Abstract
To evaluate the sympathetic innervation of the female diabetic heart, resting heart rate and sympathetic tone were assessed in vivo, and effect of tyramine on spontaneous beating rate, norepinephrine atrial concentrations, uptake, and release were determined in vitro in streptozotocin- (STZ-) treated rats and respective controls aged 3 months to 2 years. Resting bradycardia, decreased sympathetic tone, deceleration of spontaneous beating rate, and slightly declining carrier-mediated, but preserved exocytotic norepinephrine release from the atria were found in younger diabetic rats while the reactivity of the right atria to tyramine was not affected with age and disease duration. Diabetic two-year-old animals displayed symptoms of partial spontaneous recovery including normoglycemia, increased plasma insulin concentrations, fully recovered sympathetic tone, but putative change, in releasable norepinephrine tissue stores. Our data suggested that female diabetic heart exposed to long-lasting diabetic conditions seems to be more resistant to alteration in sympathetic innervation than the male one.
Highlights
Cardiovascular autonomic neuropathy (CAN) represents the most clinically important form of diabetic autonomic neuropathy
The rats were used for further experiments at 1, 2, 4, and 22 months after the induction of diabetes or vehicle administration and designated STZ1, STZ2, STZ4, and STZ22 and CONT1, CONT2, CONT4, and CONT22, respectively
Prior to STZ administration, there were no significant differences in the body weights, blood glucose levels, and plasma insulin concentrations between the animals subjected to STZ or vehicle injection
Summary
Cardiovascular autonomic neuropathy (CAN) represents the most clinically important form of diabetic autonomic neuropathy. Autonomic dysfunction manifested by intracardiac sympathetic imbalance with predisposition to arrhythmias has been proposed as a cause of the increased incidence of sudden cardiac death in diabetic patients [2]. Multiple data indicated an abnormal activity of the sympathetic nervous system in both diabetic human patients and animals with various experimental models of diabetes, their results are contradictory showing decrease, increase, or no change in plasma catecholamine levels, cardiac norepinephrine content, release, or uptake [3, 4]. The regulation of norepinephrine tissue stores is very complex involving control of expression and/or activity of the key synthesizing enzyme tyrosine hydroxylase, catecholamine exocytotic and nonexocytotic release, its uptake, and metabolism [5,6,7]. The inconsistent results of studies dealing with norepinephrine turnover in the tissues of streptozotocin- (STZ-) diabetic animals were attributed mostly to the duration and severity of diabetes [8]
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