Poggioli J, Putney J W
Pflugers Arch. 1982 Jan;392(3):239-43. doi: 10.1007/BF00584303.
The effects of receptor stimulation on net fluxes of 45Ca in parotid acinar cells were investigated. When cellular 45Ca content was near steady-state, muscarinic receptor activation by carbachol caused a net efflux of 45Ca (not always reproducible) followed by a net influx. In the presence of excess ethylene glycol bis (beta-aminoethyl ether) N,N,N,N-tetraacetic acid, net efflux invariably occurred, but the influx phase was prevented. When the muscarinic receptor antagonist atropine was added to the medium during the influx phase, an abrupt transient influx occurred followed by a return of net influx to the prestimulation level. When cellular responses believed to reflect intracellular ionized Ca (k + permeability, protein secretion) were examined under similar conditions, atropine invariably had an inhibitory effect. The Ca taken up in response to atropine apparently replenishes the hormone-sensitive pool of cellular Ca since it can be released subsequently by adrenoceptor activation. Taken together, these observations suggest that when atropine is administered to cholinergically activated cells, the hormone-sensitive Ca pool rapidly refills from the extracellular fluid without a concomitant increase in ionized intracellular Ca. Thus, it is suggested that this Ca pool is most likely associated with the plasma membrane.
研究了受体刺激对腮腺腺泡细胞中45Ca净通量的影响。当细胞45Ca含量接近稳态时，卡巴胆碱激活毒蕈碱受体导致45Ca净流出（并非总是可重复的），随后是净流入。在存在过量乙二醇双（β-氨基乙基醚）N，N，N，N-四乙酸的情况下，总是会发生净流出，但流入阶段被阻止。当在流入阶段向培养基中加入毒蕈碱受体拮抗剂阿托品时，会出现突然的短暂流入，随后净流入恢复到刺激前水平。当在类似条件下检查被认为反映细胞内游离钙的细胞反应（钾通透性、蛋白质分泌）时，阿托品总是具有抑制作用。对阿托品反应所摄取的钙显然补充了细胞钙的激素敏感池，因为它随后可通过肾上腺素能受体激活而释放。综上所述，这些观察结果表明，当向胆碱能激活的细胞施用阿托品时，激素敏感钙池迅速从细胞外液重新填充，而细胞内游离钙没有相应增加。因此，有人认为这个钙池很可能与质膜有关。
