| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Received April 26, 2004
Revised May 12, 2004
Accepted after revision June 8, 2004
1 Kings College London
2 University of Southampton
* To whom correspondence should be addressed. E-mail: paul.taylor{at}kcl.ac.uk.
We recently reported vascular dysfunction in adult offspring of rats fed a fat-rich (animal lard) diet in pregnancy. This study reports further characterisation of constrictor and dilator function in mesenteric and caudal femoral arteries from 180 day-old offspring of dams fed the high fat die (OHF). Endothelium-dependent relaxation to acetylcholine (10-9-10-5M) was impaired in mesenteric small arteries from male and female OHF compared to offspring of dams fed normal chow (males, [max % relaxation] OHF 67.92±2.89, n=8 versus control 92.08±2.19, P<0.01). Substantial relaxation to acetycholine in control mesenteric arteries remained after inhibition of nitric oxide synthase, soluble guanylate cyclase and cyclo-oxygenase but was blocked by 25mM 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 [max % 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.
This article has been cited by other articles:
|
|
 |
|
  N. Igosheva, P. D. Taylor, L. Poston, and V. Glover Prenatal stress in the rat results in increased blood pressure responsiveness to stress and enhanced arterial reactivity to neuropeptide Y in adulthood J. Physiol., July 15, 2007; 582(2): 665 - 674. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Douglas, J. A. Armitage, P. D. Taylor, J. R. Lawson, G. E. Mann, and L. Poston Cardiovascular consequences of life-long exposure to dietary isoflavones in the rat J. Physiol., March 1, 2006; 571(2): 477 - 487. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Armitage, P. D. Taylor, and L. Poston Experimental models of developmental programming: consequences of exposure to an energy rich diet during development J. Physiol., May 15, 2005; 565(1): 3 - 8. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Armitage, L. Lakasing, P. D. Taylor, A. A. Balachandran, R. I. Jensen, V. Dekou, N. Ashton, J. R. Nyengaard, and L. Poston Developmental programming of aortic and renal structure in offspring of rats fed fat-rich diets in pregnancy J. Physiol., May 15, 2005; 565(1): 171 - 184. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
