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. 2014 Dec 1;172(4):1005–1019. doi: 10.1111/bph.12964

Figure 5.

Figure 5

The role of G-protein coupling in serelaxin-mediated cGMP accumulation in human primary umbilical vascular cells. Pretreatment of HUASMC (n = 6) in (A) and of HUVSMC (n = 6) in (B) with the selective Gαs inhibitor NF449 (10 μM, 30 min) caused a rightward shift and reduced the E-max of the cGMP CRC to serelaxin without modifying the shape of the curve. Pretreatment of HUASMC (n = 7) in (C) and of HUVSMC (n = 6) in (D) with the selective Gαi/o inhibitor NF023 (10 μM, 30 min) reduced the E-max of the cGMP CRC to serelaxin and changed the shape of the curve observed with HUVSMC (D) from bell-shaped to sigmoidal. In both (E) HUASMC (n = 6) and (F) HUVSMC (n = 6), pretreatment with both NF449 and NF023 completely abolished serelaxin-mediated cGMP responses, showing that the responses result entirely from RXFP1 receptors interaction with G proteins. In (G) HUASMC (n = 6) and in (H) HUVSMC (n = 6), pretreatment with filipin III (1 μg·mL−1, 1 h), which disrupts lipid rafts, mimicked the effect of the Gαi/o inhibitor NF023 – reducing E-max and converting CRCs from bell-shaped to sigmoidal in HUVSMC.