Neural and hormonal control mechanisms in excitatory cardiac regulation of the hermit crabs

我们研究了甲壳类动物心包肽proctolin对A. aniculus心脏的影响。通过记录心肌收缩力、心肌细胞内膜电位和心肌神经节细胞外电位的方法，研究了这些作用。我们使用了半完整的心脏，与背甲一起分离，以及完全分离的心脏。正性肌力作用和正性张力作用的阈值浓度分别约为10 μ M和10 μ M。<-13><-10>在10 μ M时，变力效应超过正常搏动幅度的150%。<-7>在用proctolin（10 μ M-10 μ M）灌注期间，最初的正变时效应随后是负效应。<-6><-5>其变力作用主要是由于增加了心脏神经节细胞的爆发内脉冲频率。正性变时效应（&lt;50%）反映了神经节爆发率的增加。应用丙诺啡后，复合EJPs和肌肉动作电位的幅度增加，而心肌细胞膜的电导没有改变。即使在含TTX的生理盐水中也观察到正性张力作用，如挛缩。在含有蛋白激酶抑制剂H-7的盐水中消除挛缩。H-7不影响心肌膜电位，但略有增强神经节的活动。腺苷酸环化酶激活剂，毛喉素，和G蛋白激活剂，霍乱毒素，增强神经节的活动，但不挛缩。在A1F_4 ^-存在时，proctolin的作用没有增强。某些磷酸二酯酶抑制剂，咖啡因，茶碱，3-甲基黄嘌呤和IBMX影响神经节，但不影响心肌活动本身。也就是说，在抑制剂的存在下，proctolin对心脏神经节的作用，但不是对心肌细胞，显着增强。不是二丁酰cGMP，而是

We studied the effects, on the A.aniculus heart, of a crustacean pericardial peptide, proctolin. Those effects were investigated by means of recording contractile force, intracellular membrane potential of the myocardium and extracellular potential from cardiac ganglionic cells. We used semi-intact hearts, isolated together with the dorsal, carapace, as well as totally isolated hearts. Threshold concentrations for positively inotropic and positively tonotropic effects were approximately 10^<-13> M and 10^<-10> M, respectively. At 10^<-7> M, inotropic effects amounted to more than 150% of the normal beat amplitude. Initially positive chronotropic effects were followed by negative effects during a period of perfusion with proctolin (10^<-6> M - 10^<-5> M). The inotropic effects resulted mainly from augmentation of the intra-burst impulse rate of cardiac ganglionic cells. The positively chronotropic effects (<50%) reflected increases in burst rate of the ganglion. The amplitude of the compound EJPs and that of the muscle action potentials were augmented, while conductance of the myocardial cell membrane was not changed, during proctolin application. Positively tonotropic effects were observed as contracture even in TTX-containing saline. The contracture was abolished in saline containing a protein kinase inhibitor, H-7. H-7 did not affect myocardial membrane potential but slightly enhanced ganglionic activity. An adenylate cyclase activator, forskolin, and a G-protein activator, cholera toxin, enhanced ganglionic activity but not contracture. In the presence of A1F_4^-, proctolin effects were not augmented. Certain phosphodiesterase inhibitors, caffeine, theophylline, 3-methylxanthine and IBMX affected the ganglion but not myocardial activity itself. That is, in the presence of the inhibitors, proctolin actions on the cardiac ganglion, but not on the myocardial cells, were significantly augmented. Not dibutyryl cGMP, but instead