Ball D, Elliott M E, Hadjokas N, Goodfriend T L, Green M J
Clin Exp Hypertens A. 1986;8(3):323-45. doi: 10.3109/10641968609039608.
Veratridine inhibited angiotensin binding to its receptors in bovine adrenal glomerulosa cells and vascular smooth muscle. Fifty percent inhibition of adrenal receptors required about 2 X 10(-5) M veratridine. Receptors from vascular tissue were less sensitive. Graphic analysis showed that inhibition resulted primarily from a reduction of receptor number. Angiotensin stimulation of phosphatidylinositol turnover and of aldosterone production was inhibited by veratridine. Analogues of veratridine varied in their receptor inhibitory potency, but these variations did not correlate with the potencies of analogues as hypotensive agents or inhibitors of aldosteronogenesis. Very low extracellular sodium concentrations inhibited the adrenal effects of angiotensin. Neither veratridine nor grayanotoxin, both of which open sodium channels in excitable tissues, had a detectable effect on sodium fluxes in adrenal cells. Inhibition of aldosteronogenesis by veratridine is more likely the result of receptor and post-receptor effects than an alteration of the sodium channel.
藜芦碱抑制血管紧张素与牛肾上腺球状带细胞及血管平滑肌中其受体的结合。肾上腺受体50%的抑制率需要约2×10⁻⁵ M的藜芦碱。血管组织中的受体敏感性较低。图像分析表明，抑制主要是由于受体数量减少所致。藜芦碱抑制血管紧张素对磷脂酰肌醇周转及醛固酮生成的刺激作用。藜芦碱类似物在受体抑制效力方面存在差异，但这些差异与类似物作为降压剂或醛固酮生成抑制剂的效力无关。极低的细胞外钠浓度抑制血管紧张素对肾上腺的作用。藜芦碱和灰藜毒素（二者均可在可兴奋组织中打开钠通道）对肾上腺细胞中的钠通量均未产生可检测到的影响。藜芦碱对醛固酮生成的抑制作用更可能是受体及受体后效应的结果，而非钠通道改变所致。
