The Effects Of Peptidic Transmitter CGRP And Classical Neurotransmitte's NE And ACh On Primary Cultured Cardiac Myocytes

Objective: It is an important research topic of cardiovascular system disease's high incidence rate. The dysfunction of autonomic nervous system (the sympathetic and parasympathetic systems) plays an important role on cardiovascular diseases. The NE and ACh are the traditional transmitters of the sympathetic and parasympathetic systems respectively. In addition to the classical transmitters (NE or ACh) peptidic transmitters are clearly present and have direct or indirect actions on cardiac function. The peptidic transmitters may coexist with the classical transmitters and may be released from the nerve terminals when they are stimulated. The classical neurotransmitters and nerve peptides play an important role not only on cardiovascular physiological regulation, but also the pathological process of myocardial hypertrophy and heart failure. The previous studies showed that the basic mechanism of congestive heart failure is ventricle remodeling. The myocardial hypertrophy is the characteristic change of ventricle remodeling. The hemodynamics mechanism is the earliest focus during the onset of myocardium hypertrophy. The recently research showed that the non-hemodynamics factors played an important role during the onset and development of myocardium hypertrophy process. The cardiac muscle cell hypertrophy is a complicated dynamic process with many regulation factors to participate in .There are manyfactors can induce cardiac muscle cell hypertrophy, such as the neurotrophic factors> chemical factors and mechanical stimulation factors. The factor regulation includes sympathetic, vagus, and peptidergic nerve fiber .It has been confirmed that the sympathetic transmitter NE had the role of inducing cardiac muscle cell hypertrophy. The animal experiments showed that long-term of higher dosage NE injection can induce the myocardial hypertrophy. It gives us the cue that catecholamine play an important direct auxetic role in the myocardial cell hypertrophy in addition to the hemodynamics effects. The hypertrophy role of CGRP has been reported in domestic and international literature being the peptide nerve fiber transmitter but have different views. So it is necessary to further study the mechanism of CGRP in myocardial cell hypertrophy. ACh as the parasympathetic transmitter to myocardial cell hypertrophy role has never been reported, so the purpose of this research is to investigate different myocardial cell hypertrophy role of simple factor between the classical neurotransmitter NE, ACh and peptidic CGRP as well as their antagonists in the primary culture myocardial cell. The aim of this study is to further investigate the possible mechanism of myocardial hypertrophy and provide the theoretical evidence for clinical treatment. Methods: Put the four-days live primary culture rat myocardial cell in different concentration NEs ACh> and CGRP solution respectively to detect the spontaneous contraction rate^ morphological changes> protein content and volume of a single cardiac muscle cell. Based on the above experiments, we put the antagonists in the four-days living cells prior to neurotransmitter exposure. There effects on cardiac muscle cell will be observed.Results: The different concentrations of NE, ACh and CGRP have different effects on the spontaneous contraction rate^ morphological changes> protein content and volume of a single cardiac muscle cell.NE, ACh's actions can be blocked by their relative antagonists but CGRP's action cannot be blocked by the antagonists of NE. Conclusions: NE can increase the spontaneous contraction rate in dosage-dependence and time-dependence manner as well as the volume of a single cardiac muscle cell and the protein contents. ACh can decrease the spontaneous contraction rate in dosage-dependence and time-dependence manners. But there are no effect on the volume of a single cardiac muscle cell and the protein contents. CGRP can increase the spontaneous contraction rate in dosage-dependence and time-dependence manner as well as the volume of a single cardiac muscle cell and the protein contents. But the antagonists of NE cannot block CGRP's action.