title: Direct effects of angiotensin I, angiotensin II, an ACE inhibitor and a serine proteinase inhibitor on cultured heart cells from spontaneously hypertensive rats.
abstract: 1. The purpose of the present study was to investigate how angiotensin I (AI), angiotensin II (AII), an angiotensin converting enzyme inhibitor (ACE inhibitor; ACE-I) and a serine proteinase inhibitor contribute to the protein metabolism of cultured newborn spontaneously hypertensive rats (SHR) heart cells. We examined the uptake of [3H]-uridine and [3H]-proline into cultured cardiac myocytes and fibroblasts, respectively. 2. Both AI and AII increased the uptake of [3H]-uridine into myocytes in a concentration-dependent manner. However, the effect of AI was denied in the presence of the ACE-I with the concentration of 10(-6) g/mL. Both AI and AII increased the uptake of [3H]-proline into cardiac fibroblasts in a concentration-dependent manner. However, this effect was only partially abolished in the presence of 10(-6) g/mL of the ACE-I, which was the maximal concentration that did not exert any effect on the [3H]-proline uptake. In the presence of AII receptor antagonist, [Sar1, Leu8]-AII, the uptake of [3H]-proline into cardiac fibroblasts was completely inhibited. Moreover, the stimulatory effects of AI on the uptake of [3H]-proline into cardiac fibroblasts were completely inhibited in the presence of a serine proteinase inhibitor in addition to the ACE-I. 3. These results suggest that an ACE-I has different effects on protein metabolism in the heart and also suggest the presence of serine proteinase in cultured cardiac fibroblasts from SHR.
authors.affiliation: 4th Department of Internal Medicine, Shimane Medical University, Izumo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kuzuo
authors.forename: M
authors.initials: M
authors.lastname: Honda
authors.forename: K
authors.initials: K
authors.lastname: Tanaka
authors.forename: T
authors.initials: T
authors.lastname: Kuramochi
authors.forename: S
authors.initials: S
authors.lastname: Morioka
authors.forename: T
authors.initials: T
authors.lastname: Takabatake
authors.forename: Y
authors.initials: Y
authors.lastname: Yamori
mesh_terms: D000803:Angiotensin I / Q000494:pharmacology*; D000804:Angiotensin II / Q000494:pharmacology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D005347:Fibroblasts / Q000648:ultrastructure; D006973:Hypertension / Q000378:metabolism*; D007150:Immunohistochemistry; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D015842:Serine Proteinase Inhibitors / Q000494:pharmacology*; D014529:Uridine / Q000378:metabolism
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D015842:Serine Proteinase Inhibitors; D000804:Angiotensin II; D000803:Angiotensin I; D014529:Uridine