title: Lymphocyte beta2-adrenergic receptors and plasma catecholamine levels in lead-exposed workers.
abstract: The effect of lead exposure on beta2-adrenoceptor density and catecholamine response was studied in 26 male workers and 1 female worker, exposed to lead on average for 6 years. The systolic blood pressure in lead workers (101-160 mmHg, 124.4 +/- 14.7 mmHg) was found to be significantly higher than in controls (97-134 mmHg, 115.4 +/- 10.4 mmHg, p < 0.01) as was plasma norepinephrine (0.51 +/- 0.1 microg/liter vs 0.24 +/- 0.05 microg/liter, p < 0.01). The density of lymphocyte beta2-adrenergic receptors (Bmax) in lead-exposed workers was 86% lower than that in controls (0.15 +/- 0.08 vs 1.08 +/- 0.29 fmol/0.1 x 10(6) cells; p < 0.01). The dissociation constants (Kd) of [125I]iodocyanopindolol were 93.6 +/- 42.6 and 87.9 +/- 42.7 pM in lead-exposed workers and controls, respectively. Multiple linear regression analysis showed that elevation of systolic pressure was closely related to (a) blood lead levels, (b) decreased beta2-adrenergic receptor density, and (c) increased plasma catecholamine levels in lead-exposed workers. Linear regression analysis revealed that both plasma norepinephrine levels and beta2-adrenoceptor density (Bmax) were highly correlated with both systolic blood pressures and blood lead levels in lead-exposed workers, and a highly significant negative correlation was found to exist between Bmax and plasma norepinephrine levels (r = -0.82, p < 0.001). These data therefore demonstrate that there is a close relationship between elevated plasma catecholamine levels, decreased beta2-adrenergic receptors, and elevated blood pressure in lead-exposed workers.
authors.affiliation: Department of Physiology, Graduate Institute of Medicine, Kaohsiung Medical College, Koahsuing City, Taiwan.
authors.forename: H R
authors.initials: HR
authors.lastname: Chang
authors.forename: S S
authors.initials: SS
authors.lastname: Chen
authors.forename: T J
authors.initials: TJ
authors.lastname: Chen
authors.forename: C H
authors.initials: CH
authors.lastname: Ho
authors.forename: H C
authors.initials: HC
authors.lastname: Chiang
authors.forename: H S
authors.initials: HS
authors.lastname: Yu
mesh_terms: D000328:Adult; D001665:Binding Sites; D001794:Blood Pressure / Q000187:drug effects; D002851:Chromatography, High Pressure Liquid; D004791:Enzyme Inhibitors / Q000097:blood; D004837:Epinephrine / Q000097:blood*; D005260:Female; D006419:Heme Oxygenase (Decyclizing) / Q000037:antagonists & inhibitors; D006801:Humans; D020120:Iodocyanopindolol; D007553:Isotope Labeling; D007854:Lead / Q000009:adverse effects*; D007855:Lead Poisoning / Q000503:physiopathology; D016014:Linear Models; D008214:Lymphocytes / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood*; D016273:Occupational Exposure; D010869:Pindolol / Q000031:analogs & derivatives / Q000378:metabolism; D011524:Protoporphyrins / Q000097:blood; D011869:Radioligand Assay; D018343:Receptors, Adrenergic, beta-2 / Q000187:drug effects* / Q000378:metabolism; D013054:Spectrophotometry, Atomic
chemical_list: D004791:Enzyme Inhibitors; D011524:Protoporphyrins; D018343:Receptors, Adrenergic, beta-2; C017803:zinc protoporphyrin; D007854:Lead; D020120:Iodocyanopindolol; D010869:Pindolol; D006419:Heme Oxygenase (Decyclizing); D009638:Norepinephrine; D004837:Epinephrine