Gestation increases nitric oxide–mediated vasodilation in rat uterine arteries

• Published in: American journal of obstetrics and gynecology Vol. 176; no. 4; pp. 856 - 864
• Main Authors: Ni, Yajun, Meyer, Marjorie, Osol, George
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Philadelphia, PA Mosby, Inc 01.04.1997; Elsevier
• Subjects: Acetylcholine - pharmacology; Animals; Arteries - drug effects; Arteries - physiology; Biological and medical sciences; endothelium; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiology; Enzyme Inhibitors - pharmacology; Female; Fundamental and applied biological sciences. Psychology; Mother. Fetoplacental unit. Mammary gland. Milk; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - physiology; nitric oxide; Nitric Oxide - blood; Nitric Oxide - physiology; Nitric Oxide Synthase - antagonists & inhibitors; Nitroarginine - pharmacology; Nitroprusside - pharmacology; Phenylephrine - pharmacology; Pregnancy; Pregnancy, Animal - physiology; Pregnancy. Parturition. Lactation; Rats; Rats, Sprague-Dawley; uterine arteries; Uterus - blood supply; Vasoconstrictor Agents - pharmacology; Vasodilation - drug effects; Vasodilation - physiology; Vasodilator Agents - pharmacology; Vertebrates: reproduction; Pregnancy; endothelium; nitric oxide; uterine arteries; Vasodilator agent; Rat; Rodentia; In vitro; Artery; Vasodilation; Endothelium; Vertebrata; Mammalia; Uterus; Animal; Nitric oxide; Female genital system; Phenylephrine; Arterial pressure; Acetylcholine
• ISSN: 0002-9378; 1097-6868
• DOI: 10.1016/S0002-9378(97)70611-2

OBJECTIVE: The purpose of this study was to determine the influence of endothelium-released nitric oxide on uterine arterial tone and reactivity during pregnancy. STUDY DESIGN: The effects of pregnancy on endothelial function were evaluated in isolated pressurized rat uterine arteries from late-pregnant rats (day 19 to 20) versus age-matched nonpregnant controls. The effects of nitric oxide synthase inhibition (Nω-nitro- l-arginine) on arterial tone and reactivity under basal and activated (phenylephrine) conditions were determined, as was arterial reactivity to endothelium-dependent (acetylcholine) and endothelium-independent (sodium nitroprusside) vasodilators, by evaluating changes in lumen diameter. RESULTS: (1) Maximal constriction to Nω-nitro- l-arginine was significantly enhanced under basal (nonstimulated) conditions in arteries from late-pregnant versus nonpregnant rats (changes in lumen diameter 37% ± 8% vs 9.3 ± 6.2%, respectively, p < 0.05). (2) Nitric oxide synthase blockade with 1 nmol/L Nω-nitro- l-arginine significantly increased phenylephrine sensitivity in arteries from late-pregnant animals (median effective concentration 115 ± 23 nmol/L vs 33 ± 8 nmol/L, control vs treated vessels, p < 0.05) but was without statistically significant effect on arteries from nonpregnant animals (control 255 ± 164 nmol/L, treated 250 ± 102 nmol/L, p > 0.05). (3) The threshold concentration of acetylcholine required to elicit endothelium-dependent dilation was significantly lower in late-pregnant versus nonpregnant arteries (1.4 ± 0.2 nmol/L vs 12.2 ± 3.8 nmol/L, p < 0.05). (4) Vascular smooth muscle sensitivity to an exogenous nitrodilator (sodium nitroprusside) was identical in late-pregnant versus nonpregnant vessels. CONCLUSION: Endothelial vasodilator influences are augmented during pregnancy under basal, activated (phenylephrine), and chemically provoked (acetylcholine) conditions in uterine arteries by enhanced release of nitric oxide. (Am J Obstet Gynecol 1997;176:856-64.)