TY - JOUR
T1 - Vasoconstrictor components in the Arabian Gulf catfish (Arius thalassinus, Ruppell) Proteinaceous skin secretion
AU - Al-Hassan, Jassim M.
AU - Thomson, Martha
AU - Ali, Muslim
AU - Fayad, Sanaa
AU - Elkhawad, Abdullah
AU - Thulesius, Olav
AU - Criddle, Richard S.
PY - 1986
Y1 - 1986
N2 - J. M. Al-Hassan, M. Thomson, M. Ali, S. Fayad, A. Elkhawad, O. Thulesius and R. S. Criddle. Vasoconstrictor components in the Arabian Gulf catfish (Arius thalassinus, Ruppell) proteinaceous skin secretion. Toxicon 24, 1009 - 1014, 1986. - The Arabian Gulf catfish (Arius thalassinus, Ruppell) produces toxic substances from its skin and from venom glands located near the base of the pectoral fins. Investigation of the pharmacological properties of the skin toxin have previously shown cholinergic vasoconstrictor activity in umbilical arteries. Cholinergic vasoconstriction was confirmed in sheep renal arteries. This activity was partially blocked by atropine, while most of the residual contraction was eliminated by simultaneous addition of indomethacin. Skin toxin treatment of arterial specimens caused a release of prostaglandin (PGE2, TXB2 and 6-keto-PGF1α) into the organ bath. Prostaglandin release was blocked by pretreatment with indomethacin. Heat denaturation of skin toxin caused a loss of only the indomethacinsensitive muscle contraction activity; most of the residual activity was blocked by atropine.
AB - J. M. Al-Hassan, M. Thomson, M. Ali, S. Fayad, A. Elkhawad, O. Thulesius and R. S. Criddle. Vasoconstrictor components in the Arabian Gulf catfish (Arius thalassinus, Ruppell) proteinaceous skin secretion. Toxicon 24, 1009 - 1014, 1986. - The Arabian Gulf catfish (Arius thalassinus, Ruppell) produces toxic substances from its skin and from venom glands located near the base of the pectoral fins. Investigation of the pharmacological properties of the skin toxin have previously shown cholinergic vasoconstrictor activity in umbilical arteries. Cholinergic vasoconstriction was confirmed in sheep renal arteries. This activity was partially blocked by atropine, while most of the residual contraction was eliminated by simultaneous addition of indomethacin. Skin toxin treatment of arterial specimens caused a release of prostaglandin (PGE2, TXB2 and 6-keto-PGF1α) into the organ bath. Prostaglandin release was blocked by pretreatment with indomethacin. Heat denaturation of skin toxin caused a loss of only the indomethacinsensitive muscle contraction activity; most of the residual activity was blocked by atropine.
UR - http://www.scopus.com/inward/record.url?scp=0022969231&partnerID=8YFLogxK
U2 - 10.1016/0041-0101(86)90007-3
DO - 10.1016/0041-0101(86)90007-3
M3 - Article
C2 - 3824400
AN - SCOPUS:0022969231
SN - 0041-0101
VL - 24
SP - 1009
EP - 1014
JO - Toxicon
JF - Toxicon
IS - 10
ER -