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Vascular reactivity is altered in mice with a conditional knockout of relaxin receptor in endothelial cells (681.11)
Author(s) -
Woodward Lawrence,
Rusnak Margaret,
Ramirez Rolando,
Huang Zaohua,
Lopez Carolina,
Agoulnik Alexander,
Conrad Kirk,
Novak Jacqueline
Publication year - 2014
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.28.1_supplement.681.11
Subject(s) - relaxin , endocrinology , medicine , vasodilation , receptor , endothelium , knockout mouse , biology
The ovarian hormone relaxin (RLX) has been traditionally thought of as a reproductive hormone; however, the effects of RLX outside the reproductive organs have gained a better appreciation. Relaxin is a vasodilator and increases arterial compliance. These beneficial effects have opened up the therapeutic potential for RLX and have focused our studies on the physiological role for arterial‐derived RLX. The RLX receptor RXFP1 has been identified in both endothelium and vascular smooth muscle. For this study, conditional knockout mice with RXFP1 ablation in endothelial cells were used. Floxed allele of RXFP1 was deleted using endothelial‐specific Cdh5‐cre transgene. The littermate control group maintained functional RXFP1 receptor gene. Mice lacking the RXFP1 receptor in their endothelium displayed an altered vascular reactivity compared to control animals. Isolated resistance sized renal interlobar arties were studied in a isobaric arteriograph. Myogenic reactivity was reduced in control mouse arteries treated with L‐arginine but not in those arteries treated with D‐arginine. Percent change in diameter was 5.8±0.8% with L‐arg compared 0.90±.8% to D‐arg treated arteries. However, the arteries isolated from conditional knockout mice failed to respond to L‐arg and remained very myogenic (‐0.81±.2%). These data suggest that the endothelial RLX receptor is important for the reduced myogenic response to RLX.