Search Results

You are looking at 1 - 1 of 1 items for

  • Author: K Ashida x
  • Refine by access: All content x
Clear All Modify Search
K Hamano
Search for other papers by K Hamano in
Google Scholar
PubMed
Close
,
ML Tierney
Search for other papers by ML Tierney in
Google Scholar
PubMed
Close
,
K Ashida
Search for other papers by K Ashida in
Google Scholar
PubMed
Close
,
Y Takei
Search for other papers by Y Takei in
Google Scholar
PubMed
Close
, and
N Hazon
Search for other papers by N Hazon in
Google Scholar
PubMed
Close

Arterial rings were prepared from the branchial artery, coeliac artery and ventral aorta of the Japanese dogfish Triakis scyllia and used to determine arterial contraction in a myograph. Noradrenaline caused a dose-dependent contraction (10(-9)-3 x 10(-6) M) that was completely inhibited by pre-treatment with 10(-7) M phentolamine. Homologous dogfish angiotensin II (ANG II) ([Asn1, Pro3, Ile5]-ANG II) also caused dose-dependent contraction (10(-9)-3 x 10(-6) M), but phentolamine had no effect on this response. Administration of dogfish angiotensin I (ANG-I) ([Asn1, Pro3, Ile5, Gln9]-ANG I) resulted in a contraction similar to that produced by ANG II and the effect could be blocked with 10(-7) M captopril. The mammalian ANG II receptor antagonists [Sar1, Ile8]-ANG II and [Sar1, Ala8]-ANG II caused dose-dependent contractions of coeliac artery rings, but were less potent than homologous ANG I and ANG II. These results show that the contractile effect of [Asn1, Pro3, Ile5]-ANG II is not mediated by the alpha-adrenergic system and contractions of arterial rings by noradrenaline and elasmobranch ANG II are mediated by separate vascular receptors. The elasmobranch ANG II vascular receptor may have co-evolved with the unusual structure of this peptide.

Free access