| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Centre Hospitalier Universitaire de Québec, Centre de Recherche du Pavillon l'Hôtel-Dieu de Québec, Quebec, Canada G1R 2J6
To determine whether kinin receptor expression is regulated by kinins, prostaglandins, and/or nitric oxide (NO), rabbits were treated with a B1 receptor (B1R) antagonist, a B2 receptor (B2R) antagonist, a prostacyclin mimetic, or inhibitors of NO synthase, cyclooxygenase, or angiotensin-converting enzyme. The mRNA concentrations for B1R and B2R (multiplex RT-PCR) were measured in several organs. The B2R mRNA expression was not significantly upregulated by any of the treatments; it was notably downregulated by angiotensin-converting enzyme or cyclooxygenase blockade or B2R antagonism in the heart and duodenum. A treatment with bacterial lipopolysaccharide (LPS), known to induce B1R expression, has also been applied and was the most consistent in upregulating the expression of B1R mRNA (kidney, duodenum, and striated muscle). The contractile responses mediated by kinin receptors in blood vessels isolated from the treated rabbits also indicated that LPS was the only B1R inducer (aorta). Icatibant, a nonequilibrium antagonist of the rabbit B2R, was the sole tested drug to alter the contractions mediated by the B2R in the jugular vein or the intensity of the immunohistochemical B2R staining in several organs (inhibition in both cases). B2R mRNA expression was downregulated in some organs by several of the applied treatments, but the data did not support generally applicable feedback for the regulation of B2R expression involving endogenous kinins, prostanoids, or NO. There was no indication of compensatory or reciprocal regulation of B1Rs, relative to B2Rs, inasmuch as B1R expression was restricted to LPS-treated animals.
lipopolysaccharide; kinin-induced vascular contraction; mediators secondarily released by kinins; noncompetitive pharmacological antagonism; nitric oxide
This article has been cited by other articles:
|
|
 |
|
  F. Lang, C. Bohmer, M. Palmada, G. Seebohm, N. Strutz-Seebohm, and V. Vallon (Patho)physiological Significance of the Serum- and Glucocorticoid-Inducible Kinase Isoforms. Physiol Rev, October 1, 2006; 86(4): 1151 - 1178. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Ongali, H. d. S. Buck, F. Cloutier, F. Legault, D. Regoli, C. Lambert, G. Thibault, and R. Couture Regulation of Cardiovascular Signaling by Kinins and Products of Similar Converting Enzyme Systems: Chronic effects of angiotensin-converting enzyme inhibition on kinin receptor binding sites in the rat spinal cord Am J Physiol Heart Circ Physiol, June 1, 2003; 284(6): H1949 - H1958. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Sabourin, G. Morissette, J. Bouthillier, L. Levesque, and F. Marceau Expression of kinin B1 receptor in fresh or cultured rabbit aortic smooth muscle: role of NF-kappa B Am J Physiol Heart Circ Physiol, July 1, 2002; 283(1): H227 - H237. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Duka, E. Kintsurashvili, I. Gavras, C. Johns, M. Bresnahan, and H. Gavras Vasoactive Potential of the B1 Bradykinin Receptor in Normotension and Hypertension Circ. Res., February 16, 2001; 88(3): 275 - 281. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Houle, J.-F. Larrivee, M. Bachvarova, J. Bouthillier, D. R. Bachvarov, and F. Marceau Antagonist-Induced Intracellular Sequestration of Rabbit Bradykinin B2 Receptor Hypertension, June 1, 2000; 35(6): 1319 - 1325. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
