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This study tested whether altered SMC Ca<jats:sup>2+<\/jats:sup> signals to sympathetic (NE) and sensory (CGRP) neurotransmitters underlie aging\u2010related deficits in vasodilation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>MAs from young and old mice were pressurized and loaded with Fluo\u20104 dye for confocal measurement of SMC Ca<jats:sup>2+<\/jats:sup> sparks and waves. Endothelial denudation resolved the influence of ECs. SMCs were immunolabeled for RyR isoforms and compared with transcript levels for RyRs and CGRP receptor components.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>SMCs from young vs old mice exhibited more spontaneous Ca<jats:sup>2+<\/jats:sup> spark sites with no difference in Ca<jats:sup>2+<\/jats:sup> waves. NE reduced spark sites and increased waves for both groups; addition of CGRP restored sparks and reduced waves only for young mice. Endothelial denudation attenuated Ca<jats:sup>2+<\/jats:sup> responses to CGRP for young but not old mice, which were already attenuated, suggesting a diminished role for ECs with aging. CGRP receptor expression was similar between ages with increased serum CGRP in old mice, where RyR1 expression was replaced by RyR3.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>With aging, we suggest that altered RyR expression in SMCs contributes to impaired ability of sensory neurotransmission to restore Ca<jats:sup>2+<\/jats:sup> signaling underlying vasomotor control during sympathetic activation.<\/jats:p><\/jats:sec>","DOI":"10.1111\/micc.12607","type":"journal-article","created":{"date-parts":[[2020,1,29]],"date-time":"2020-01-29T07:13:16Z","timestamp":1580281996000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Aging alters spontaneous and neurotransmitter\u2010mediated Ca<sup>2+<\/sup> signaling in smooth muscle cells of mouse mesenteric 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