Bentley P J, Yorio T, Fleisher L
J Endocrinol. 1975 Aug;66(2):273-8. doi: 10.1677/joe.0.0660273.
Cadmium, 10(-3) mol/l on the mucosal or 10(-5) mol/l on the serosal side of the toad urinary bladder, inhibits the hydro-osmotic effect of vasopressin. This inhibition is irreversible. The osmotic transfer of water in the absence of vasopressin was unaffected by the presence of the Cd2+. The hydro-osmotic response to cyclic AMP was also reduced by the Cd2+, but the response due to hypertonicity of the serosal bathing solution was unaffected. The short-circuit current (reflecting active transmural Na+ transport) was inhibited by 10(-3) mol Cd2+/l on the serosa, but was increased by 10(-3) mol/l at the mucosa or 10(-4) mol/l at the serosa. The natriferic response of the bladder to vasopressin was unaffected when Cd2+ was present under conditions that inhibited the hydro-osmotic response, further emphasizing that separate effector mechamisms may be involved for each effect.
镉,蟾蜍膀胱黏膜侧浓度为10⁻³mol/l或浆膜侧浓度为10⁻⁵mol/l时,会抑制血管加压素的水渗透效应。这种抑制是不可逆的。在没有血管加压素的情况下,水的渗透转运不受Cd²⁺存在的影响。Cd²⁺也会降低对环磷酸腺苷的水渗透反应,但浆膜侧沐浴溶液高渗引起的反应不受影响。浆膜侧10⁻³mol Cd²⁺/l会抑制短路电流(反映主动跨膜Na⁺转运),但黏膜侧10⁻³mol/l或浆膜侧10⁻⁴mol/l时短路电流会增加。当在抑制水渗透反应的条件下存在Cd²⁺时,膀胱对血管加压素的排钠反应不受影响,这进一步强调每种效应可能涉及不同的效应机制。