title: [Regeneration of perivascular nerve and role of angiotensin receptors].
abstract: The present study was designed to investigate involvement of angiotensin (Ang) II type 2 receptors (AT2R) in restoration of perivascular nerve innervation injured by topical phenol treatment. Male Wistar rats underwent in vivo topical application of 10% phenol around the superior mesenteric artery to induce nerve injure. Phenol treatment markedly reduced densities of both calcitonin gene-related peptide (CGRP)-like immunoreactivity (LI)- and neuropeptide Y (NPY)-LI-containing fibers. NGF restored densities of both nerve fibers to the Sham control level. Coadministration of Ang II and losartan (AT1R antagonist) significantly increased the density of CGRP-LI-fibers but not NPY-LI-fibers compared with saline control. The increase of the density of CGRP-LI-fibers by coadministration of Ang II and losartan was suppressed by adding PD123319 (AT2R antagonist). Furthermore, NGF-induced CGRP-LI nerve regeneration was inhibited by PD123319 treatment. NGF-induced increase of AT2R mRNA level was significantly suppressed by AT1R antagonist treatment in phenol treated rats dorsal root ganglia. These results suggest that selective stimulation of AT2R by Ang II facilitates reinnervation of mesenteric perivascular CGRP-containing nerves injured by topical phenol application in the rat.
authors.affiliation: Department of Life Science, Okayama University of Science, Okayama, Japan. hobara@dls.ous.ac.jp
authors.forename: Narumi
authors.initials: N
authors.lastname: Hobara
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Goda
authors.forename: Namika
authors.initials: N
authors.lastname: Yoshida
authors.forename: Naoya
authors.initials: N
authors.lastname: Hashikawa
authors.forename: Hiromu
authors.initials: H
authors.lastname: Kawasaki
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D019808:Losartan / Q000494:pharmacology; D008297:Male; D008638:Mesenteric Arteries / Q000294:innervation*; D020932:Nerve Growth Factor / Q000494:pharmacology; D009416:Nerve Regeneration / Q000187:drug effects; D009478:Neuropeptide Y / Q000378:metabolism; D059348:Peripheral Nerve Injuries; D010525:Peripheral Nerves / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D019800:Phenol / Q000009:adverse effects; D011725:Pyridines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D044139:Receptor, Angiotensin, Type 2 / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D013268:Stimulation, Chemical
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D007093:Imidazoles; D009478:Neuropeptide Y; D011725:Pyridines; D044139:Receptor, Angiotensin, Type 2; D000804:Angiotensin II; C073402:PD 123319; D019800:Phenol; D020932:Nerve Growth Factor; D015740:Calcitonin Gene-Related Peptide; D019808:Losartan