neuropeptide-y and alpha-methyltyrosine-methyl-ester

To assess the effects of long-term pressure overload on sympathetic presynaptic components in the left ventricle, young adult male rats were subjected to surgical constriction of the suprarenal abdominal aorta. At 4 and 8 wk postsurgery, but not at 1 wk, left ventricular sympathetic activity, measured by the net fractional norepinephrine (NE) decrease after alpha-methyl-p-tyrosine methyl ester administration, was elevated in the aortic-banded rats. However, left ventricular NE was reduced only at 8 wk. Scatchard analysis of saturation binding of [3H]nisoxetine, a specific ligand for NE uptake sites, determined that left ventricular NE transporter sites were also reduced at 8 wk, suggesting a relationship between a reduced number of uptake sites and loss of NE stores. In contrast, aortic constriction did not reduce neuropeptide Y (NPY), tyrosine hydroxylase, dopamine beta-hydroxylase, nervegrowth factor, and low-affinity nerve growth factor receptors at any time point. Thus long-term pressure overload can cause a selective reduction in ventricular NE stores without a reduction in NPY, a colocalized sympathetic neurotransmitter.

Topics: Animals; Aorta, Abdominal; Binding Sites; Carrier Proteins; Fluoxetine; Hypertension; Ligation; Male; Methyltyrosines; Myocardium; Neuropeptide Y; Norepinephrine; Norepinephrine Plasma Membrane Transport Proteins; Presynaptic Terminals; Rats; Rats, Sprague-Dawley; Sympathetic Nervous System; Symporters; Time Factors; Ventricular Function, Left