{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,17]],"date-time":"2026-01-17T21:31:29Z","timestamp":1768685489772,"version":"3.49.0"},"reference-count":79,"publisher":"The Endocrine Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>We used SK-N-SH human neuroblastoma cells to test the hypothesis that adrenomedullin (ADM), a multifunctional neuropeptide, stimulates nitric oxide (NO) release by modulating intracellular free calcium concentration ([Ca2+]i) in neuron-like cells. We used a nitrite assay to demonstrate that ADM (10 pm to 100 nm) stimulated NO release from the cells, with a maximal response observed with 1 nm at 30 min. This response was blocked by 1 nm ADM22\u201352, an ADM receptor antagonist or 2 \u03bcm vinyl-l-NIO, a neuronal NO synthase inhibitor. In addition, 5 \u03bcm 1,2-bis(2-aminophenoxy)ethane-N,N,N\u2032,N\u2032-tetraacetic acid acetoxymethyl ester, an intracellular calcium chelator, eliminated the ADM-induced NO release. Similar results were observed when the cells were incubated in calcium-free medium or when l-type calcium channels were inhibited with 5 \u03bcm nifedipine or 10 \u03bcm nitrendipine. Depletion of calcium stores in the endoplasmic reticulum (ER) with 1 \u03bcm cyclopiazonic acid or 150 nm thapsigargin, or inhibition of ryanodine-sensitive receptors in the ER with 10 \u03bcm ryanodine attenuated the ADM-induced NO release. NO responses to ADM were mimicked by 1 mm dibutyryl cAMP, a cAMP analog, and were abrogated by 5 \u03bcm H-89, a protein kinase A inhibitor. Furthermore, Fluo-4 fluorescence-activated cell sorter analysis showed that ADM (1 nm) significantly increased [Ca2+]i at 30 min. This response was blocked by nifedipine (5 \u03bcm) or H-89 (5 \u03bcm) and was reduced by ryanodine (10 \u03bcm). These results suggest that ADM stimulates calcium influx through l-type calcium channels and ryanodine-sensitive calcium release from the ER, probably via cAMP-protein kinase A-dependent mechanisms. These elevations in [Ca2+]i cause activation of neuronal NO synthase and NO release.<\/jats:p>","DOI":"10.1210\/en.2004-1354","type":"journal-article","created":{"date-parts":[[2005,1,28]],"date-time":"2005-01-28T01:25:30Z","timestamp":1106875530000},"page":"2295-2305","source":"Crossref","is-referenced-by-count":23,"title":["Adrenomedullin Stimulates Nitric Oxide Release from SK-N-SH Human Neuroblastoma Cells by Modulating Intracellular Calcium Mobilization"],"prefix":"10.1210","volume":"146","author":[{"given":"Yong","family":"Xu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Teresa L.","family":"Krukoff","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"80","reference":[{"key":"2020071612410880300_R1","doi-asserted-by":"crossref","first-page":"553","DOI":"10.1006\/bbrc.1993.1451","article-title":"Adrenomedullin: a novel hypotensive peptide isolated from human 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