Effect of exogenous angiotensin II on renal tissue nitric oxide and intrarenal circulation in anaesthetized rats.
OBJECTIVE
The renal medullary circulation is protected against depressor action of angiotensin II (Ang II) because of the opposed action of a vasodilator agent, possibly nitric oxide (NO). This possibility was evaluated by a simultaneous determination of the effect of exogenous Ang II on renal cortical and medullary tissue NO and on intrarenal circulation.


METHODS
In anaesthetized rats effects were determined of pressor and subpressor Ang II doses on tissue NO concentration in the renal cortex and inner medulla (selective NO electrodes), total renal blood flow (RBF, Transonic renal artery probe) and inner medullary blood flow (IMBF, laser Doppler flux). The measurements were repeated in rats treated with tempol, a scavenger of superoxide.


RESULTS
Moderately pressor Ang II infusion significantly decreased tissue NO signal from 5.7 +/- 0.2 to 5.3 +/- 0.2 nA in the cortex and from 10.7 +/- 0.6 to 10.1 +/- 0.6 nA in the medulla. The RBF, a measure of cortical perfusion, decreased, and IMBF did not change. Subpressor doses of Ang II did not change medullary or cortical tissue NO. Tempol prevented an Ang II dependent decrease in medullary (but not cortical) NO without affecting RBF or IMBF responses.


CONCLUSIONS
An absence of an increase in renal cortical or medullary tissue NO after infusion of subpressor or pressor doses of Ang II speaks against the role of this agent in buffering the intrarenal vasoconstrictor action of the hormone. Elimination of the post-Ang II decrease in medullary NO in animals pre-treated with tempol suggests that tissue superoxide generation stimulated by the hormone might reduce local bioavailability of NO.
Badzyńska
B
B
Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
Grzelec-Mojzesowicz
M
M
Sadowski
J
J
D000758:Anesthesia / Q000379:methods; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D003497:Cyclic N-Oxides / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D007672:Kidney Cortex / Q000187:drug effects / Q000378:metabolism; D007679:Kidney Medulla / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009569:Nitric Oxide / Q000032:analysis*; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000187:drug effects* / Q000502:physiology; D013113:Spin Labels; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
D000975:Antioxidants; D003497:Cyclic N-Oxides; D013113:Spin Labels; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D009569:Nitric Oxide; C001803:tempol