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Mesenteric resistance arteries from control ( n = 43) and HU ( n = 44) rats were isolated, cannulated, and pressurized to 108 cm H<jats:sub>2<\/jats:sub>O for in vitro experimentation. Myogenic (intralumenal pressure ranging from 30 to 180 cm H<jats:sub>2<\/jats:sub>O), KCl (2\u2013100 mM), norepinephrine (NE, 10<jats:sup>\u22129<\/jats:sup>\u201310<jats:sup>\u22124<\/jats:sup>M) and caffeine (1\u201320 mM) induced vasoconstriction, as well as the temporal dynamics of vasoconstriction to NE, were determined. The active myogenic and passive pressure responses were unaltered by HU when pressures remained within physiological range. However, vasoconstrictor responses to KCl, NE, and caffeine were diminished by HU, as well as the rate of constriction to NE (C, 14.8 \u00b1 3.6 \u03bcm\/s vs. HU 7.6 \u00b1 1.8 \u03bcm\/s). Expression of sarcoplasmic reticulum Ca<jats:sup>2+<\/jats:sup>ATPase 2 and ryanodine 3 receptor mRNA was unaffected by HU, while ryanodine 2 receptor mRNA and protein expression were diminished in mesenteric arteries from HU rats. These data suggest that HU-induced and microgravity-associated orthostatic intolerance may be due, in part, to an attenuated vasoconstrictor responsiveness of mesenteric resistance arteries resulting from a diminished ryanodine 2 receptor Ca<jats:sup>2+<\/jats:sup>release mechanism.<\/jats:p>","DOI":"10.1152\/ajpregu.00084.2008","type":"journal-article","created":{"date-parts":[[2008,3,20]],"date-time":"2008-03-20T00:46:53Z","timestamp":1205974013000},"page":"R1577-R1585","source":"Crossref","is-referenced-by-count":27,"title":["Simulated microgravity alters rat mesenteric artery vasoconstrictor dynamics through an intracellular Ca<sup>2+<\/sup>release mechanism"],"prefix":"10.1152","volume":"294","author":[{"given":"Patrick N.","family":"Colleran","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bradley J.","family":"Behnke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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