Cellular and receptor mechanisms of impairment of myocardium and aorta contractilityat Alzheimers disease model

Introduction. Recent studies certify the existence of link
between Alzheimers disease and cardiovascular pathology,
however the mechanisms of this phenomenon is unclear. Here
we studied the influence of Alzheimers β-amyloid peptide
(βAP) on the contractility of rat myocardium and aorta.
Material and methods. Contractility of myocardium ventricle
strips and transverse fragments of abdominal aorta was
measured at Power Lab setup using conventional myographic
technique. Contractile responses of aorta strips were evoked
by application of receptor agonists, contractile responses of
myocardium - by electrical stimulation. Contractile responses
of aorta strips after application of carbachol (10-6-10-4 М),
histamine (10-6-10-4 М), norepinephrine (10-5-10-3 М) and
ATP (10-6-10-4 М) were measured.
Results and discussion. We found the impairment of
carbachol- and histamine-induced contractility of aorta,
appearing as perverse contractile reactions (relaxation instead
of contraction) under the action of βAP (10-6 М). Next, we
found βAP-induced impairments of ventricle myocardium
contractility, appearing as decrease of relaxation phase
duration and increase of relaxation speed (positive lusitropic
effect). Also, own positive lusitropic effect of norepinephrine
was absent in presence of βAP (10-6М).
Thus, βAP(25-35) significantly impairs the contractility
of rat myocardium and aorta, as well as processes of its
regulation. Obtained data significantly broad our understanding
of mechanisms of Alzheimers disease pathogenesis and
pathophysiology of cardiovascular system.

β-amyloid peptide, Alzheimer's disease, myocardium, aorta, contractility, lusitropic effect