Upregulation of corticotropin-releasing hormone gene expression in the paraventricular nucleus of cyclophosphamide-induced cystitis in male rats.
We examined the effects of cyclophosphamide (CP)-induced cystitis on the expression of corticotropin-releasing hormone (CRH) mRNA in the paraventricular nucleus (PVN) and the serum levels of adrenocorticotropic hormone (ACTH) using in situ hybridization histochemistry and radioimmunoassay. In addition, the expression of AVP heteronuclear (hn) RNA and neuronal nitric oxide synthase (nNOS) mRNA was also examined in the PVN of a CP-induced cystitis model. We found that the levels of CRH mRNA were significantly increased in the PVN at 2 h after intraperitoneal administration of CP compared to those in saline-treated rats. The CRH mRNA levels in the PVN peaked at 12 h after CP administration and the levels were still significantly higher than those in saline-treated group at 24 h after CP administration. The serum ACTH levels in CP-treated group were also significantly higher compared to those in saline-treated group at any of the time points examined. Unlike previous findings showing upregulation of nNOS mRNA and AVP hnRNA under somatic nociceptive states, the levels of nNOS mRNA and AVP hnRNA were unchanged in the PVN following CP-induced cystitis, visceral nociceptive stimulation. These results suggest that visceral nociceptive stimulation as well as somatic nociceptive stimulation may activate the hypothalamo-pituitary axis but the hypothalamic neuroendocrine responses produced by visceral nociceptive stimulation may be different from those produced by somatic nociceptive stimulation.
Mineta
Kaori
K
Department of Urology, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahakanishi, Kitakyushu 807-8555, Japan.
Nomura
Masayoshi
M
Terado
Michikazu
M
Fujimoto
Naohiro
N
Sasaguri
Takakazu
T
Ueta
Yoichi
Y
Matsumoto
Tetsuro
T
D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000818:Animals; D001127:Arginine Vasopressin / Q000235:genetics / Q000378:metabolism; D003346:Corticotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism*; D003520:Cyclophosphamide; D003556:Cystitis / Q000139:chemically induced / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D017403:In Situ Hybridization; D008297:Male; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I; D009619:Nociceptors / Q000503:physiopathology; D010146:Pain / Q000209:etiology / Q000378:metabolism*; D010286:Paraventricular Hypothalamic Nucleus / Q000378:metabolism*; D012313:RNA / Q000032:analysis; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D015854:Up-Regulation; D001743:Urinary Bladder / Q000294:innervation / Q000473:pathology; D017833:Visceral Afferents / Q000503:physiopathology
D012333:RNA, Messenger; D001127:Arginine Vasopressin; D012313:RNA; D003520:Cyclophosphamide; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat