| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Physiology, Hypertension and Renal Center, Tulane University Health Sciences Center, New Orleans, Louisiana
Submitted 23 May 2006 ; accepted in final form 3 July 2006
Heme oxygenases (HO-1 and HO-2) catalyze the conversion of heme to carbon monoxide (CO), iron, and biliverdin. CO causes vasorelaxation via stimulation of soluble guanylate cyclase (sGC) and/or activation of calcium-activated potassium channels. Because nitric oxide (NO) exerts effects via the same pathways, we tested the interaction between CO and NO on rat afferent arterioles (AAs) using the blood-perfused juxtamedullary nephron preparation. AAs were superfused with either tricarbonyldichlororuthenium (II) dimer, known as CO releasing molecule (CORM-2), 10 µmol/l CO solution, or 15 µmol/l chromium mesoporphyrin (CrMP, HO inhibitor). AAs were also superfused with 1 mmol/l N
-nitro-L-arginine (L-NNA) to inhibit NO synthase (NOS) or 10 µmol/l 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one to inhibit sGC, and then CrMP was superfused during NOS inhibition or sGC inhibition. Treatment with 150 and 300 µmol/l CORM-2 or with CO (10 µmol/l) significantly dilated AAs (22.0 ± 0.9 and 22.8 ± 0.9 vs. 18.3 ± 0.9 µm, n = 5, P < 0.05; and 26.0 ± 1.4 vs. 18.8 ± 0.7 µm, n = 5, P < 0.05). In untreated vessels, HO inhibition did not alter AA diameter (17.5 ± 0.7 vs. 17.2 ± 0.6 µm, n = 7, P > 0.05); however, during inhibition of NO production, which constricted arterioles to 14.6 ± 1.2 µm, n = 6, P < 0.05, concurrent HO inhibition led to further vasoconstriction (11.7 ± 1.6 µm, n = 6, P < 0.05). CORM-2 attenuated the L-NNA-induced vasoconstriction. Inhibition of sGC caused significant constriction (15.7 ± 0.4 vs. 18.8 ± 0.4 µm, n = 6, P < 0.05). HO inhibition during sGC inhibition did not cause further change in AAs (15.5 ± 0.7 µm, n = 6). We conclude that endogenously produced CO does not exert a perceptible influence on AA diameter in the presence of intact NO system; however, when NO production is inhibited, CO serves as an important renoprotective reserve mechanism to prevent excess afferent arteriolar constriction.
heme oxygenase; renal circulation; soluble guanylate cyclase
This article has been cited by other articles:
|
|
 |
|
  D. E. Stec, T. Vera, M. V. Storm, G. R. McLemore Jr, and M. J. Ryan Blood pressure and renal blow flow responses in heme oxygenase-2 knockout mice Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2009; 297(6): R1822 - R1828. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. T. Botros, M. C. Prieto-Carrasquero, V. L. Martin, and L. G. Navar Heme oxygenase induction attenuates afferent arteriolar autoregulatory responses Am J Physiol Renal Physiol, October 1, 2008; 295(4): F904 - F911. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Ren, M. A. D'Ambrosio, H. Wang, R. Liu, J. L. Garvin, and O. A. Carretero Heme oxygenase metabolites inhibit tubuloglomerular feedback (TGF) Am J Physiol Renal Physiol, October 1, 2008; 295(4): F1207 - F1212. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. E. Stec, H. A. Drummond, and T. Vera Role of Carbon Monoxide in Blood Pressure Regulation Hypertension, March 1, 2008; 51(3): 597 - 604. [Full Text] [PDF]
|
|
|
|
|
|
A. Patzak, A. Steege, E. Y. Lai, J. O. Brinkmann, E. Kupsch, N. Spielmann, A. Gericke, A. Skalweit, J. Stegbauer, P. B. Persson, et al. Angiotensin II response in afferent arterioles of mice lacking either the endothelial or neuronal isoform of nitric oxide synthase Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2008; 294(2): R429 - R437. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Herrera and J. L. Garvin Novel role of AQP-1 in NO-dependent vasorelaxation Am J Physiol Renal Physiol, May 1, 2007; 292(5): F1443 - F1451. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
