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Vasoactive peptides neuropeptide

Hosli, L., Hosli, E., Kaeser, H. Lefkovits, M. (1992) Colocalization of receptors for vasoactive peptides on astrocytes of cultured rat spinal cord and brain stem electrophysiological effects of atrial and brain natriuretic peptide, neuropeptide Y and bradykinin. Neurosci. Lett. 148, 114-116. [Pg.82]

VASOACTIVE INTESTINAL PEPTIDE, SUBSTANCE P, CALCITONIN GENE-RELATED PEPTIDE, NEUROPEPTIDE Y... [Pg.170]

Melatonin [73-31-4] C 2H N202 (31) has marked effects on circadian rhythm (11). Novel ligands for melatonin receptors such as (32) (12), C2yH2gN202, have affinities in the range of 10 Af, and have potential use as therapeutic agents in the treatment of the sleep disorders associated with jet lag. Such agents may also be usehil in the treatment of seasonal affective disorder (SAD), the depression associated with the winter months. Histamine (see Histamine and histamine antagonists), adenosine (see Nucleic acids), and neuropeptides such as corticotropin-like intermediate lobe peptide (CLIP) and vasoactive intestinal polypeptide (VIP) have also been reported to have sedative—hypnotic activities (7). [Pg.534]

Peptides are used by most tissues for cell-to-cell communication. As noted in Chapters 6 and 21, they play important roles in the autonomic and central nervous systems. Several peptides exert important direct effects on vascular and other smooth muscles. These peptides include vasoconstrictors (angiotensin II, vasopressin, endothelins, neuropeptide Y, and urotensin) and vasodilators (bradykinin and related kinins, natriuretic peptides, vasoactive intestinal peptide, substance P, neurotensin, calcitonin gene-related peptide, and adrenomedullin). This chapter focuses on the smooth muscle actions of the peptides. [Pg.373]

Finally, peptides such as galanin, leptin, neuropeptide Y, vasoactive intestinal polypeptide (VIP), and pituitary adenylate cyclase-activating polypeptide (PACAP) have been identified in various areas of the CNS. These and other peptides may affect various CNS functions, either by acting directly as neurotransmitters or by acting as cotransmitters moderating the effects of other neurotransmitters.7 24,27,34... [Pg.59]

The heterogeneity of dopaminergic neurons may also be judged by the fact that the cotransmitter systems involving dopamine and peptides are varied in the central nervous system. For example, in the corpus striatum, in addition to dopamine, acetylcholine, y-aminobutyric acid, serotonin, glutamate, and aspartate, one also finds peptides such as enkephalin, substance P, somatostatin, neuropeptide Y, cholecystokinin, neurotensin, and vasoactive intestinal peptide. Although many neuroleptics block dopamine receptors, they may have selective effects on the peptides and other parts of the brain. A few examples will be cited. [Pg.176]

Macrophages/DCs and lymphocytes express a variety of adrenergic receptors. Increased concenh ations of NE or dopamine can modulate T cells polarization toward Th2 profile, stimulate IL-4, IL-5, and IL-13 secretion (Kohm and Sanders, 2001). The same Th2 polarization can be induced by histamine, serotonin, neuropeptides such as substance P, vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating polypeptide, calcitonin gene-related peptide, a-melanocyte-stimulating hormone, and leptin (Steinman, 2004). [Pg.148]

The effects of both ACh and NE can be enhanced by the CO-localization of agents such as the neuropeptides vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY). For example, VIP can increase ACh induced salivary secretion (Lundberg and Hokfelt, 1983) and NPY can enhance the vasoconstrictive effects of NE (Wahlestedt et al., 1985). In theory, agents mimicking or blocking the effects of these neuropeptides should expand the opportunities for conh ol of various disease conditions such as Sjogren s disease and hypertension. How ever, significant advances in such therapy are yet to be realized. [Pg.549]

Maggi. C. A. et al. (1995) Neuropeptides as regulators of airway function Vasoactive intestinal peptide and the tachykinins. Physiol. Rev.. 75.277-322. Alexander. S.P.H. et al (1998) Receptors and ion channel nomenclature supplement. Ninth Edition. Trends Pharmacol. Sci., Suppl.. 19.1 -98. [Pg.288]

Fig. 15. Hypothetical model of how initiators and modulators that affect insulin release may reach A-, B- and D-cells. The first target of arterial blood containing nutrients, hormones, peptides and drugs is the B-cell. From there, via an intraislet portal vein system, blood which now also contains released insulin flows to the mantle where A- and D-cells are localized and from there enters the circulation. Nerves derived from the autonomous nervous system which contain neurotransmitters (acetylcholine, noradrenaline) and neuropeptides (including vasoactive intestinal peptide (VIP), gastrin-releasing peptide (GRP), galanin) are connected to islet cells. Glucagon (A-cells) and somatostatin (D-cells) reach other endocrine cells in the islet in a paracrine manner. The B-cell may also be the target of previously released insulin via a short loop. Fig. 15. Hypothetical model of how initiators and modulators that affect insulin release may reach A-, B- and D-cells. The first target of arterial blood containing nutrients, hormones, peptides and drugs is the B-cell. From there, via an intraislet portal vein system, blood which now also contains released insulin flows to the mantle where A- and D-cells are localized and from there enters the circulation. Nerves derived from the autonomous nervous system which contain neurotransmitters (acetylcholine, noradrenaline) and neuropeptides (including vasoactive intestinal peptide (VIP), gastrin-releasing peptide (GRP), galanin) are connected to islet cells. Glucagon (A-cells) and somatostatin (D-cells) reach other endocrine cells in the islet in a paracrine manner. The B-cell may also be the target of previously released insulin via a short loop.

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See also in sourсe #XX -- [ Pg.168 , Pg.170 ]




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