Renal tissue NO and intrarenal haemodynamics during experimental variations of NO content in anaesthetised rats.
Direct renal nitric oxide (NO) measurements were infrequent and no simultaneous measurements of renal cortical and medullary NO and local perfusion. Large-surface NO electrodes were placed in renal cortex and medulla of anaesthetised rats; simultaneously, renal blood flow (RBF, index of cortical perfusion) and medullary laser-Doppler flux (MBF) were determined. NO synthase inhibitors: nonselective (L-NAME) or selective for neuronal NOS (nNOS) (S-methyl-thiocitrulline, SMTC), and NO donor (SNAP), were used to manipulate tissue NO. Baseline tissue NO was significantly higher in medulla (703+/-49 NM) than in cortex (231+/-17 nM). Minimal cortical and medullary NO current measured after maximal L-NAME dose (2.4 mg kg(-1) i.v.) was taken as tissue NO zero kevel. This dose decreased RBF and MBF significantly (-43%). SMTC, 1.2 mg kg(-1) h(-1) i.v., significantly decreased tissue NO by 105+/-32 nM in cortex and 546+/-64 nM in medulla, RBF and MBF decreased 30% and 20%, respectively. Renal artery infusion of SNAP, 0.24 mg kg(-1) min(-1) significantly increased tissue NO by 139+/-18 nM in cortex and 948+/-110 nM in medulla. Since inhibition of nNOS decreased medullary NO by 80% and MBF by 20% only, this isoform has probably minor role in the maintenance of medullary perfusion.
Grzelec-Mojzesowicz
M
M
Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
Sadowski
J
J
D000758:Anesthesia; D000818:Animals; D001783:Blood Flow Velocity; D002956:Citrulline / Q000031:analogs & derivatives / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007191:Indazoles / Q000494:pharmacology; D017736:Ion-Selective Electrodes; D007668:Kidney / Q000098:blood supply* / Q000187:drug effects / Q000378:metabolism*; D007672:Kidney Cortex / Q000098:blood supply / Q000378:metabolism; D007679:Kidney Medulla / Q000098:blood supply / Q000378:metabolism; D017078:Laser-Doppler Flowmetry; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I; D011048:Polarography / Q000295:instrumentation; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000187:drug effects; D015203:Reproducibility of Results; D026423:S-Nitroso-N-Acetylpenicillamine / Q000494:pharmacology; D013890:Thiourea / Q000031:analogs & derivatives / Q000494:pharmacology; D013997:Time Factors
D004791:Enzyme Inhibitors; D007191:Indazoles; D020030:Nitric Oxide Donors; D002956:Citrulline; D009569:Nitric Oxide; D026423:S-Nitroso-N-Acetylpenicillamine; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat; D013890:Thiourea; C086717:S-methylthiocitrulline; C080122:7-nitroindazole; D019331:NG-Nitroarginine Methyl Ester