Integrated autonomic and behavioral responses to L/N Ca2(+)-channel blocker omega-conotoxin in conscious rats
| Autor: | S. Shapira, G. Feuerstein, O. M. Adeyemo |
|---|---|
| Rok vydání: | 1990 |
| Předmět: |
Agonist
Male medicine.medical_specialty Physiology medicine.drug_class Hemodynamics Propranolol Motor Activity Autonomic Nervous System Nervous System Peptides Cyclic omega-Conotoxins Body Temperature chemistry.chemical_compound Diltiazem Catecholamines Nifedipine Physiology (medical) Internal medicine medicine Animals Injections Intraventricular Behavior Animal business.industry Rats Inbred Strains 3-Pyridinecarboxylic acid 1 4-dihydro-2 6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl ester Omega-Conotoxins Calcium Channel Blockers Rats Epinephrine Endocrinology Muscimol chemistry business Blood Chemical Analysis medicine.drug |
| Zdroj: | The American journal of physiology. 259(3 Pt 2) |
| ISSN: | 0002-9513 |
| Popis: | omega-Conotoxin (omega-ctx) was used as a probe for studying the putative role of brain L/N-type Ca2+ channels in regulation of autonomic functions. Rats were injected intracerebroventricularly (icv) with omega-ctx, and hemodynamic, biochemical and behavioral variables were monitored. omega-Ctx (0.032-10 nmol/kg) caused a persistent, dose-dependent shaking behavior, complex thermoregulatory changes, and motor deficits lasting up to 48 h. Cardiovascular responses to omega-ctx included tachycardia (+71 +/- 16%, P less than 0.01) and elevated arterial blood pressure (+16 +/- 1%, P less than 0.05) associated with increased circulating levels of norepinephrine and epinephrine. Higher doses, 1 or 10 nmol/kg, resulted in circulatory shock and death. Central administration of 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8), diltiazem (100 or 1,000 nmol/kg), neomycin (100 nmol/kg, each), nifedipine (10 nmol/kg), and CdCl2 (100 nmol/kg), which represent intracellular, non-specific N-, L-, and L/N-type Ca2(+)-channel blockers, respectively, did not cause any behavioral or hemodynamic effects, whereas the L-channel agonist BAY K 8644 (100 nmol/kg icv) caused a mild transient pressor response. Pretreatment with the gamma-aminobutyric acid (GABA) agonist muscimol (icv) or a combined intravenous pretreatment with propranolol and N-methylatropine blocked the omega-ctx effects. Our data suggest that omega-ctx actions in the brain involve central GABAergic mechanisms modulated by yet a different type of Ca2+ channels not characterized by any of the known voltage-operated Ca2+ channels. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|