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AJP - Renal Physiology, Vol 271, Issue 3 653-F658, Copyright © 1996 by American Physiological Society
ARTICLES |
N. Parekh and A. P. Zou
Department of Physiology, University of Heidelberg, Germany. parekh@novsrv1.pio1.uni-heidelberg.de
This study investigated effects of renal prostaglandins and their interaction with different vasoactive agents in regulating regional renal blood flow. Using intravenous infusions, we compared effects of different pressor hormones and a nitric oxide (NO) inhibitor under control conditions and after inhibition of cyclooxygenase. Because vasodilator effects of prostanoids are considered to be mediated via opening of ATP-dependent K+ channels, we also studied effects of a prostacyclin analogue (iloprost), a channel opener (lemakalim), and a channel blocker (glibenclamide). Blood flow in renal cortex (CBF) and medulla (MBF) was determined with previously described platinum electrodes inserted into the kidney of anesthetized rats. Angiotensin II and norepinephrine reduced predominantly only CBF (-24 and -19%, respectively). After indomethacin, which selectively reduced MBF (-25%), angiotensin II and norepinephrine also reduced MBF (-45 and -35%, respectively), whereas the corresponding changes in CBF were not affected by indomethacin. Arginine vasopressin and the NO inhibitor NG-nitro-L-arginine methyl ester reduced both CBF and MBF by approximately 30% both under control conditions and after indomethacin. Iloprost and lemakalim increased selectively MBF (15 and 27%, respectively), whereas glibenclamide selectively decreased MBF (-19%). Our data indicate that renal prostaglandins are predominantly involved in regulating medullary circulation. They probably exert their dilatory action on medullary vessels via opening of ATP-dependent K+ channels and are involved in antagonizing medullary effects of pressor hormones in an agonist-specific manner.
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