The vascular response to pregnancy has been frequently studied in mesenteric artery models, by investigating endothelial cell (EC) and smooth muscle cell (SMC) dependent responses to mechanical (flow-mediated vasodilation, myogenic reactivity, and vascular compliance) and pharmacological stimuli (G-protein coupled receptor responses: GqEC, GsSMC, GqSMC). It is unclear to what extent these pathways contribute to normal pregnancy-induced vasodilatation across species, strains, and/or gestational age, and at which receptor level pregnancy affects the pathways. We performed a meta-analysis on responses to mechanical and pharmacological stimuli associated with pregnancy-induced vasodilation of mesenteric arteries and included 55 (188 responses) out of 398 studies. Most included studies (84%) were performed in Wistar rats (WR) and Sprague Dawley (SDR), and compared late gestation versus non-pregnant controls (80%). Pregnancy promotes flow-mediated vasodilation in all investigated species. Only in SDR, pregnancy additionally stimulates both vasodilator GqEC sensitivity (EC50 reduced by -0.76 [-0.92, - 0.60] log[M]) and GsSMC sensitivity (EC50 reduced by -0.51 [-0.82, -0.20] log[M]), depresses vasopressor GqSMC sensitivity (EC50 increase in SDR by 0.23 [0.16, 0.31] log[M]) and enhances arterial compliance. We conclude that 1) Pregnancy facilitates flow-mediated vasodilation at term, amongst all investigated species; the contribution of additional vascular responses is species and strain specific, 2) Late pregnancy mediates vasodilation through changes at the receptor level, for the substances tested. The initial steps of vasodilation in early pregnancy remain to be elucidated.
- systematic review
- Copyright © 2011, American Journal of Physiology - Heart and Circulatory Physiology