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Impaired EDHF‐mediated vasodilatation in adult offspring of rats exposed to a fat‐rich diet in pregnancy
Author(s) -
Taylor P. D.,
Khan I. Y.,
Hanson M. A.,
Poston L.
Publication year - 2004
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2002.018879
Subject(s) - offspring , mesenteric arteries , endocrinology , medicine , vasodilation , nitric oxide , acetylcholine , chemistry , nitric oxide synthase , electrical impedance myography , anatomy , pregnancy , biology , artery , genetics
We recently reported vascular dysfunction in adult offspring of rats fed a fat‐rich (animal lard) diet in pregnancy. This study reports further characterization of constrictor and dilator function in mesenteric and caudal femoral arteries from 180‐day‐old offspring of dams fed the high fat diet (OHF). Endothelium‐dependent relaxation in response to acetylcholine (10 −9 –10 −5 m ) was impaired in mesenteric small arteries from male and female OHF compared with offspring of dams fed normal chow (males (maximum percentage relaxation): OHF 67.92 ± 2.89, n = 8 versus control 92.08 ± 2.19, n = 8, P < 0.01). Substantial relaxation in response to acetycholine in control mesenteric arteries remained after inhibition of nitric oxide synthase, soluble guanylate cyclase and cyclo‐oxygenase but was blocked by 25 m m potassium. This component of relaxation, attributed to EDHF, was significantly reduced in OHF mesenteric arteries compared with controls. However, EDHF played a minor role in acetylcholine‐induced relaxation in both control and OHF femoral caudal arteries (male and female). In these arteries, in contrast to mesenteric vessels, acetylcholine‐induced relaxation was significantly enhanced in OHF but only in males (ACh (maximum percentage relaxation): OHF 58.40 ± 4.39, n = 8 versus male controls 32.18 ± 6.36, P < 0.05). This was attributable to enhanced nitric oxide‐mediated relaxation. In conclusion, reduced endothelium‐dependent relaxation in OHF mesenteric arteries is due to impaired EDHF‐mediated relaxation. This defect was not apparent in femoral arteries in which EDHF has a less prominent role.