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Nitric oxide does not mediate the vasodilation of early human pregnancy
Matthias R Langenfeld1, Lisa A Simmons, Jane A McCrohon
1Department of Cardiology University of Sydney, Camperdown, NSW, Australia.
Background:
In early pregnancy, a substantial drop in arterial blood pressure occurs, that might be attributed to enhanced vascular nitric oxide synthesis. We investigated whether nitric oxide mediates the vasodilation that occurs in early human pregnancy.
Methods:
Resting and stimulated forearm vascular resistance were measured (venous occlusion plethysmograph) in six women at 10 +/- 3 weeks of uncomplicated pregnancy and in the same women 7 +/- 5 weeks after elective termination of pregnancy. Forearm vascular resistance was also measured in six non-pregnant, healthy controls.
Results:
Resting forearm vascular resistance was similar during pregnancy (33 +/- 16 arbitrary units (AU)), after pregnancy (31 +/- 10 AU) and in controls (41 +/- 13 AU, P > 0.05). The decreases in forearm vascular resistance to intrabrachial infusions of acetylcholine (2 and 20 microg/min), serotonin (10 and 100 ng/min) and sodium nitroprusside (1 and 2.5 microg/min) were similar in all groups. The nitric oxide synthase inhibitor NG-monomethyl-L-arginine (16 micromol/min) produced similar increases in vascular resistance in pregnant women (38 +/- 17 AU), after pregnancy (36 +/- 14 AU) and in control subjects (42 +/- 8 AU, P = NS).
Conclusions:
These results indicate that neither basal nor stimulated nitric oxide levels are altered in the forearm circulation during first trimester pregnancy.
