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Disparate roles of AT2 receptors in the renal cortical and medullary circulations of anesthetized rabbits.
Hypertension. 2003 Aug; 42(2):200-5.H

Abstract

The contributions of angiotensin II type 1 (AT1) and type 2 (AT2) receptors to the control of regional kidney blood flow were determined in pentobarbital-anesthetized rabbits. Intravenous candesartan (AT1 antagonist; 10 microg/kg plus 10 microg x kg(-1) x h(-1)) reduced mean arterial pressure (12%) and increased total renal blood flow (29%) and cortical laser-Doppler flux (18%) but not medullary laser-Doppler flux. Neither intravenous PD123319 (AT2 antagonist; 1 mg/kg plus 1 mg x kg(-1) x h(-1)) nor saline vehicle significantly affected these variables, and the responses to candesartan plus PD123319 were indistinguishable from those of candesartan alone. In vehicle-treated rabbits, renal-arterial infusions of angiotensin II (1 to 25 ng x kg(-1) x min(-1)) and angiotensin III (5 to 125 ng x kg(-1) x min(-1)) dose-dependently reduced renal blood flow (up to 51%) and cortical laser-Doppler flux (up to 50%) but did not significantly affect medullary laser-Doppler flux or arterial pressure. Angiotensin(1-7) (20 to 500 ng x kg(-1) x min(-1)) had similar effects but of lesser magnitude. CGP42112A (20 to 500 ng x kg(-1) x min(-1)) did not significantly affect these variables. After PD123319 administration, angiotensin II and angiotensin III dose-dependently increased medullary laser-Doppler flux (up to 84%), and reductions in renal blood flow in response to angiotensin II were enhanced. Candesartan abolished renal hemodynamic responses to the angiotensin peptides, even when given in combination with PD123319. We conclude that AT2 receptor activation counteracts AT1-mediated vasoconstriction in the renal cortex but also counteracts AT1-mediated vasodilatation in vascular elements controlling medullary perfusion. These mechanisms might have an important effect on the control of medullary perfusion under conditions of activation of the renin-angiotensin system.

Authors+Show Affiliations

Department of Physiology, PO Box 13F, Monash University, Victoria 3800, Australia. Lisa.Duke@med.monash.edu.auNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12847115

Citation

Duke, Lisa M., et al. "Disparate Roles of AT2 Receptors in the Renal Cortical and Medullary Circulations of Anesthetized Rabbits." Hypertension (Dallas, Tex. : 1979), vol. 42, no. 2, 2003, pp. 200-5.
Duke LM, Eppel GA, Widdop RE, et al. Disparate roles of AT2 receptors in the renal cortical and medullary circulations of anesthetized rabbits. Hypertension. 2003;42(2):200-5.
Duke, L. M., Eppel, G. A., Widdop, R. E., & Evans, R. G. (2003). Disparate roles of AT2 receptors in the renal cortical and medullary circulations of anesthetized rabbits. Hypertension (Dallas, Tex. : 1979), 42(2), 200-5.
Duke LM, et al. Disparate Roles of AT2 Receptors in the Renal Cortical and Medullary Circulations of Anesthetized Rabbits. Hypertension. 2003;42(2):200-5. PubMed PMID: 12847115.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Disparate roles of AT2 receptors in the renal cortical and medullary circulations of anesthetized rabbits. AU - Duke,Lisa M, AU - Eppel,Gabriela A, AU - Widdop,Robert E, AU - Evans,Roger G, Y1 - 2003/07/07/ PY - 2003/7/9/pubmed PY - 2003/8/9/medline PY - 2003/7/9/entrez SP - 200 EP - 5 JF - Hypertension (Dallas, Tex. : 1979) JO - Hypertension VL - 42 IS - 2 N2 - The contributions of angiotensin II type 1 (AT1) and type 2 (AT2) receptors to the control of regional kidney blood flow were determined in pentobarbital-anesthetized rabbits. Intravenous candesartan (AT1 antagonist; 10 microg/kg plus 10 microg x kg(-1) x h(-1)) reduced mean arterial pressure (12%) and increased total renal blood flow (29%) and cortical laser-Doppler flux (18%) but not medullary laser-Doppler flux. Neither intravenous PD123319 (AT2 antagonist; 1 mg/kg plus 1 mg x kg(-1) x h(-1)) nor saline vehicle significantly affected these variables, and the responses to candesartan plus PD123319 were indistinguishable from those of candesartan alone. In vehicle-treated rabbits, renal-arterial infusions of angiotensin II (1 to 25 ng x kg(-1) x min(-1)) and angiotensin III (5 to 125 ng x kg(-1) x min(-1)) dose-dependently reduced renal blood flow (up to 51%) and cortical laser-Doppler flux (up to 50%) but did not significantly affect medullary laser-Doppler flux or arterial pressure. Angiotensin(1-7) (20 to 500 ng x kg(-1) x min(-1)) had similar effects but of lesser magnitude. CGP42112A (20 to 500 ng x kg(-1) x min(-1)) did not significantly affect these variables. After PD123319 administration, angiotensin II and angiotensin III dose-dependently increased medullary laser-Doppler flux (up to 84%), and reductions in renal blood flow in response to angiotensin II were enhanced. Candesartan abolished renal hemodynamic responses to the angiotensin peptides, even when given in combination with PD123319. We conclude that AT2 receptor activation counteracts AT1-mediated vasoconstriction in the renal cortex but also counteracts AT1-mediated vasodilatation in vascular elements controlling medullary perfusion. These mechanisms might have an important effect on the control of medullary perfusion under conditions of activation of the renin-angiotensin system. SN - 1524-4563 UR - https://www.unboundmedicine.com/medline/citation/12847115/Disparate_roles_of_AT2_receptors_in_the_renal_cortical_and_medullary_circulations_of_anesthetized_rabbits_ L2 - https://www.ahajournals.org/doi/10.1161/01.HYP.0000083341.64034.00?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -