Aarsen P N
Br J Pharmacol. 1977 Dec;61(4):523-32. doi: 10.1111/j.1476-5381.1977.tb07544.x.
1 By means of the double sucrose-gap technique, the effects of bradykinin and the bradykinin potentiating peptide BPP(5a) were compared on the guinea-pig taenia coli under a number of experimental conditions.2 In normal Krebs solution the response to bradykinin was mostly a slight stimulation, characterized by a depolarization, an increase in spontaneous spike activity and a contraction. If BPP(5a) caused any effect at all, it was stimulation of the spike activity but without depolarization. Since the effect of bradykinin was little affected by an increase in dose, a potentiating effect of BPP(5a) could not be determined.3 Spontaneous spikes with a 5 to 7 s rhythm and prepotentials at their base were inhibited by bradykinin, whereas they were stimulated by BPP(5a).4 Oscillatory potentials (slow waves) induced by a calcium and magnesium-free medium were also suppressed by bradykinin and stimulated by BPP(5a). This effect of bradykinin was accompanied by a depolarization and a decrease in membrane resistance, phenomena not found after administration of BPP(5a).5 The amplitude of spontaneous spikes induced by potassium-depolarization was suppressed by bradykinin, even though the membrane resistance and potential had been decreased. BPP(5a) produced either no effect or a small stimulatory effect without influencing the membrane resistance.6 Reduction of the calcium concentration to 0.25 mM enhanced the stimulatory responses to both bradykinin and BPP(5a), especially the spike activity and depolarization. In this case the membrane resistance was increased by bradykinin as well as BPP(5a). These effects, especially those of BPP(5a), were inhibited by reduction of the sodium concentration to 15.5 mM. Reduction of the chloride concentration to 9.7 mM decreased rather than increased the stimulatory effects of both bradykinin and BPP(5a). Under these conditions bradykinin did not decrease the membrane resistance.7 Bradykinin can have both inhibitory and stimulatory effects on the taenia coli whereas BPP(5a) has only a stimulatory effect. Since under certain conditions both responses to bradykinin are accompanied by a sodium-dependent depolarization and decrease in membrane resistance, not influenced by lanthanum to any extent, it is suggested that bradykinin induces an increase in sodium conductance of the membrane. Under all the conditions investigated, except in low calcium, BPP(5a) did not affect the membrane potential and resistance. Thus, the underlying cause of its stimulatory effect is probably different from that of bradykinin.
采用双蔗糖间隙技术,在多种实验条件下比较了缓激肽和缓激肽增强肽BPP(5a)对豚鼠结肠带的作用。
在正常的 Krebs 溶液中,对缓激肽的反应大多是轻微刺激,其特征为去极化、自发棘波活动增加和收缩。如果BPP(5a)确实有任何作用的话,那就是刺激棘波活动但无去极化。由于缓激肽的作用几乎不受剂量增加的影响,所以无法确定BPP(5a)的增强作用。
具有5至7秒节律且基部有预电位的自发棘波被缓激肽抑制,而被BPP(5a)刺激。
无钙镁培养基诱导的振荡电位(慢波)也被缓激肽抑制,被BPP(5a)刺激。缓激肽的这种作用伴随着去极化和膜电阻降低,而给予BPP(5a)后未发现这些现象。
钾去极化诱导的自发棘波幅度被缓激肽抑制,即使膜电阻和电位已经降低。BPP(5a)要么没有作用,要么有轻微刺激作用,且不影响膜电阻。
将钙浓度降至0.25 mM可增强对缓激肽和BPP(5a)的刺激反应,尤其是棘波活动和去极化。在这种情况下,缓激肽和BPP(5a)都会使膜电阻增加。这些作用,尤其是BPP(5a)的作用,会被将钠浓度降至15.5 mM所抑制。将氯浓度降至9.7 mM会降低而非增加缓激肽和BPP(5a)的刺激作用。在这些条件下,缓激肽不会降低膜电阻。
缓激肽对结肠带既有抑制作用又有刺激作用,而BPP(5a)只有刺激作用。由于在某些条件下,对缓激肽的两种反应都伴随着钠依赖性去极化和膜电阻降低,且不受镧的任何影响,因此表明缓激肽会诱导膜钠电导增加。在除低钙外的所有研究条件下,BPP(5a)均不影响膜电位和电阻。因此,其刺激作用的潜在原因可能与缓激肽不同。