Search

Your search keyword '"BUCKLEY, C. H."' showing total 323 results
Start Over Author "BUCKLEY, C. H."
323 results on '"BUCKLEY, C. H."'

23. Pregnancy

Author

Fox, H., Buckley, C. H., Gresham, G. Austin, editor, Fox, H., and Buckley, C. H.

Published
1983
Full Text
View/download PDF

47. Endothelium-derived hyperpolarizing factor and potassium use different mechanisms to induce relaxation of human subcutaneous resistance arteries

Author

McIntyre, C-A, Buckley, C H, Jones, G C, Sandeep, T C, Andrews, R C, Elliott, A I, Gray, G A, Williams, B C, McKnight, J A, Walker, B R, and Hadoke, P W F

Subjects
Adult, Male, Time Factors, Charybdotoxin, Vasodilator Agents, Barium Compounds, Indomethacin, In Vitro Techniques, Nitroarginine, Biological Factors, Norepinephrine, Chlorides, Humans, Enzyme Inhibitors, Ouabain, Aged, Skin, Dose-Response Relationship, Drug, Arteries, Middle Aged, Acetylcholine, Vasodilation, Apamin, Papers, Potassium, Female, Endothelium, Vascular, Nitric Oxide Synthase
Abstract

This investigation examined the hypothesis that release of K(+) accounts for EDHF activity by comparing relaxant responses produced by ACh and KCl in human subcutaneous resistance arteries. Resistance arteries (internal diameter 244+/-12 microm, n=48) from human subcutaneous fat biopsies were suspended in a wire myograph. Cumulative concentration-response curves were obtained for ACh (10(-9) - 3x10(-5) M) and KCl (2.5 - 25 mM) following contraction with noradrenaline (NA; 0.1 - 3 microM). ACh (E(max) 99.07+/-9.61%; -LogIC(50) 7.03+/-0.22; n=9) and KCl (E(max) 74.14+/-5.61%; -LogIC(50) 2.12+/-0.07; n=10)-induced relaxations were attenuated (P0.0001) by removal of the endothelium (E(max) 8.21+/-5.39% and 11.56+/-8.49%, respectively; n=6 - 7). Indomethacin (10 microM) did not alter ACh-induced relaxation whereas L-NOARG (100 microM) reduced this response (E(max) 61.7+/-3.4%, P0.0001; n=6). The combination of ChTx (50 nM) and apamin (30 nM) attenuated the L-NOARG-insensitive component of ACh-induced relaxation (E(max): 15.2+/-10.5%, P0.002, n=6) although these arteries retained the ability to relax in response to 100 microM SIN-1 (E(max) 127.6+/-13.0%, n=3). Exposure to BaCl(2) (30 microM) and Ouabain (1 mM) did not attenuate the L-NOARG resistant component of ACh-mediated relaxation (E(max), 76.09+/-8.92, P=0.16; n=5). KCl-mediated relaxation was unaffected by L-NOARG+indomethacin (E(max); 68.1+/-5.6%, P=0.33; n=5) or the combination of L-NOARG/indomethacin/ChTx/apamin (E(max); 86.61+/-14.02%, P=0.35; n=6). In contrast, the combination of L-NOARG, indomethacin, ouabain and BaCl(2) abolished this response (E(max), 5.67+/-2.59%, P0.0001, n=6). The characteristics of KCl-mediated relaxation differed from those of the nitric oxide/prostaglandin-independent component of the response to ACh, and were endothelium-dependent, indicating that K(+) does not act as an EDHF in human subcutaneous resistance arteries.

Published
2001

Catalog

Books, media, physical & digital resources
See catalog results