Department of Chemistry, University of Toronto Mississauga, Mississauga, Ontario, Canada L5L 1C6.
Gen Comp Endocrinol. 2011 Apr 1;171(2):218-24. doi: 10.1016/j.ygcen.2011.01.015. Epub 2011 Feb 3.
Like vertebrate cardiovascular systems, the dorsal vessel of the Orthopteran insects Baculum extradentatum and Locusta migratoria is under myogenic as well as neural control, through the action of neurotransmitters, neuromodulators and neurohormones. It was previously shown that the excitatory neuropeptide, crustacean cardioactive peptide (CCAP), triggers an increase in heart rate in B. extradentatum, and CCAP-like immunoreactivity is present in the innervation to the heart in many insects. In the present study, CCAP resulted in a dose-dependent increase in heart rate and hemolymph flow velocity, or cardiac output, in B. extradentatum. In contrast, CCAP led to a significant increase in stroke volume and cardiac output in L. migratoria without modifying heart rate or aortic contraction frequency. Hemolymph flow through the excurrent ostia of L. migratoria, small openings or valves on the posterior aorta and anterior heart, was inhibited with increasing concentrations of CCAP, with complete inhibition seen at 10(-7) M CCAP. In the locust, CCAP increases the volume of hemolymph in the dorsal vessel by the synchronous closing of the excurrent ostia, resulting in more forceful heart contractions and increased stroke volume and cardiac output, without modifying heart rate through a physiological mechanism analogous to the Frank-Starling mechanism in vertebrates. Therefore, crustacean cardioactive peptide alters the contractile properties of cardiac tissue in both B. extradentatum and L. migratoria, allowing for an increase in blood flow and circulation.
与脊椎动物心血管系统一样,直翅目昆虫 Baculum extradentatum 和 Locusta migratoria 的背血管受到肌源性和神经源性控制,通过神经递质、神经调质和神经激素的作用。先前的研究表明,兴奋性神经肽甲壳动物心脏活性肽(CCAP)可引起 Baculum extradentatum 的心率增加,并且在许多昆虫的心脏神经支配中存在 CCAP 样免疫反应性。在本研究中,CCAP 导致 Baculum extradentatum 的心率和血淋巴流速(或心输出量)呈剂量依赖性增加。相比之下,CCAP 导致 L. migratoria 的搏出量和心输出量显著增加,而不改变心率或主动脉收缩频率。随着 CCAP 浓度的增加,通过 L. migratoria 的后主动脉和前心的传出孔的血淋巴流动被抑制,在 10(-7) M CCAP 时完全抑制。在蝗虫中,CCAP 通过同步关闭传出孔,增加背血管中的血淋巴量,从而导致更有力的心脏收缩和增加的搏出量和心输出量,而不会通过类似于脊椎动物的 Frank-Starling 机制改变心率。因此,甲壳动物心脏活性肽改变了 Baculum extradentatum 和 L. migratoria 中心肌组织的收缩特性,允许增加血流量和循环。