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Augmented endothelin‐1 constriction in pudendal arteries from ETB receptor‐deficient rats: linking hypertension and female sexual dysfunction.
Author(s) -
Allahdadi Kyan J,
Hannan Johanna L,
Boesen Erika I,
Webb R. Clinton
Publication year - 2010
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.24.1_supplement.985.5
Subject(s) - endocrinology , medicine , constriction , endothelin receptor , endothelin 1 , anatomy , receptor
Female sexual dysfunction (FSD) afflicts 40% of women, reduces quality of life and is linked with hypertension. One potential commonality between these disorders is augmented vascular sensitivity to endothelin‐1 (ET‐1). The pudendal artery is critical in blood delivery to female genitalia. We hypothesize that pudendal arteries from hypertensive ETB receptor‐deficient (ETBR‐) rats have elevated constrictor sensitivity to ET‐1. Pudendal arteries from ETBR‐ and wild type (WT) rats were mounted in wire myographs and submitted to increasing concentrations of ET‐1 in the presence or absence of ETAR (Atrasentan; 10–9 and 10–8 M) and rho‐kinase (Y‐27632; 10–6M) antagonists. Western blot measured protein levels of the ETAR. Pudendal arteries from ETBR‐ rats display increased ET‐1‐mediated constriction (pD2=9.8±0.1) compared to WT rats (pD2=8.8±0.1). ETAR antagonism reduced ET‐1‐mediated constriction in pudendal arteries from ETBR‐ (pD2=8.7±0.1); however no antagonism was observed in WT. Rho‐kinase inhibition did not reduce ET‐1‐mediated constriction in pudendal arteries from ETBR‐ or WT rats. PE‐mediated contraction and ACh‐mediated relaxation were not different between groups. ETAR protein was increased in ETBR‐ pudendal arteries. Pudendal arteries from ETBR‐ rats show greater sensitivity and elevated ETAR expression, suggesting a common abnormality in hypertension and FSD. (NIH HL066993‐06)