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Dietary protein restriction in pregnancy induces hypertension and vascular defects in rat male offspring

Dietary protein restriction in pregnancy induces hypertension and vascular defects in rat male offspring
Dietary protein restriction in pregnancy induces hypertension and vascular defects in rat male offspring
It is established that dietary protein restriction of pregnant rats results in their offspring developing hypertension. However, to date no studies have investigated peripheral vascular function of offspring using the low protein model. Therefore, the aim of the study was to assess isolated resistance artery function from adult male offspring of control (C, 18% casein) and protein-restricted (PR, 9% casein) pregnant dams at two different ages. The birthweight of PR offspring did not significantly differ from that of C offspring. Systolic blood pressure was significantly elevated in PR compared with C (p < 0.05). Maximal vascular contraction to phenylephrine and the thromboxane analog U46619 were similar in C and PR offspring at postnatal d 87 and 164. Relaxation induced by the endothelium-dependent vasodilators acetylcholine or bradykinin was significantly reduced in the PR group (p < 0.05). Relaxation to the endothelium-independent vasodilator sodium nitroprusside and phosphodiesterase type 3 inhibitor cilostamide was less in the PR offspring compared with C (p < 0.01). Dietary protein restriction in pregnancy induces hypertension and vascular dysfunction in male offspring. Abnormalities in the nitric oxide–cGMP pathway may explain the defect in endothelium-dependent and -independent relaxation. Reduced vasodilation may be a potential mechanism underlying the elevated systolic blood pressure observed in this model.
0031-3998
83-90
Brawley, Lee
acce4d5e-03c8-48da-b391-45fbc1b384b1
Itoh, Shigeru
ee32ea77-f41b-486b-a687-dae80f4a244e
Torrens, Christopher
15a35713-0651-4249-8227-5901e2cfcd22
Barker, Alison
030dbfdb-0216-40f4-81c7-05502d176e8f
Bertram, Caroline
bd8d2058-c047-4dd6-a1f2-8191fcbe1b08
Poston, Lucilla
916aced2-462e-445f-9efa-83ed4b7b3a9f
Hanson, Mark
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Brawley, Lee
acce4d5e-03c8-48da-b391-45fbc1b384b1
Itoh, Shigeru
ee32ea77-f41b-486b-a687-dae80f4a244e
Torrens, Christopher
15a35713-0651-4249-8227-5901e2cfcd22
Barker, Alison
030dbfdb-0216-40f4-81c7-05502d176e8f
Bertram, Caroline
bd8d2058-c047-4dd6-a1f2-8191fcbe1b08
Poston, Lucilla
916aced2-462e-445f-9efa-83ed4b7b3a9f
Hanson, Mark
1952fad1-abc7-4284-a0bc-a7eb31f70a3f

Brawley, Lee, Itoh, Shigeru, Torrens, Christopher, Barker, Alison, Bertram, Caroline, Poston, Lucilla and Hanson, Mark (2003) Dietary protein restriction in pregnancy induces hypertension and vascular defects in rat male offspring. Pediatric Research, 54 (1), 83-90. (doi:10.1203/01.PDR.0000065731.00639.02).

Record type: Article

Abstract

It is established that dietary protein restriction of pregnant rats results in their offspring developing hypertension. However, to date no studies have investigated peripheral vascular function of offspring using the low protein model. Therefore, the aim of the study was to assess isolated resistance artery function from adult male offspring of control (C, 18% casein) and protein-restricted (PR, 9% casein) pregnant dams at two different ages. The birthweight of PR offspring did not significantly differ from that of C offspring. Systolic blood pressure was significantly elevated in PR compared with C (p < 0.05). Maximal vascular contraction to phenylephrine and the thromboxane analog U46619 were similar in C and PR offspring at postnatal d 87 and 164. Relaxation induced by the endothelium-dependent vasodilators acetylcholine or bradykinin was significantly reduced in the PR group (p < 0.05). Relaxation to the endothelium-independent vasodilator sodium nitroprusside and phosphodiesterase type 3 inhibitor cilostamide was less in the PR offspring compared with C (p < 0.01). Dietary protein restriction in pregnancy induces hypertension and vascular dysfunction in male offspring. Abnormalities in the nitric oxide–cGMP pathway may explain the defect in endothelium-dependent and -independent relaxation. Reduced vasodilation may be a potential mechanism underlying the elevated systolic blood pressure observed in this model.

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Published date: 2003

Identifiers

Local EPrints ID: 25277
URI: http://eprints.soton.ac.uk/id/eprint/25277
ISSN: 0031-3998
PURE UUID: 8168d5b9-8c3e-41cb-a23c-b2254300696c
ORCID for Mark Hanson: ORCID iD orcid.org/0000-0002-6907-613X

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Date deposited: 10 Apr 2006
Last modified: 16 Mar 2024 03:17

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Contributors

Author: Lee Brawley
Author: Shigeru Itoh
Author: Christopher Torrens
Author: Alison Barker
Author: Caroline Bertram
Author: Lucilla Poston
Author: Mark Hanson ORCID iD

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