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v The heart is the organ of the endocrine function can generate and secretion of natriuretic peptide hormones. Natriuretic peptide hormone natriuretic peptide family (the family of natriuretic peptides. NPs) in the form exists in and mammals, members of atrial natriuretic peptide (atrial natriuretic peptide, ANP), brain natriuretic peptide (brainnatriuretic peptide, BNP ), C-type natriuretic peptide (C-type natriuretic peptide, CNP) and D-type natriuretic peptide (dendroaspis natriuretic peptide, DNP). Biological effects of such hormones natriuresis, diuresis, and to participate in the water and salt balance and blood pressure regulation. ANP is mainly synthesized by atrial myocytes and release, with the presence of the heart, blood vessels, central nervous system, lymphatic tissue, genital and kidney tissue natriuretic peptide receptor (natriuretic peptidereceptor, NPR) combined, and thus play a diastolic blood vessels, lower blood pressure, natriuretic, and inhibition of cell proliferation, the role of regulating immune and protect cells and involved in lipid metabolism. ANP is found for the first time in the natriuretic peptide family peptide hormones. Studies have shown that many factors involved in the regulation of ANP secretion, such as atrial expansion or pressure can stimulate atrial myocytes Golgi secretory granules increased ANP secretion. Some humoral factors also could affect ANP secretion, such as the overall condition, glucocorticoids stimulate ANP secretion, intravenous injection of angiotensin II, phentolamine, endothelin, vasopressin and prostaglandin plasma ANP concentrations can increase; contrary, nitric oxide can inhibit atrial ANP secretion. Cells under in vitro conditions, high osmotic pressure, the the high K , hypoxia and Na concentration can promote the secretion of the isolated heart of ANP. In addition, adrenergic, cholinergic and peptide receptor ANP secretion has a regulatory role. However, the atrial myocytes Distraction (stretch) stimulus is considered to be the most critical stimulus for ANP secretion. Currently, of Ca , 2 and cyclic adenosine monophosphate (cyclic adenosine monophosphate, cAMP) and ANP secretion relationship between research concern. While Ca 2 regulation of ANP secretion in dispute. Ca 2 as a second messenger in cardiac myocyte excitation - contraction coupling (excitation-contractioncoupling ECC) process is important intermediary substance. Depolarization of myocardial cells can be activated on the cell membrane of the L-type Ca 2 channel (L-type Ca 2 channels) to promote the Ca 2 influx and activation of the sarcoplasmic reticulum (sarcoplasmic reticulum, SR) membrane Ryanodine receptors (RyRs) in turn trigger SR Ca 2 release within this process is called the Ca 2 trigger Ca 2 release (Calcium-induced release ofcalcium, CICR). CICR mechanism can rapidly increase-intracellular Ca 2 concentration of to enhanced cytoplasmic Ca 2 and troponin sensitivity, causing the contraction of myocardial cells and improve the myocardial tissue mechanical activity. Some studies suggest that in the atrium and in vitro pulsatile perfusion heart model, activation of plasma membrane L-type Ca 2 channel promote Ca 2 influx inhibit ANP secretion . On the contrary, to promote the secretion of ANP. Studies have shown that activation of plasma membrane L-type Ca 2 channels can promote the secretion of ANP in the the atrial perfusion model, and cultured atrial myocytes. In addition, Jin et study found that extracellular hypertonic conditions to promote atrial myocytes release of ANP, its role may be on the cell membrane of the L-type Ca 2 channel activity and activation of SR. But the the SR the freed Ca 2 ANP secretion and intracellular Ca 2 concentration of ANP secretion relationship is unclear. Therefore, the present study, rabbits pulsatile perfusion model of isolated atrial ANP secretion observed SR release of Ca 2 , then investigate the changes in intracellular Ca 2 concentration the regulating role of ANP secretion. The results of this study are as follows: 1.SR release Ca significantly 2 inhibitors Ryanodine (succeedingly 3.0 μmol of / L) was significantly promote rabbit atrial ANP secretion (P <0.01), while the inhibition of atrial stroke volume (P <0.001) and atrial pulse pressure (P <0.001). 2.SR release the Ca 2 agonist caffeine (1.0 mmol / L) significantly inhibited ANP secretion, significantly increased atrial stroke volume and atrial pulse pressure, compared with the control loop has significant difference (P <0.001). 3. The adenylate cyclase direct activator blessing Division Colin (1.0μmol / L) significantly increased atrial stroke volume and the amount of cAMP escape, while a significant inhibition of ANP secretion, respectively, compared with the control loop has a significant difference (P < 0.01). 4.L-type Ca 2 channel blocker nifedipine (1.0μmol / L) and diltiazem (10.0μmol / L) could stimulate ANP secretion (P <0.05), but can not change inhibitory effect of caffeine on ANP secretion. Cardiac excitation - contraction coupling desensitizer 2,3 - butanedione monoxime (10.0 mmol / L) significantly inhibited atrial stroke volume and atrial pulse pressure significantly promote ANP secretion, respectively, compared with the control loop has a significant difference (P <0.001). These results suggest that: 1. Activate the SR membrane RyRs or membrane L-type Ca 2 channel intracellular Ca 2 concentration increased inhibitory regulatory role of ANP secretion. 2. Inhibition of extracellular Ca 2 influx can not change the inhibitory effect of caffeine on ANP secretion. Atrial mechanical activity to reduce the role of the ANP secretion increased might of Ca 2 and troponin binding force to the weakening.
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