Characterization of vascular postsynaptic NPY receptor function and regulation and differential sensitivity of Y1 and Y2 receptor function to changes in extracellular calcium availability and prior in vitro peptide exposure
| Autor: | Richard E. Tessel, X. Dong, Michael B. Doughty, D.W. Miller, G. A. Misse |
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| Rok vydání: | 1993 |
| Předmět: |
Male
Agonist medicine.medical_specialty Indanidine medicine.drug_class In Vitro Techniques Clonidine Muscle Smooth Vascular Rats Sprague-Dawley Norepinephrine (medication) Cellular and Molecular Neuroscience chemistry.chemical_compound Endocrinology Nifedipine Postsynaptic potential Internal medicine mental disorders medicine Animals Vasoconstrictor Agents Neuropeptide Y Receptor Endocrine and Autonomic Systems Chemistry General Medicine 3-Pyridinecarboxylic acid 1 4-dihydro-2 6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl ester Neuropeptide Y receptor Peptide Fragments humanities Rats Receptors Neuropeptide Y Neurology Synapses Calcium medicine.symptom Peptides Adrenergic alpha-Agonists Vasoconstriction medicine.drug |
| Zdroj: | Neuropeptides. 25:289-298 |
| ISSN: | 0143-4179 |
| DOI: | 10.1016/0143-4179(93)90046-d |
| Popis: | Effects of calcium-free buffer, nifedipine, or prior cumulative neuropeptide Y (NPY) receptor agonist concentration exposure on vasoconstrictive responsiveness to the agonists were assessed in norepinephrine (NE)-conditioned isolated rat femoral artery rings. Calcium-free buffer and nifedipine partially inhibited responsiveness to initial NPY exposure; residual responsiveness to NPY re-exposure was unaffected. In contrast, these treatments markedly inhibited responsiveness to the Y 2 agonist NPY 13–36 , the calcium channel agonist BAY K 8644 (BAY) and the partial alpha 1 adrenoceptor agonist indanidine but did not alter that to the Y 1 agonist [Leu 31 , Pro 34 ]NPY. Responsiveness to NPY and NPY 13–36 but not to BAY or indanidine was markedly reduced 120 min following conditioning regardless of prior ring exposure to the same peptide; only prior exposure reduced responsiveness to [Leu 31 , Pro 34 ]NPY. Responsiveness changes to NPY at various times or after various numbers of NE and/or NPY exposures indicated that pre-exposure and time-related responsiveness reductions were discriminable and temporally unrelated to conditioning. Postsynaptic vascular Y 2 receptor activation therefore accounts for the known sensitivity of NPY-induced pressor and vasoconstrictive actions to nifedipine. The ‘time-dependent’ loss of Y 2 receptor function may also explain prior failures to observe postsynaptic arterial Y 2 receptors in vitro. |
| Databáze: | OpenAIRE |
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