Blockade of hyperpolarization-activated channels modifies the effect of beta-adrenoceptor stimulation.
Experiments on rats showed that blockade of hyperpolarization-activated currents moderates tachycardia induced by beta-adrenoceptor agonist isoproterenol and potentiates the increase in stroke volume produced by this agonist. Electrical stimulation of the vagus nerve against the background of isoproterenol treatment augmented bradycardia and increased stroke volume. Blockade of hyperpolarization-activated currents followed by application of isoproterenol moderated vagus-induced bradycardia and had no effect on the dynamics of stroke volume.
Zefirov
T L
TL
Department of Anatomy, Physiology, and Human Health Protection, Kazan State Pedagogical University. nafisa@kmu-mf.kcn.ru
Ziyatdinova
N I
NI
Gainullin
A A
AA
Zefirov
A L
AL
D000818:Animals; D001919:Bradycardia; D002317:Cardiovascular Agents / Q000494:pharmacology; D004594:Electrophysiology; D006321:Heart / Q000187:drug effects; D007545:Isoproterenol / Q000494:pharmacology*; D011743:Pyrimidines / Q000494:pharmacology; D051381:Rats; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D013997:Time Factors; D014628:Vagotomy; D014630:Vagus Nerve
D002317:Cardiovascular Agents; D011743:Pyrimidines; D011943:Receptors, Adrenergic, beta; C082246:ICI D2788; D007545:Isoproterenol