Evans D H, Weingarten K E, Walton J S
Center for Membrane Toxicity Studies, Mount Desert Island Biological Laboratory, Salsbury Cove, ME 04672.
Toxicology. 1990 May 14;62(1):89-94. doi: 10.1016/0300-483x(90)90033-d.
We investigated the effect of blockade of muscarinic, cholinergic receptors by atropine on the Cd2(+)- and Ni2(+)-induced vasoconstriction of rings of endothelium-free, vascular smooth muscle from the ventral aorta of the dogfish shark, Squalus acanthias. Atropine reduced the Cd2(+)-induced vasoconstriction by approximately 50%, but did not alter the Ni2(+)-induced vasoconstriction, suggesting that the vasoactivity of these two metals may be, at least partially, via different pathways. In addition, this is the first demonstration that one component of Cd2+ vaso-toxicity may be via stimulation of muscarinic receptors.
我们研究了阿托品对毒蕈碱型胆碱能受体的阻断作用，对镉离子（Cd2+）和镍离子（Ni2+）诱导的皱唇鲨（Squalus acanthias）腹主动脉无内皮血管平滑肌环收缩的影响。阿托品使镉离子诱导的血管收缩降低了约50%，但未改变镍离子诱导的血管收缩，这表明这两种金属的血管活性可能至少部分通过不同途径发挥作用。此外，这首次证明了镉离子血管毒性的一个组成部分可能是通过刺激毒蕈碱型受体。
