Popular Conclusion:
1. Diastolic dysfunction (a decrease in peak ventricular filling after systole or a prolonged relaxation of contracted muscle) results from in part a downregulation of the sarcoplasmic reticulum's (SR) calcium ATPase that sequesters cytosolic calcium via the hydrolysis of ATP. Exercise training of sedentary old mammals produces a faster relaxation and an upregulation of the SR calcium ATPase.
2.Phosphorylation of chromosomal proteins is a function of age and its modulation by calcium.
3...alterations in calcium homeostasis underlie some of the cholinergic and behavioral deficits that accompany senescence.
4.The decline in synaptosomal calcium uptake may alter neuronal metabolism which leads to the reduction in mental function that accompanies aging.
5.The effects of decreased ion movement may be further aggravated by an age-related decline in other calcium-dependent processes. Depression of some of these calcium-dependent functions appears physiologically significant, since increasing calcium availability ameliorates age-related deficits in neurotransmission and behavior.
6.Indomethacin and dexamethasone inhibited calcium release from untreated 5- and 75-day-old calvaria suggesting that prostaglandin biosynthesis was involved in the calcium release process.
7.Parathyroid hormone-sensitive Na+/Ca2+ exchange activity was markedly blunted in cells from senescent rats. Parathyroid hormone-stimulated adenylate cyclase was also decreased in aging. In contrast, forskolin-stimulated Na(+)-dependent Ca2+ efflux and adenylate cyclase did not change with senescence. ... the age related blunting in responses of renal cells to PTH was due, at least in part, to the elevated serum iPTH level in old rats.
8....the age-dependent decline in T lymphocyte function is largely the result of the accumulation of memory T lymphocytes with over-active plasma membrane calcium pumps.
9.... the plasma calcium level in response to calcitonin is decreased in rats uring aging. The reduction of the hypocalcemic effect of calcitonin in old female rats at least was estradiol-independent.
10.It is believed that pineal calcification may be age-associated and that the well-demonstrated age-related decline in melatonin biosynthesis may be an expression of an alteration in calcium homeostasis in the pinealocyte.
11. The combined deficiency in calcium and vitamin D stimulates the secretion of parathyroid hormone which tends to normalize serum calcium levels and causes the bone disorders of senile osteoporosis.
"...Aging is associated both with calcium deficiency, due to low
dietary intake and decreased intestinal absorption, and with vitamin D
deficiency, secondary to depletion of body stores resulting from inadequate
exposure to sunlight. Hepatic hydroxylation of vitamin D remains normal
in elderly individuals. Renal hydroxylation of vitamin D, previously believed
to decrease with advancing age, also remains virtually normal even when
creatinine clearance declines, as is very often the case in elderly patients.
The combined deficiency in calcium and vitamin D stimulates the secretion
of parathyroid hormone which tends to normalize serum calcium levels and
causes the bone disorders of senile osteoporosis." (
Rev Rhum Ed Fr 1993 Jun;60(6):445-9: Benhamou CL; Tourliere
D; Asselin F
[Influence of aging on vitamin D metabolism].)
"...Many aspects of calcium homeostasis change with aging. Numerous
calcium compartments complicate studies of altered calcium regulation.
However, age-related decreases in calcium permeation acros membranes and
mobilization from organelles may be a common fundamental change. Deficits
in ion movements appear to lead to altered coupling of calcium-dependent
biochemical and neurophysiological processes and may lead to pathological
and behavioral changes. The calcium-associated changes during aging probably
do not occur with equal intensity in all cell types or in different parts
of the same cell. Thus, cells or compartments with a high proportion of
calcium activated processes would be more sensitive to diminished calcium
availability. These age-related changes may predispose the brain to the
development of age-related neurological disorders. The effects of decreased
ion movement may be further aggravated by an age-related decline in other
calcium-dependent processes. Depression of some of these calcium-dependent
functions appears physiologically significant, since increasing calcium
availability ameliorates age-related deficits in neurotransmission and
behavior." (
Neurobiol Aging 1987 Jul-Aug;8(4):329-43: Gibson GE; Peterson
C
Calcium and the aging nervous system.)
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