ROLE OF PROSTAGLANDINS IN RENAL MEDULLARY CIRCULATION - RESPONSE TO DIFFERENT VASOCONSTRICTORS

Authors
Citation
N. Parekh et Ap. Zou, ROLE OF PROSTAGLANDINS IN RENAL MEDULLARY CIRCULATION - RESPONSE TO DIFFERENT VASOCONSTRICTORS, American journal of physiology. Renal, fluid and electrolyte physiology, 40(3), 1996, pp. 653-658
Citations number
34
Categorie Soggetti
Physiology
ISSN journal
03636127
Volume
40
Issue
3
Year of publication
1996
Pages
653 - 658
Database
ISI
SICI code
0363-6127(1996)40:3<653:ROPIRM>2.0.ZU;2-E
Abstract
This study investigated effects of renal prostaglandins and their inte raction with different vasoactive agents in regulating regional renal blood flow. Using intravenous infusions, we compared effects of differ ent presser hormones and a nitric oxide (NO) inhibitor under control c onditions and after inhibition of cyclooxygenase. Because vasodilator effects of prostanoids are considered to be mediated via opening of AT P-dependent K+ channels, we also studied effects of a prostacyclin ana logue (iloprost), a channel opener (lemakalim), and a channel blocker (glibenclamide). Blood flow in renal cortex (CBF) and medulla (MBF) wa s determined with previously described platinum electrodes inserted in to the kidney of anesthetized rats. Angiotensin II and norepinephrine reduced predominantly only CBF (-24 and -19%, respectively). After ind omethacin, which selectively reduced MBF (-25%), angiotensin II and no repinephrine also reduced MBF (-45 and -35%, respectively), whereas th e corresponding changes in CBF were not affected by indomethacin. Argi nine vasopressin and the NO inhibitor NG-nitro-L-arginine methyl ester reduced both CBF and MBF by similar to 30% both under control conditi ons and after indomethacin. Iloprost and lemakalim increased selective ly MBF (15 and 27%, respectively), whereas glibenclamide selectively d ecreased MBF (-19%). Our data indicate that renal prostaglandins are p redominantly involved in regulating medullary circulation. They probab ly exert their dilatory action on medullary vessels via opening of ATP -dependent K+ channels and are involved in antagonizing medullary effe cts of presser hormones in an agonist-specific manner.