology
MH  - Indazoles/pharmacology
MH  - Juxtaglomerular Apparatus/*enzymology
MH  - Kidney Glomerulus/*blood supply/physiology
MH  - Kidney Tubules, Proximal/physiology
MH  - Male
MH  - Methylguanidine/pharmacology
MH  - Nitric Oxide/*physiology
MH  - Nitric Oxide Synthase/antagonists & inhibitors
MH  - Nitroarginine/pharmacology
MH  - Pressure
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Time Factors
MH  - Vasoconstriction/drug effects
EDAT- 1996/02/01 00:00
MHDA- 1996/02/01 00:01
CRDT- 1996/02/01 00:00
PHST- 1996/02/01 00:00 [pubmed]
PHST- 1996/02/01 00:01 [medline]
PHST- 1996/02/01 00:00 [entrez]
AID - S0085-2538(15)59356-3 [pii]
AID - 10.1038/ki.1996.62 [doi]
PST - ppublish
SO  - Kidney Int. 1996 Feb;49(2):430-6. doi: 10.1038/ki.1996.62.