Tags

Type your tag names separated by a space and hit enter

Opposed effects of prostaglandin E2 on perfusion of rat renal cortex and medulla: interactions with the renin-angiotensin system.
Exp Physiol. 2008 Dec; 93(12):1292-302.EP

Abstract

While prostaglandin E(2) (PGE(2)) is an established renal vasodilator, studies of prostaglandin EP receptors suggest that it also has vasoconstrictor potential. Prostaglandin E(2) is much more abundant in the medulla than in the cortex, yet likely differences in effects between zones have not been defined. This study is focused on different vascular effects in the cortex and medulla and interaction with the renin-angiotensin system (RAS). In anaesthetized rats, the effects of cyclo-oxygenase blockade and of PGE(2) infused into the renal artery or renal interstitium were examined. Total renal blood flow was measured by ultrasonic renal artery probe, and local perfusion, separately, of the superficial cortex, outer- and inner medulla, as laser-Doppler fluxes. Indomethacin (5 mg kg(-1) i.v.) increased cortical perfusion (by approximately 10%) and decreased medullary perfusion (by approximately 20%). Renal artery infusion of PGE(2) (15-30 microg kg(-1) h(-1)) increased cortical and medullary perfusion only transiently. Previous inactivation of the RAS using losartan or captopril, and background infusion of exogenous angiotensin II, prevented the transient increase and enhanced the subsequent stable decrease in perfusion. Prostaglandin E(2) infused into the medullary interstitium (7-22 microg kg(-1) h(-1)) increased medullary perfusion by 13%, while cortical perfusion decreased by 6%. Misoprostol, an agonist of constrictor EP(3) receptors, decreased perfusion of the cortex and medulla, with both renal artery and medullary interstitial infusion. In conclusion, in rat renal cortex the dominating stable PGE(2) effect is vasoconstriction, most probably mediated by EP(3) receptors and unrelated to activation of the RAS. Prostaglandin E(2) applied to the cortical or medullary interstitium, a natural route for paracrine agents, induces medullary vasodilatation.

Authors+Show Affiliations

Laboratory of Renal and Body Fluid Physiology, Medical Research Centre of the Polish Academy of Sciences, Pawińskiego 5, 02-106 Warsaw, Poland.No affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18586855

Citation

Badzynska, Bozena, and Janusz Sadowski. "Opposed Effects of Prostaglandin E2 On Perfusion of Rat Renal Cortex and Medulla: Interactions With the Renin-angiotensin System." Experimental Physiology, vol. 93, no. 12, 2008, pp. 1292-302.
Badzynska B, Sadowski J. Opposed effects of prostaglandin E2 on perfusion of rat renal cortex and medulla: interactions with the renin-angiotensin system. Exp Physiol. 2008;93(12):1292-302.
Badzynska, B., & Sadowski, J. (2008). Opposed effects of prostaglandin E2 on perfusion of rat renal cortex and medulla: interactions with the renin-angiotensin system. Experimental Physiology, 93(12), 1292-302. https://doi.org/10.1113/expphysiol.2008.043604
Badzynska B, Sadowski J. Opposed Effects of Prostaglandin E2 On Perfusion of Rat Renal Cortex and Medulla: Interactions With the Renin-angiotensin System. Exp Physiol. 2008;93(12):1292-302. PubMed PMID: 18586855.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Opposed effects of prostaglandin E2 on perfusion of rat renal cortex and medulla: interactions with the renin-angiotensin system. AU - Badzynska,Bozena, AU - Sadowski,Janusz, Y1 - 2008/06/27/ PY - 2008/7/1/pubmed PY - 2009/1/14/medline PY - 2008/7/1/entrez SP - 1292 EP - 302 JF - Experimental physiology JO - Exp Physiol VL - 93 IS - 12 N2 - While prostaglandin E(2) (PGE(2)) is an established renal vasodilator, studies of prostaglandin EP receptors suggest that it also has vasoconstrictor potential. Prostaglandin E(2) is much more abundant in the medulla than in the cortex, yet likely differences in effects between zones have not been defined. This study is focused on different vascular effects in the cortex and medulla and interaction with the renin-angiotensin system (RAS). In anaesthetized rats, the effects of cyclo-oxygenase blockade and of PGE(2) infused into the renal artery or renal interstitium were examined. Total renal blood flow was measured by ultrasonic renal artery probe, and local perfusion, separately, of the superficial cortex, outer- and inner medulla, as laser-Doppler fluxes. Indomethacin (5 mg kg(-1) i.v.) increased cortical perfusion (by approximately 10%) and decreased medullary perfusion (by approximately 20%). Renal artery infusion of PGE(2) (15-30 microg kg(-1) h(-1)) increased cortical and medullary perfusion only transiently. Previous inactivation of the RAS using losartan or captopril, and background infusion of exogenous angiotensin II, prevented the transient increase and enhanced the subsequent stable decrease in perfusion. Prostaglandin E(2) infused into the medullary interstitium (7-22 microg kg(-1) h(-1)) increased medullary perfusion by 13%, while cortical perfusion decreased by 6%. Misoprostol, an agonist of constrictor EP(3) receptors, decreased perfusion of the cortex and medulla, with both renal artery and medullary interstitial infusion. In conclusion, in rat renal cortex the dominating stable PGE(2) effect is vasoconstriction, most probably mediated by EP(3) receptors and unrelated to activation of the RAS. Prostaglandin E(2) applied to the cortical or medullary interstitium, a natural route for paracrine agents, induces medullary vasodilatation. SN - 0958-0670 UR - https://www.unboundmedicine.com/medline/citation/18586855/Opposed_effects_of_prostaglandin_E2_on_perfusion_of_rat_renal_cortex_and_medulla:_interactions_with_the_renin_angiotensin_system_ L2 - https://doi.org/10.1113/expphysiol.2008.043604 DB - PRIME DP - Unbound Medicine ER -