title: Modulation of angiotensin II type 1 receptor mRNA expression in human blood cells: comparison of platelets and mononuclear leucocytes.
abstract: The objective of the present study was to quantify the expression of angiotensin II type 1 (AT1) receptor transcripts in human blood cells--platelets and mononuclear leukocytes--from 10 normal healthy volunteers during the alterations in the renin-angiotensin system. A quantitative assay employing reverse transcription-polymerase chain reaction (RT-PCR) was utilized. Oral administration of furosemide, 40 mg for 2 days, under mild salt restriction (50 mEq NaCl/day) for 6 days stimulated the renin-angiotensin system resulting in significant increases in plasma renin activity (PRA) (1.84 +/- 0.12 vs. 1.05 +/- 0.17 ng/l/s; P < 0.01), plasma angiotensin II concentration, and plasma aldosterone concentration (PAC). The ratio of AT1 receptor mRNA to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA expression in mononuclear leucocytes was significantly (P < 0.05) increased from the basal level (0.49 +/- 0.05 vs. 0.29 +/- 0.03) (P < 0.01), while in platelets these changes were opposite (0.11 +/- 0.05 vs. 0.25 +/- 0.05) (P < 0.01). Compared to these significant changes, salt loading (200 mEq NaCl/day) for 6 days decreased PRA(0.49 +/- 0.10 vs. 1.05 +/- 0.17 ng/l/s; P < 0.01) and induced the opposite changes in the ratio of AT1 receptor/GAPDH mRNA. These data suggest that AT1 receptors in human blood cells may be of two different types--platelets and mononuclear leucocytes.
authors.affiliation: Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: H
authors.initials: H
authors.lastname: Shibata
authors.forename: M
authors.initials: M
authors.lastname: Murakami
authors.forename: A
authors.initials: A
authors.lastname: Sato
authors.forename: M
authors.initials: M
authors.lastname: Naito
authors.forename: A
authors.initials: A
authors.lastname: Ichihara
authors.forename: A
authors.initials: A
authors.lastname: Matsumoto
authors.forename: G
authors.initials: G
authors.lastname: Tsujimoto
authors.forename: A
authors.initials: A
authors.lastname: Hirasawa
authors.forename: K
authors.initials: K
authors.lastname: Horie
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood / Q000187:drug effects; D001483:Base Sequence; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D004039:Diet, Sodium-Restricted; D005665:Furosemide / Q000494:pharmacology*; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D011945:Receptors, Angiotensin / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D012083:Renin / Q000097:blood / Q000187:drug effects; D014158:Transcription, Genetic
chemical_list: D012333:RNA, Messenger; D011945:Receptors, Angiotensin; D000804:Angiotensin II; D000450:Aldosterone; D005665:Furosemide; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D012083:Renin