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Strathprints serves world leading Open Access research by the University of Strathclyde, including research by the Strathclyde Institute of Pharmacy and Biomedical Sciences (SIPBS), where research centres such as the Industrial Biotechnology Innovation Centre (IBioIC), the Cancer Research UK Formulation Unit, SeaBioTech and the Centre for Biophotonics are based.

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Aging and Ca2+ signaling in murine mesenteric arterial myocytes

Angermann, J.E. and Mcallister, C. and del Corsso, C. and Gurney, A.M. and Wilson, S.M. (2004) Aging and Ca2+ signaling in murine mesenteric arterial myocytes. FASEB Journal, 18 (4-5). A703-A703. ISSN 0892-6638

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Abstract

Vascular reactivity may be reduced in old individuals and the (Ca2+)i is important to smooth muscle contractility. Experiments were therefore performed to determine if Ca2+ signaling is altered in mesenteric arterial smooth muscle cells (MASMCs) from 5-6 (young (Y)) and 29-30 month (old (O)) C57bl/6 mice. (Ca2+)i was measured using fura-2 imaging of individual MASMCs. The basal (Ca2+)i of MASMCs from Y (36+/-6 nM n=48) and O (51+/-4 nM n=101) were not significantly different. Total cytosolic Ca2+ (CaT) released by 30s 10 mM caffeine (CAF) or 10 ?M phenylephrine (PE) exposures were estimated by integrating the Ca2+ transient. CaT was proportional to peak (Ca2+)i in both Y and O, but the slope of CaT to peak (Ca2+)i was 2-fold greater in Y for both CAF and PE. The (Ca2+)i increase above basal following SR Ca2+ depletion in Y 66+/-8 nM n=19 was greater than in O 18+/-3 nM n=34. Following store depletion the (Ca2+)i clearance rate (Mclear) with extracellular Ca2+ removal in Y 0.0073+/-0.0009 s-1 n=19 was slower than in O 0.0161+/-0.0008 s-1 n=34. The (Ca2+)i cleared from the cytosol (Mclear*CaT) was proportional to the peak (Ca2+)i and was the same between Y and O for CAF, while that due to PE was greater in O. Aging modifies agonist-induced cytosolic Ca2+ increases and our data imply that altered cytosolic Ca2+ clearance mechanisms are an important component to the Ca2+ signaling impairments. NIH P20 RR15581 from NCRR, AG20400, HL10476, AI55462.