| pubmed-article:2526225 | pubmed:abstractText | Atrial natriuretic peptide (ANP) is a circulating hormone produced by atrial muscle cells which acts upon renal vascular smooth muscle to raise glomerular filtration pressure, thereby increasing salt and water excretion and reducing blood pressure [2, 5, 8]. As in other peptide hormone-secreting cells, ANP is packaged and stored in dense Golgi-derived secretory granules [4-6]. These atrial specific granules [6] occur predominantly in large clusters deep in the myocyte's interior, associated with Golgi cisternae in myofibril-free cytoplasm at the nuclear poles [5, 6]. Smaller clusters and individual granules are distributed beneath the sarcolemma and between myofibrils [6, 10]. Expansion of the blood volume raises the level of circulating ANP [7], a response mediated by mechanical stretch of the atrial wall [1, 3, 9]. The mechanism by which cell stretch induces release of ANP from atrial myocytes is, however, unknown. We show here that one component of this unusual secretory mechanism involves a sudden centrifugal movement of atrial specific granules toward the cell surface. | lld:pubmed |
