title: Concentration of tissue angiotensin II increases with severity of experimental pancreatitis.
abstract: Necrotizing pancreatitis is a serious condition that is associated with high morbidity and mortality. Although vasospasm is reportedly involved in necrotizing pancreatitis, the underlying mechanism is not completely clear. In addition, the local renin‑angiotensin system has been hypothesized to be involved in the progression of pancreatitis and trypsin has been shown to generate angiotensin II under weakly acidic conditions. However, to the best of our knowledge, no studies have reported elevated angiotensin II levels in tissue with pancreatitis. In the present study, the concentration of pancreatic angiotensin II in rats with experimentally induced acute pancreatitis was measured. Acute pancreatitis was induced by retrograde injection of 6% sodium taurocholate into the biliopancreatic duct. Control rats were sacrificed without injection into the biliopancreatic duct. The concentration of tissue angiotensin II was measured using the florisil method. Angiotensin II concentration in tissues with acute pancreatitis measured at 3, 6, 12 and 24 h following taurocholate injection were significantly higher than that of normal pancreatic tissue. In addition, the concentration of angiotensin II increased in a time‑dependent manner. The results demonstrated that the angiotensin II generating system is involved in the transition from edematous to necrotizing pancreatitis in experimental animals. We hypothesize that locally formed angiotensin II affects the microenvironment in pancreatitis.
authors.affiliation: Department of Gastroenterological Surgery, Division of Cancer Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa 920‑8641, Japan. keijuhospital@hotmail.co.jp
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Furukawa
authors.forename: Atsushi
authors.initials: A
authors.lastname: Shinmura
authors.forename: Hidehiro
authors.initials: H
authors.lastname: Tajima
authors.forename: Tomoya
authors.initials: T
authors.lastname: Tsukada
authors.forename: Shin-Ichi
authors.initials: S
authors.lastname: Nakanuma
authors.forename: Koichi
authors.initials: K
authors.lastname: Okamoto
authors.forename: Seisho
authors.initials: S
authors.lastname: Sakai
authors.forename: Isamu
authors.initials: I
authors.lastname: Makino
authors.forename: Keishi
authors.initials: K
authors.lastname: Nakamura
authors.forename: Hironori
authors.initials: H
authors.lastname: Hayashi
authors.forename: Katsunobu
authors.initials: K
authors.lastname: Oyama
authors.forename: Masafumi
authors.initials: M
authors.lastname: Inokuchi
authors.forename: Hisatoshi
authors.initials: H
authors.lastname: Nakagawara
authors.forename: Tomoharu
authors.initials: T
authors.lastname: Miyashita
authors.forename: Hideto
authors.initials: H
authors.lastname: Fujita
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Takamura
authors.forename: Itasu
authors.initials: I
authors.lastname: Ninomiya
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Kitagawa
authors.forename: Sachio
authors.initials: S
authors.lastname: Fushida
authors.forename: Takashi
authors.initials: T
authors.lastname: Fujimura
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Ohta
authors.forename: Tomohiko
authors.initials: T
authors.lastname: Wakayama
authors.forename: Shoichi
authors.initials: S
authors.lastname: Iseki
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D004195:Disease Models, Animal; D008297:Male; D008954:Models, Biological; D010195:Pancreatitis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D012720:Severity of Illness Index; D013656:Taurocholic Acid / Q000009:adverse effects; D013997:Time Factors
chemical_list: D000804:Angiotensin II; D013656:Taurocholic Acid; D000681:Amylases