RESUMO
The alkaloid neurotoxin veratridine has the unique property of functionally distinguishing sodium channel subtypes in the rat through differences in single channel conductances, channel substates and probability of channel opening. Veratridine-activated cardiac sodium channels from rat ventricular muscle displayed a single channel conductance of 8.4 pS with no evidence of subconductance states or channel subtypes. Rat skeletal muscle sodium channels displayed both high (8.5 pS) and low conductance (4.7 pS) openings as well as a lower probability of opening (approximately 50%) at depolarized potentials than shown with brain or cardiac sodium channels (90-95%). Rat brain veratridine-activated sodium channels displayed primarily subconductance states at depolarized potentials (3-6 pS) and full conductance of approximately 9.5 pS at hyperpolarized potentials.
Assuntos
Encéfalo/fisiologia , Coração/fisiologia , Músculos/fisiologia , Canais de Sódio/fisiologia , Veratridina/farmacologia , Animais , Condutividade Elétrica/efeitos dos fármacos , Ventrículos do Coração , Ativação do Canal Iônico/efeitos dos fármacos , Ativação do Canal Iônico/fisiologia , Bicamadas Lipídicas , Potenciais da Membrana/efeitos dos fármacos , Especificidade de Órgãos , Probabilidade , Quinuclidinil Benzilato/metabolismo , Ensaio Radioligante , Ratos , Ratos Sprague-Dawley , Sarcolema/fisiologia , Saxitoxina/metabolismo , Canais de Sódio/efeitos dos fármacos , Canais de Sódio/isolamento & purificaçãoRESUMO
The calcium-complexing abilities of acetate, bicarbonate, lactate, succinate, and citrate were quantified, and were found to differ substantially. Acetate was a more potent vasodilator than lactate, and the vasorelaxant potencies of acetate and lactate failed to correlate with their calcium-complexing ability. The vasodilator action of acetate was not abolished after correction for complexing of ionized calcium. Strips constricted with vasopressin were especially sensitive to the vasodilator effects of acetate.
Assuntos
Acetatos/farmacologia , Cálcio/metabolismo , Canais Iônicos/efeitos dos fármacos , Lactatos/farmacologia , Vasodilatação/efeitos dos fármacos , Ácido Acético , Animais , Bicarbonatos/farmacologia , Quelantes , Citratos/farmacologia , Ácido Cítrico , Ácido Láctico , Masculino , Músculo Liso Vascular/efeitos dos fármacos , Ratos , Ratos Endogâmicos , Sódio/farmacologia , Bicarbonato de Sódio , Succinatos/farmacologia , Ácido SuccínicoRESUMO
Studies in a conscious, nonuremic dog model suggest that use of dialysate hyponatric to plasma tends to cause hypotension during dialytic ultrafiltration by accelerating the rate of contraction of plasma volume. No adverse effect of hyponatric dialysate on total peripheral resistance response could be demonstrated.
Assuntos
Sangue , Hemodinâmica , Sódio/sangue , Ultrafiltração/métodos , Animais , CãesRESUMO
Sodium acetate caused dose-dependent relaxation of helical rat tail artery strips constricted by phenylephrine, potassium chloride and arginine vasopressin. Substantial relaxation was evident at acetate concentrations as low as 4 mM. The results suggest that the vasodilatation of acetate is not limited to receptor-dependent or voltage-dependent mechanisms. Acute increases in bath sodium chloride concentration resulted in marked relaxation of vessel strips constricted by phenylephrine and potassium chloride. Arginine vasopressin-constricted strips were quite resistant to the vasorelaxant effect of increased bath sodium chloride.
