Adrenomedullin in the rostral ventrolateral medulla increases arterial pressure and heart rate: roles of glutamate and nitric oxide
| Autor: | Yong Xu, Teresa L. Krukoff |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Male
medicine.medical_specialty Indazoles Microinjections Receptors Peptide Physiology medicine.drug_class Glutamic Acid Blood Pressure Nitric Oxide Synthase Type I Nitric Oxide Receptors N-Methyl-D-Aspartate Synaptic Transmission Article Rats Sprague-Dawley Adrenomedullin chemistry.chemical_compound Heart Rate Physiology (medical) Internal medicine medicine Animals Glutamate receptor antagonist Enzyme Inhibitors Receptors Adrenomedullin 6-Cyano-7-nitroquinoxaline-2 3-dione Medulla Oblongata Chemistry Glutamate receptor Rostral ventrolateral medulla Receptor antagonist Peptide Fragments Stimulation Chemical Rats Dizocilpine Endocrinology NMDA receptor Dizocilpine Maleate Nitric Oxide Synthase Peptides Soluble guanylyl cyclase Excitatory Amino Acid Antagonists medicine.drug |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 287:R729-R734 |
| ISSN: | 1522-1490 0363-6119 |
| DOI: | 10.1152/ajpregu.00188.2004 |
| Popis: | This study was done to investigate the effects of microinjections of adrenomedullin (ADM), a vasoactive neuropeptide, in the rostral ventrolateral medulla (RVLM) on mean arterial pressure (MAP) and heart rate (HR) in urethane-anesthetized rats, and to assess the potential roles of glutamate and nitric oxide (NO) in these effects. Unilateral injections of ADM (0.01 or 0.1 pmol) into the RVLM significantly increased MAP and HR in a dose-dependent manner, whereas ADM at 0.001 pmol was ineffective. Microinjections of ADM (0.01 pmol) outside the RVLM had no effects on MAP or HR. Coinjections of a putative ADM receptor antagonist, ADM22–52 (0.01 pmol), abolished the increases in MAP and HR evoked by ADM (0.01 pmol). The vasopressor effects of ADM (0.01 pmol) in the RVLM were abolished by coinjections of either dizocilpine hydrogen maleate (a selective NMDA glutamate receptor antagonist, 500 pmol) or 6-cyano-7-nitroquinoxaline-2,3-dione (a selective non-NMDA glutamate receptor antagonist, 50 pmol). The ADM-induced vasopressor effects were also abolished by coadministration of either 7-nitroindazole sodium salt (a selective neuronal NO synthase inhibitor, 0.05 pmol) or methylene blue (a soluble guanylyl cyclase inhibitor, 100 pmol). These results suggest that ADM in the RVLM stimulates increases in MAP and HR through ADM receptor-mediated mechanisms. These effects are mediated by glutamate via both NMDA and non-NMDA receptors. NO, derived from neuronal NO synthase, also contributes to the ADM-induced vasopressor effects via a soluble guanylyl cyclase-associated signaling pathway. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|