Gruber K A, Callahan M F
Department of Medicine, Wake Forest University Medical Center, Winston-Salem, North Carolina 27103.
Am J Physiol. 1989 Oct;257(4 Pt 2):R681-94. doi: 10.1152/ajpregu.1989.257.4.R681.
Examination of the cardiovascular effects produced by peripheral administration of peptide sequences derived from adrenocorticotropic hormone (ACTH) led to the discovery of the pressor, cardioaccelerator, and natriuretic actions of intravenous (iv) ACTH-(4-10). Based on pharmacological studies in rats with alpha- and beta-adrenergic receptor antagonists, the cardiovascular effects of this peptide appeared to be mediated by the release of catecholamines. A peptide sequence analogous to ACTH-(4-10), gamma-melanocyte-stimulating hormone (gamma-MSH), possesses greater than 100-fold more cardiovascular activity and 1,000-fold more natriuretic activity than ACTH-(4-10). The pressor effect of iv gamma-MSH peptides appears to be dependent on the maintenance of preganglionic sympathetic drive, with no significant contribution of circulating vasopressin or angiotensin II. However, the presence of central vasopressinergic, and perhaps angiotensinergic, pathways appears to be crucial for expression of the full pressor effect of circulating gamma-MSH. Further evidence for the potential importance of the central nervous system (CNS) in these cardiovascular effects was obtained from central lesion experiments and a comparison of intracarotid vs. intrajugular infusions. Structure-activity studies suggested that the cardiovascular effects of ACTH-(4-10) or gamma-MSH are dependent on an Arg-hydrophobic amino acid sequence, located at or near their COOH-terminal. A similar requirement for biological activity is found in molluscan cardioexcitatory peptides, and the molluscan peptides have cardiovascular effects in rats, which resemble ACTH-(4-10) or gamma-MSH. This suggests that peptides of the gamma-MSH family are the pharmacological analogues, and perhaps the physiological homologues, of a cardioexcitatory family of peptides found in molluscs and birds. Elevated circulating levels of peptides derived from the NH2-terminal of pro-opiomelanocortin (POMC) have been found in psychological stress, cardiovascular distress, and hemorrhage. Increases in central sympathetic drive are common to all of these states. gamma-MSH peptides have been localized to POMC neurons in the arcuate nucleus and nucleus commissuralis of the rat. Projections from the latter nucleus innervate hindbrain vasomotor centers. Intraventricular administration of gamma-MSH produces prolonged elevation of mean arterial pressure. gamma-MSH peptides may provide a link between humoral and neurogenic mechanisms in cardiovascular regulation and could potentially be important neurotransmitters for central control of the cardiovascular system.
对外周给予促肾上腺皮质激素(ACTH)衍生的肽序列所产生的心血管效应进行研究后,发现了静脉注射ACTH-(4 - 10)的升压、心脏加速和利钠作用。基于对大鼠使用α和β肾上腺素能受体拮抗剂的药理学研究,该肽的心血管效应似乎是由儿茶酚胺的释放介导的。一种与ACTH-(4 - 10)类似的肽序列,γ-黑素细胞刺激素(γ-MSH),其心血管活性比ACTH-(4 - 10)高100倍以上,利钠活性高1000倍以上。静脉注射γ-MSH肽的升压作用似乎依赖于节前交感神经驱动的维持,循环中的血管加压素或血管紧张素II没有显著作用。然而,中枢血管加压素能通路以及可能的血管紧张素能通路的存在似乎对循环γ-MSH的完全升压作用的表达至关重要。通过中枢损伤实验以及颈内动脉与颈静脉输注的比较,获得了进一步的证据,证明中枢神经系统(CNS)在这些心血管效应中具有潜在重要性。结构-活性研究表明,ACTH-(4 - 10)或γ-MSH的心血管效应依赖于位于其COOH末端或附近的精氨酸-疏水氨基酸序列。在软体动物心脏兴奋肽中也发现了对生物活性的类似要求,并且这些软体动物肽在大鼠中具有类似于ACTH-(4 - 10)或γ-MSH的心血管效应。这表明γ-MSH家族的肽是软体动物和鸟类中发现的心脏兴奋肽家族的药理学类似物,也许还是生理学同源物。在心理应激、心血管窘迫和出血情况下,已发现源自阿片-促黑素细胞皮质素原(POMC)NH2末端的肽的循环水平升高。所有这些状态都有中枢交感神经驱动增加的情况。γ-MSH肽已定位在大鼠弓状核和连合核的POMC神经元中。后一个核的投射支配后脑血管运动中枢。脑室内注射γ-MSH会使平均动脉压长时间升高。γ-MSH肽可能在心血管调节的体液和神经源性机制之间提供联系,并且可能是心血管系统中枢控制的重要神经递质。