![]() LaToya Colenberg |
School: Alcorn State University
Major: Biology Mentor: Dr. Sean Wilson Expected Graduation Date: May 2007 Organizations and Activities: • Honors Student OrganizationE-MAIL: LColnbrg2003@yahoo.com COMMENTS:
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ABSTRACT
An Analysis of Changes in Arterial Smooth Muscle Calcium Signaling with Aging
It is well known that with aging there are many physiological changes.
These changes include but are not limited to an increase in arterial stiffness,
arterial wall thickening and reduced vascular reactivity (Gros et al.,
2002 & Robert, 1999). According to the information published
in the 2004 American Heart Association statistics on heart disease and
stroke, more than a third of the 64 million individuals with cardiovascular
disease are over the age of 65 in the United States. The prevalence
of stroke, heart attack, and kidney failure increases with age, making
it important to understand the aging vasculature.
The aim of this project is to discover if excitation mediated
intracellular Ca2+ elevations are reduced with aging in mesenteric arterial
smooth muscle cells. The experimental models for this research
include murine mesenteric smooth muscle cells from mice that are 4-6 months
(mature) and 24-30 months (old). With these cells, agonists involved
in autocrine signaling, paracrine, neurotransmission (synaptic signaling),
and endocrine signaling were examined. These agonists include caffeine,
phenylephrine, adenosine triphosphate, arginine vasopressin, and fluflenamic
acid. Ca2+ was measured using fura2 AM. Quality of response was unchanged
with aging in cells excited with the agonists caffeine, phenylephrine,
and adenosine triphosphate. There was not a mature data set for arginine
vasopressin and flufenamic acid, therefore quality of response with aging
could not be determined. A trend was identified between PE and ATP
in which responsiveness decrease in the old for the former and increase
in the old for the latter. This suggests that with aging, the vasculature
may come more dependent on purinergic stimulation rather than adrenergic
stimulation.
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