Expression and functional evidence of the prostaglandin F2α receptor mediating contraction in human umbilical vein

Umbilical vein vasomotion detectedin vivoby serial three-dimensional pixelwise spatially angle-corrected volume flow measurements

“…In contrast to traditional PI, RI and flow velocity measurements, the novel flow volume measurements reflect the fetal supply of blood more precisely since a certain quantity of blood is necessary to transport certain amounts of oxygen and nutrients. Spontaneous contractions observed in vitro can be modified by pharmaceuticals or intrinsically produced substances. In order to understand these mechanisms and to find an approach to their meaning in vivo , we conducted a study to monitor spontaneous changes in fetal volume perfusion in healthy fetuses.…”

Prostaglandin FP receptor antagonists: discovery, pharmacological characterization and therapeutic utility

“…In endotoxin‐treated porcine coronary arteries, the bradykinin (BK) B 1 receptor agonist, des‐Arg 9 ‐BK, caused endothelium‐independent contractions of the tissue that were inhibited by COX‐2 inhibitors and a TP receptor antagonist but neither by a COX‐1 inhibitor (aspirin) nor by DP/EP (AH‐6809)‐, FP (AL‐8810)‐ and IP (RO1138452) receptor antagonists (More et al, ,b). However, since AL‐8810 potently and competitively antagonized the contractile effects of free acids of latanoprost, bimatoprost and PGF 2α in isolated rings of human umbilical vein, the involvement of FP receptors in causing these responses was confirmed (Errasti et al, ). Likewise, AL‐8810 proved useful in ascribing an FP receptor‐mediated vasoconstrictor effect of endogenously released PGF 2α in freshly regenerated rat femoral arteries in a rat model of atherosclerosis (Hirao et al, ).…”

Prostaglandin F 2α evokes vasoconstrictor and vasodepressor activities that are both independent of the F prostanoid receptor

“…Thus, the vasoconstrictor and pressor effects of PGF 2α appear to be mainly mediated through the non‐FP receptors TP and/or EP3. However, there are studies suggesting FP also mediates vasoconstriction 24–26 . Indeed, FP −/− has been reported to abolish the pressor response of PGF 2α , whereas the over‐expression of FP is reported to not only give rise to hypertension, but also increase the ex vivo vasoconstrictor response to PGF 2α 14,27 .…”

“…However, there are studies suggesting FP also mediates vasoconstriction. [24][25][26] Indeed, FP −/− has been reported to abolish the pressor response of PGF 2α , whereas the overexpression of FP is reported to not only give rise to hypertension, but also increase the ex vivo vasoconstrictor response to PGF 2α . 14,27 Interestingly, FP is found to be readily detected in resistance vessels of the intra-renal vascular beds.…”