Effect of nutritional restriction in early pregnancy on isolated femoral artery function in mid-gestation fetal sheep.
Unbalanced maternal nutrition affects fetal endocrine and cardiovascular systems, sometimes accompanied by changes in growth, although this is usually in late gestation. We determined the effect of moderate restriction for the first half of gestation of maternal dietary protein, or of total calorific intake on isolated resistance artery function of mid-gestation fetal sheep. Welsh Mountain ewes were nutritionally restricted by 30 % of the recommended nutrient intake (globally restricted) or 30 % of the recommended protein intake (protein-restricted), compared to control ewes fed 100 % of recommended nutrient intake, for ~12 days prior to conception and for the subsequent 70 days of gestation. At mid-gestation, fetal and placental weights were similar in all dietary groups. In isolated femoral arteries, the response curve to noradrenaline was reduced in protein-restricted group fetuses (P < 0.05). Maximal relaxation (P < 0.01) and sensitivity (P < 0.05) to acetylcholine were markedly reduced in protein-restricted group fetuses, and to a smaller extent in globally restricted group fetuses (response curve, P < 0.05). The dilator response (P < 0.05) and sensitivity (P < 0.05) to the alpha2 agonist UK14304 was lower in protein-, but not in globally restricted group fetuses. The response (P < 0.05) and sensitivity (P < 0.05) to the nitric oxide donor sodium nitroprusside were reduced in protein-restricted group fetuses compared to controls. Our data show that dietary imbalance, in particular restricted protein, of the ewe can produce blunting of endothelial-dependent and -independent relaxation in systemic arteries from the mid-gestation fetus. These changes may precede perturbed late-gestation fetal and postnatal cardiovascular control.
Nishina
Hidenori
H
Department of Obstetrics and Gynaecology, University College London, 86-96 Chenies Mews, London WC1 6HX, UK.
Green
Lucy R
LR
McGarrigle
Hugh H G
HH
Noakes
David E
DE
Poston
Lucilla
L
Hanson
Mark A
MA
D020155:3-Hydroxybutyric Acid / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood; D001798:Blood Proteins / Q000032:analysis; D005314:Embryonic and Fetal Development / Q000502:physiology; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005263:Femoral Artery / Q000187:drug effects / Q000502:physiology*; D005312:Fetal Blood / Q000737:chemistry; D020567:Fetal Weight; D005508:Food Deprivation / Q000502:physiology; D005865:Gestational Age; D006854:Hydrocortisone / Q000097:blood; D066298:In Vitro Techniques; D009929:Organ Size; D010920:Placenta / Q000737:chemistry; D011247:Pregnancy; D039401:Prenatal Nutritional Physiological Phenomena / Q000502:physiology*; D011374:Progesterone / Q000097:blood; D012083:Renin / Q000097:blood; D012756:Sheep; D014508:Urea / Q000097:blood; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
D001798:Blood Proteins; D005230:Fatty Acids, Nonesterified; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D000804:Angiotensin II; D001127:Arginine Vasopressin; D011374:Progesterone; D014508:Urea; D012083:Renin; D020155:3-Hydroxybutyric Acid; D006854:Hydrocortisone