Gisbert M P, Fischmeister R
Laboratoire de Physiologie Cellulaire Cardiaque, INSERM U-241, Université de Paris-Sud, Orsay, France.
Circ Res. 1988 Apr;62(4):660-7. doi: 10.1161/01.res.62.4.660.
The effect of external application of synthetic atrial natriuretic factor (ANF) on calcium current (ICa) was studied in single cells isolated from frog ventricle using the whole-cell patch-clamp technique. Rat atriopeptin III (APIII) and 3-28 ANF rat (rANF) had negligible effects on basal ICa at concentrations up to 200 nM. However, when ICa was increased by isoprenaline, both peptides had significant inhibitory effects. rANF (3 nM) decreased isoprenaline-elevated ICa by an average of 33% after 3-5 minutes. APIII was slightly less effective than rANF. The effects of rANF and APIII were dose-dependent in a complex manner: one stimulatory and two different inhibitory effects were observed, one being responsible for an irreversible rundown of ICa. The effects of ANF were not blocked by atropine and desensitization of the cells to isoprenaline did not play a significant role in the response to ANF. When ICa was elevated by intracellular perfusion with cyclic adenosine 3',5'-monophosphate, added to the patch electrode solution or using a perfused pipette, rANF or APIII had less inhibitory effect, and no rundown of ICa was observed. It is proposed that adenylate cyclase may be one of several mechanisms by which ANF regulates ICa.
采用全细胞膜片钳技术，研究了合成心房钠尿肽（ANF）外用对从蛙心室分离的单细胞钙电流（ICa）的影响。大鼠心房肽III（APIII）和3 - 28 ANF大鼠（rANF）在浓度高达200 nM时对基础ICa的影响可忽略不计。然而，当ICa因异丙肾上腺素而增加时，这两种肽都有显著的抑制作用。rANF（3 nM）在3 - 5分钟后使异丙肾上腺素升高的ICa平均降低33%。APIII的效果略逊于rANF。rANF和APIII的作用以复杂的方式呈剂量依赖性：观察到一种刺激作用和两种不同的抑制作用，其中一种导致ICa不可逆的衰减。ANF的作用不受阿托品阻断，细胞对异丙肾上腺素的脱敏在对ANF的反应中不起重要作用。当通过向膜片钳电极溶液中添加或使用灌注移液管进行细胞内灌注环磷酸腺苷使ICa升高时，rANF或APIII的抑制作用较小，且未观察到ICa的衰减。有人提出腺苷酸环化酶可能是ANF调节ICa的几种机制之一。
