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Atrial natriuretic peptide (English: atrial natriuretic peptide), also known as ANP, natriuretic hormone, Lee urea, vasodilation factor. Belong natriuretic peptide (Natriuretic peptides), one member of the family, which includes cacl2 another brain natriuretic cacl2 peptide (brain natriuretic peptide) and C-type natriuretic peptide (C-type natriuretic peptide). Atrial natriuretic peptide is a polypeptide hold those (polypeptide) hormone, mainly by the atrium (atrial) the production, storage and secretion of myocardial cells, containing 28 amino acids at positions 7 and 23 by two cysteine residues acid (cysteine) residues are disulfide bonded to form a cyclic structure of a regulating factor [edit] 1. atria (atrial) stretch or increased blood volume stimulates the secretion of atrial natriuretic peptide increases blood volume of the heart or blood vessel wall when subjected to a large stretch stimulation, can cause atrial cacl2 myocytes release of atrial natriuretic peptide, causing powerful natriuretic and diuretic effect. 2. Limiting sodium and water intake or reducing venous return is able to reduce the release of atrial natriuretic peptide. cacl2 3.β-adrenergic receptor (β-adrenoceptors) secreted by the sympathetic stimulation of atrial natriuretic peptide. 4 wins decomposition of atrial natriuretic peptide peptide structure, the participation of the enzyme NEP (enzyme neutral endopeptidase). [2] Second, the main physiological function 1 in the kidney may act in ANPA kidneys, increase glomerular filtration rate (glomerular filtration rate), to promote the sodium ion exclusion, increase urine output, and inhibits renin (renin) cacl2 of secretion. Atrial natriuretic peptide action in the renal cortex cacl2 cell pellets (glomerulor), the inhibition of adrenal aldosterone synthesis, the reduction of renal sodium and water reabsorption (reabsorption). 2 The net effect of sodium atrial natriuretic peptide cardiovascular system in order to reduce the circulatory system of water, cacl2 sodium and fat content, thereby reducing blood pressure. Atrial natriuretic peptide can significantly reduce the degree of dehydration or blood loss after plasma antidiuretic hormone levels increased. By atrial natriuretic peptide cacl2 receptor guanylyl cyclase in the cell membrane to cyclic guanosine monophosphate in vascular smooth muscle cacl2 cells and exert its effect as a second messenger. [4] normal atrial natriuretic peptide synthesis in the atria, the heart failure patients with atrial pressure increased plasma atrial natriuretic peptide sodium increases. Injection of synthetic natriuretic peptide reduce pulmonary capillary pressure and arterial vascular resistance terminals, thereby increasing cardiac output. [5] 3. Increasing the free fatty acids in the form of adipose tissue (adipose tissue) released from the adipose tissue. Atrial natriuretic peptide in a blood vessel proliferation, such plasma glycerol fatty acid and non-steroidal (nonsterified cacl2 fatty acid) concentration increases. Activated adipocytes (adipocyte) A-type guanylate cyclase receptors on the cell membrane (NFR-A), increasing the content of intracellular cyclic guanosine monophosphate (cGMP), to promote hormone-sensitive lipase and lipid droplets package by protein A (perilipin A) phosphorylation. Phosphorylation through cGMP protein kinase (cGMP dependent protein kinase- ) performed. cacl2 Source: Wikipedia
amino acid derivative (Amino acid derivatives)
nucleotides (Nucleotide)
cancer mechanisms (Cancer mechanism)
cord (Spinal cacl2 cord)
Endocrinology (Endocrine)
histology (Histology)
Basic Biostatistics (Basic biostatistics)
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