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Pregnancy augments pressure‐induced calcium transients in endothelial cells of rat uteroplacental arteries
Author(s) -
Gokitalia I.,
Goecks Tara
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1167-b
Subject(s) - medicine , vasodilation , endocrinology , endothelium , distension , calcium , chemistry , vasoconstriction , basal (medicine) , insulin
Normal pregnancy is characterized by augmented endothelium‐dependent vasodilation in the maternal uteroplacental circulation, but the role of mechanical forces in modulating the endothelial function is not well understood. The objectives of the present study were to: (1) characterize endothelial cell (EC) [Ca 2+ ] i changes in response to elevation of intraluminal pressure in uterine arteries of non‐pregnant (NP) and late pregnant (LP) rats; (2) define the role of smooth muscle cell (SMC) Ca 2+ signaling in mediating pressure‐induced EC [Ca 2+ ] i elevations. Uterine radial arteries were cannulated and pressurized to 10 mmHg. We performed fura 2‐based measurements of changes in EC or SMC [Ca 2+ ] i and arterial diameter in response to pressure elevation to 50 (60) mmHg. Basal levels of EC [Ca 2+ ] i were significantly higher in vessels of LP compared to NP rats. Elevation of pressure resulted in a transient increase in EC [Ca 2+ ] i that was markedly potentiated in late pregnancy (LP: 160 ± 16 nM; NP: 7 ± 2 nM). Pressure‐induced elevations in SMC [Ca 2+ ] i was significantly smaller compared to those in ECs indicating that Ca 2+ diffusion from SMCs through gap junction is unlikely is a source of EC [Ca 2+ ] i transients. Pressurization of the arteries from both sides to minimize the effect of shear stress resulted in 18 ± 3 % reduction in EC [Ca 2+ ] i responses. In conclusion, late pregnancy is associated with a marked augmentation of EC [Ca 2+ ] i transients in response to both arterial distension and transient shear stress, and might be an important adaptive mechanism that contributes to augmented vasodilation in the maternal uterine circulation. Supported by NIH HL067250