Key result
ADRB agonists evoked weak relaxations (< 20%) in human umbilical vessels from term infants, partially mediated by the endothelium-derived NO pathway.
Human umbilical arteries and veins from term infants exhibit a low relaxing capacity to cAMP and cGMP pathway agonists, which may be physiologically important to maintain fetoplacental circulation.
Minimal ADRB relaxation in umbilical vessels may limit fetal vasodilator options; leaves open NO pathway roles in term pregnancies.
) were performed. None of the tested drugs induced a relaxation higher than 30% of the U44069-induced tone. Rings from HUAs and HUVs showed a similar relaxation to forskolin, SNP, PDE inhibitors, and ADRB agonists. BAY 41-2272 was significantly more efficient in relaxing veins than arteries. ADRB agonists evoked weak relaxations (< 20%), which were impaired in endothelium-removed vessels or in the presence of the NO synthase inhibitor L-NAME, sGC inhibitor ODQ. PKA and PKG inhibitors impaired ADBR1-mediated relaxation but did not affect ADRB2-mediated relaxation. ADRB3-mediated relaxation was impaired by PKG inhibition in HUAs and by PKA inhibition in HUVs. Although HUA and HUV rings were relaxed by BRL37344, immunohistochemistry and RT-qPCR analysis showed that, compared to ADRB1 and ADRB2, ADRB3 receptors are weakly or not expressed in umbilical vessels. In conclusion, our study confirmed the low relaxing capacity of HUAs and HUVs from term infants. ADRB-induced relaxation is partially mediated by endothelium-derived NO pathway in human umbilical vessels.
No takes yet. Share an insight, caveat, or question.
Provitera et al. (2019) studied Umbilical vessels from term infants. ADRB agonists and other relaxing agents was evaluated on Vessel relaxation. ADRB agonists evoked weak relaxations (< 20%) in human umbilical vessels from term infants, partially mediated by the endothelium-derived NO pathway.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: