Neuropeptide Y is a cotransmitter with norepinephrine in guinea pig inferior mesenteric vein
Department of Physiology and Cell Biology, University of Nevada, Reno, Reno, Nevada, United StatesPeptides (Impact Factor: 2.62). 07/2000; 21(6):835-843. DOI: 10.1016/S0196-9781(00)00217-5
Neuropeptide Y (NPY) is a cotransmitter with noradrenaline in guinea pig inferior mesenteric vein. Tyrosine hydroxylase-like immunoreactivity and NPY-like immunoreactivity were colocalized in a dense network of fibers within the adventitial layer of guinea-pig inferior mesenteric vein. Vasoconstrictor responses to electrical field stimulation (0.2–64 Hz, 0.1 ms, 12 V, for 10 s) appear to be mediated primarily by norepinephrine at 0.2 to 4 Hz and by NPY at 8 to 64 Hz. NPY Y1 receptors mediate the contractile responses to both endogenous and exogenous NPY. Norepinephrine and NPY are involved in neuromuscular transmission in guinea pig mesenteric vein suggesting that the sympathetic nervous system requires the coordinated action of norepinephrine and NPY to serve capacitance.
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ABSTRACT: An information database was created for characterization of the interaction of norepinephrine with other families of regulatory peptides on the basis of numerous literature data. This database took into consideration the following experimental parameters: doses and the method of treatment with a substance, organism species, organ-tissue systems, the character of the effects, and receptor mechanisms. A generalized scheme of inductive interactions of norepinephrine with a peptide pool was created on the basis of this database. We analyzed the possible influences of norepinephrine-induced cascade processes mediated by the regulatory peptides on the various physiological parameters of the body, including levels of depression and anxiety, memory, and blood pressure.
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ABSTRACT: Neuropeptide Y (NPY) and noradrenaline (NA) are co-transmitters at many sympathetic synapses, but it is not yet clear if their release is independently regulated. To address this question, we quantified the electrically evoked release of these co-transmitters from perivascular nerve terminals to the mesenteric circulation in control and drug-treated rats. 6-Hydroxydopamine reduced the tissue content and the electrically evoked release of ir-NPY and NA as well as the rise in perfusion pressure. A 0.001mg/kg reserpine reduced the content of ir-NPY and NA, but did not modify their release nor altered the rise in perfusion pressure elicited by the electrical stimuli. However, 0.1mg/kg reserpine reduced both the content and release of NA but decreased only the content but not the release of ir-NPY; the rise in perfusion pressure was halved. Clonidine did not affect the release of ir-NPY while it lowered the outflow of NA, not altering the rise in perfusion pressure elicited by the electrical stimuli. Yohimbine, did not modify the release of ir-NPY but increased the NA outflow, it antagonized the clonidine effect. Therefore, presynaptic α2-adrenoceptors modulate the release of NA but not NPY, implying separate regulatory mechanisms.
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