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CGRP terminates vasopressor responses to endothelin‐1 in vivo
Author(s) -
Meens Merlijn JPMT,
Nelissen Jelly,
Mattheij Nadine JA,
Steinbusch Laura KM,
Janssen Ben JA,
De Mey Jo GR
Publication year - 2011
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.25.1_supplement.816.1
Endothelin‐1 (ET‐1) activates ET A and ET B receptors. In rat mesenteric arteries ET A activation causes long‐lasting contractions that are not ended by antagonists or NO, but are terminated by CGRP (Meens et al. PLos ONE 2010). We assessed whether these findings are sufficiently common to alter local and/or total vascular resistance (R). Methods Several types of rat (WKY, male, 16 wks) arteries were investigated by wire‐myography. Hemodynamic parameters were assessed in anesthetized or conscious, unrestrained rats. Local blood flows were measured with flow probes. Results : In all arteries, ET‐1‐induced contractions were long‐lasting and not ended by ET‐receptor antagonism. CGRP permanently reduced ET‐1‐induced contractions in mesenteric, renal, spermatic, splenic, epigastric and saphenous arteries but not in basilar, coronary and gastric arteries. In anesthetized rats long‐lasting (Big‐)ET‐1‐induced pressor responses were transiently reversed by sodium nitroprusside (SNP) but were terminated by CGRP. This was at least partly due to CGRP‐induced decreases of R in skeletal muscle and the renal circulation. In conscious rats CGRP, but not SNP, terminated ET‐1‐induced pressor responses. Conclusion Vasoconstrictor responses to ET‐1 are resistant to ET A ‐antagonism and NO, but are ended by CGRP in several vascular beds and in vivo . Performed within TIPharma project T2‐108.