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Role of NO and COX pathways in mediation of adenosine A1 receptor-induced renal vasoconstriction.
Exp Biol Med (Maywood). 2007 May; 232(5):690-4.EB

Abstract

The mechanism of adenosine A1 receptor-induced intrarenal vasoconstriction is unclear; it depends on sodium intake and may be mediated by changing the intrarenal activity of the nitric oxide (NO) and/or cyclooxygenase (COX) pathway of arachidonic acid metabolism. The effects of 2-chloro-N(6)-cyclopentyl-adenosine (CCPA), a selective A1 receptor agonist, on renal hemodynamics were examined in anesthetized rats maintained on high sodium (HS) or low sodium (LS) diet. Total renal (i.e., cortical) blood flow (RBF) as well as superficial cortical (CBF), outer medullary (OMBF), and inner medullary (IMBF) flows were determined by laser-Doppler. In HS rats, suprarenal aortic infusions of 8-40 nmol/kg/hr CCPA decreased IMBF (15%) and other perfusion indices (22%-27%); in LS rats, IMBF increased 3% (insignificant) and other indices decreased 13%-24%. In LS rats, pretreatment with N-nitro-L-arginine methyl ester prevented the A1 receptor-mediated decrease in RBF and CBF but not OMBF; the response in IMBF was not altered. Pretreatment with indomethacin prevented the decreases in RBF, CBF, and OMBF and did not change the response of IMBF. Thus, within the cortex the vasoconstriction that follows A1 receptor activation results both from inhibition of NO synthesis and from stimulation of vasoconstrictor products of the COX pathway. In the outer medulla, the latter products seem exclusively responsible for CCPA-induced vasoconstriction. The observation that in LS rats IMBF was not affected by stimulation of adenosine A1 receptors suggests that limiting salt intake may help protect medullary perfusion against vasoconstrictor stimuli which have the potential to disturb long-term control of arterial pressure.

Authors+Show Affiliations

Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland. renal@cmdik.pan.plNo 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

17463166

Citation

Walkowska, Agnieszka, et al. "Role of NO and COX Pathways in Mediation of Adenosine A1 Receptor-induced Renal Vasoconstriction." Experimental Biology and Medicine (Maywood, N.J.), vol. 232, no. 5, 2007, pp. 690-4.
Walkowska A, Dobrowolski L, Kompanowska-Jezierska E, et al. Role of NO and COX pathways in mediation of adenosine A1 receptor-induced renal vasoconstriction. Exp Biol Med (Maywood). 2007;232(5):690-4.
Walkowska, A., Dobrowolski, L., Kompanowska-Jezierska, E., & Sadowski, J. (2007). Role of NO and COX pathways in mediation of adenosine A1 receptor-induced renal vasoconstriction. Experimental Biology and Medicine (Maywood, N.J.), 232(5), 690-4.
Walkowska A, et al. Role of NO and COX Pathways in Mediation of Adenosine A1 Receptor-induced Renal Vasoconstriction. Exp Biol Med (Maywood). 2007;232(5):690-4. PubMed PMID: 17463166.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of NO and COX pathways in mediation of adenosine A1 receptor-induced renal vasoconstriction. AU - Walkowska,Agnieszka, AU - Dobrowolski,Leszek, AU - Kompanowska-Jezierska,Elzbieta, AU - Sadowski,Janusz, PY - 2007/4/28/pubmed PY - 2007/6/15/medline PY - 2007/4/28/entrez SP - 690 EP - 4 JF - Experimental biology and medicine (Maywood, N.J.) JO - Exp Biol Med (Maywood) VL - 232 IS - 5 N2 - The mechanism of adenosine A1 receptor-induced intrarenal vasoconstriction is unclear; it depends on sodium intake and may be mediated by changing the intrarenal activity of the nitric oxide (NO) and/or cyclooxygenase (COX) pathway of arachidonic acid metabolism. The effects of 2-chloro-N(6)-cyclopentyl-adenosine (CCPA), a selective A1 receptor agonist, on renal hemodynamics were examined in anesthetized rats maintained on high sodium (HS) or low sodium (LS) diet. Total renal (i.e., cortical) blood flow (RBF) as well as superficial cortical (CBF), outer medullary (OMBF), and inner medullary (IMBF) flows were determined by laser-Doppler. In HS rats, suprarenal aortic infusions of 8-40 nmol/kg/hr CCPA decreased IMBF (15%) and other perfusion indices (22%-27%); in LS rats, IMBF increased 3% (insignificant) and other indices decreased 13%-24%. In LS rats, pretreatment with N-nitro-L-arginine methyl ester prevented the A1 receptor-mediated decrease in RBF and CBF but not OMBF; the response in IMBF was not altered. Pretreatment with indomethacin prevented the decreases in RBF, CBF, and OMBF and did not change the response of IMBF. Thus, within the cortex the vasoconstriction that follows A1 receptor activation results both from inhibition of NO synthesis and from stimulation of vasoconstrictor products of the COX pathway. In the outer medulla, the latter products seem exclusively responsible for CCPA-induced vasoconstriction. The observation that in LS rats IMBF was not affected by stimulation of adenosine A1 receptors suggests that limiting salt intake may help protect medullary perfusion against vasoconstrictor stimuli which have the potential to disturb long-term control of arterial pressure. SN - 1535-3702 UR - https://www.unboundmedicine.com/medline/citation/17463166/Role_of_NO_and_COX_pathways_in_mediation_of_adenosine_A1_receptor_induced_renal_vasoconstriction_ DB - PRIME DP - Unbound Medicine ER -