Microinjections of subpicomolar amounts of NPY(13–36) into the nucleus tractus solitarius of the rat counteract the vasodepressor responses of NPY(1–36) and of a NPY Y1 receptor agonist

Yang, Shao‐Nian; Narváez, JoséA.; Bjelke, Börje; Agnati, Luigi F.; Fuxé, Kjell

doi:10.1016/0006-8993(93)90307-9

Cited by 38 publications

(19 citation statements)

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“…In conclusion, NPY acts in the left DVC through Y1 receptor subtype to stimulate bile acid-independent and bicarbonatedependent bile secretion through vagus nerve. Because counteraction of NPY between Y1 and Y2 receptors in the brain has been reported on regulation of the cardiovascular system, 33 it is of interest to further investigate an interaction between Y1 and Y2 receptors on central regulation of bile secretion.…”

Section: Discussionmentioning

confidence: 99%

“…Similar findings have been reported in regard to central regulation of the cardiovascular system by NPY. 33 The left DVC represents a specific site of action for [Leu 31 , Pro 34 ]NPY to elicit central stimulation of bile secretion, because the peptide was ineffective when delivered to sites close to, but outside of, the left DVC and also delivered to the right DVC. In addition, the complete suppression of the bile response to [Leu 31 , Pro 34 ]NPY microinjected to the left DVC by hepatic branch vagotomy suggests that the peptide may primarily or secondarily activate preganglionic neurons contributing to vagal innervation of the liver.…”

Section: Discussionmentioning

confidence: 99%

“…[11][12][13] There are still few reports that have revealed the specific receptor subtypes of NPY or PYY in the central nervous system for physiological regulations. 33,41,[43][44][45] In this study, the specific receptor subtype and specific site in the brain to elicit the stimulation of bile secretion have been characterized. In conclusion, NPY acts in the left DVC through Y1 receptor subtype to stimulate bile acid-independent and bicarbonatedependent bile secretion through vagus nerve.…”

Section: Discussionmentioning

confidence: 99%

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Neuropeptide Y stimulates bile secretion via Y1 receptor in the left dorsal vagal complex in rats

et al. 1998

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Neuropeptide Y (NPY), a 36-amino acid peptide, was first isolated from porcine brain and is the member of a family of structurally related peptides that includes peptide YY (PYY) and pancreatic polypeptide. 1,2 NPY is localized in the central nervous system, as well as the peripheral nervous system. 3 In the brain, NPY immunoreactive nerve fibers and terminals and NPY receptors are localized in the paraventricular nucleus of the hypothalamus and the dorsal vagal complex (DVC), including the dorsal motor nucleus of the vagus (DMN) and the nucleus of the solitary tract (NST), 4-6 which are important sites for the autonomic nervous regulation of gastrointestinal function. 7 Central administration of NPY affects several physiological functions. 8 With respect to the gastrointestinal system, central injection of NPY modifies gastric and pancreatic secretion in animal models. 9,10 Recently, Farouk et al. observed that intracerebroventricular injection of NPY stimulates bile acid-independent bile secretion through vagal pathways in rats and dogs, 11 and we have confirmed this effect by intracisternal injection of NPY in rats. 12 Moreover, we have found very recently that the left vagal complex is the specific brain site of action for NPY to induce bile stimulation. 13 It is now generally accepted on the basis of functional and ligand binding studies that NPY binds to and activates six different receptor subtypes, designated Y1, 2, 3, 4 (PP receptor), 5, and 6. 14-18 Y1 receptors exhibit similar affinity for NPY, PYY and [Leu 31 , Pro 34 ]NPY analog, and poor affinity for the C-terminal fragments of NPY/PYY, while Y2 receptors display affinity for NPY/PYY and C-terminal fragments of the peptides but not to the Y1 and 3 selective agonist, [Leu 31 , Pro 34 ]NPY. 14,19-23 PYY has been suggested to have high affinity for Y1 and 2 receptors, and less affinity for Y3 receptors. 14,20,24 Although Y1 receptors were suggested as postsynaptic and Y2 receptors as presynaptic, 25 later studies demonstrated that Y2 receptors are also localized presynaptically. 26 Both Y1 and Y2 receptors are localized in the DVC, 27 which has been identified as the specific brain site for NPY to stimulate bile secretion. 13 Peripherally released PYY binds to the DVC, 28 and microinjection of PYY into the DVC modified gastrointestinal functions. 29,30 The identity of the receptor subtype for NPY in the medulla that mediates the stimulation of bile acid-independent and bicarbonate-dependent bile secretion remains to be established. The present studies were performed to address this question by examining the effect of microinjection of NPY and NPY analogs into the DVC on bile secretion in rats. MATERIALS AND METHODS Animals.Male Wistar rats weighing 270 to 330 g (Charles River Japan Inc., Yokohama, Japan) were housed in group cages under conditions of controlled temperature (22-24°C) and illumination (12-hour light cycle starting at 8 AM) for at least 7 days before the experiments. Animals were maintained on laboratory chow and tap water. Experiments w...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Neuropeptide Y stimulates bile secretion via Y1 receptor in the left dorsal vagal complex in rats

et al. 1998

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“…NPY microinjected into the DVC modulates gastrointestinal [92,97,100] and cardiovascular [96] functions through the vagus. Although PYY was more potent than NPY to stimulate gastric acid secretion when microinjected into the DVC [92], the suggested PYY preferring receptor in this area [44,92] has not been cloned.…”

Section: Summary and Perspectivesmentioning

confidence: 99%

Central and peripheral regulation of gastric acid secretion by peptide YY

Yang

2002

Peptides

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Peptide YY (PYY) released postprandially from the ileum and colon displays a potent inhibition of cephalic and gastric phases of gastric acid secretion through both central and peripheral mechanisms. To modulate vagal regulation of gastric functions, circulating PYY enters the brain through the area postrema and the nucleus of the solitary tract, where it exerts a stimulatory action through PYY-preferring Y1-like receptors, and an inhibitory action through Y2 receptors. In the gastric mucosa, PYY binds to Y1 receptors in the enterochromaffin-like cells to inhibit gastrin-stimulated histamine release and calcium signaling via a pertussis toxin-sensitive pathway.

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“…Among the six identified NPY receptor subtypes, Y1R, Y2R and Y5R are distributed widely in the cardiovascular system [8], with Y1R mediating a vasoconstrictor response, Y2R mediating the decrease of HR and Y5R facilitating cardiac hypertrophy [16][17][18]. And microinjection of Y1R agonist into NTS led to vasodepressor and bradycardic responses [19]. Moreover, previous studies have demonstrated that central and intravenous injections of NPY immediately affect blood pressure and baroreflex control of HR [20,21].…”

Section: Introductionmentioning

confidence: 99%

Long-term Neuropeptide Y Administration in the Periphery Induces Abnormal Baroreflex Sensitivity and Obesity in Rats

Xie

Zhang

et al. 2012

Cell Physiol Biochem

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Neuropeptide Y (NPY) is an important neuronal element involved in cardiovascular regulation. Since elevated plasma levels of NPY have been observed in numerous pathological situations, this study aimed to determine whether long-term elevated plasma concentrations of NPY could result in aberrant baroreflex sensitivity. Mini-osmotic pump containing NPY (85 µg per 30 days) was subcutaneously implanted between scapulae in male rats for 4 months. The rats treated with NPY showed the following characters compared with control group: (1) attenuated heart rate responding to the increases in mean arterial blood pressure (MABP) induced by phenylephrine, but enhanced heart rate responding to the decreases in MABP induced by sodium nitroprusside; (2) decreased protein levels of substance P (SP) and GluR2, while increased the expression of γ-aminobutyric acid A receptor (GABA_AR) in brainstem; (3) abdominal obesity indicated by increased body weight and accumulated fat mass in peritoneal cavity; (4) significant increases in total cholesterol, triglycerides, and low density lipoprotein levels in the periphery. These findings indicate that long-term NPY administration in the periphery leads to abnormal baroreflex sensitivity due, at least in part, to the down-regulated expression of SP/GluR2 and elevated expression of GABA_AR in both protein and RNA levels, which indicate the alternations in glutamate function and GABA action in the nucleus tractus solitarii in NPY-treated rats. Furthermore, long-term NPY administration results in abdominal obesity and dyslipidemia.

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Microinjections of subpicomolar amounts of NPY(13–36) into the nucleus tractus solitarius of the rat counteract the vasodepressor responses of NPY(1–36) and of a NPY Y1 receptor agonist

Cited by 38 publications

References 24 publications

Neuropeptide Y stimulates bile secretion via Y1 receptor in the left dorsal vagal complex in rats

Neuropeptide Y stimulates bile secretion via Y1 receptor in the left dorsal vagal complex in rats

Central and peripheral regulation of gastric acid secretion by peptide YY

Long-term Neuropeptide Y Administration in the Periphery Induces Abnormal Baroreflex Sensitivity and Obesity in Rats

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