Differential vagal inhibition of the positive chronotropic and inotropic responses to cardiotonics in the isolated dog atrium

Furukawa, Yoshiko; Ogiwara, Yasuhiro; Saegusa, Kimiaki; Akahane, Kunio; Chiba, Shigetoshi

doi:10.1016/0014-2999(89)90173-8

Cited by 4 publications

(2 citation statements)

References 21 publications

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“…This differ ent inhibition by pinacidil on the chronotropic and iso tropic responses to norepinephrine differs from the inhi bition by acetylcholine or adenosine on the cardiac responses to norepinephrine. In the isolated, blood-per fused canine atrial preparation, we previously reported that acetylcholine and adenosine attenuated the positive chronotropic and inotropic responses to norepinephrine (14,15). These sympathoinhibitory effects of acetyl choline or adenosine on the heart are caused at sites of the intracellular signal transduction (12,13,29,30).…”

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confidence: 98%

“…Acetylcholine and adenosine attenuate the chronotropic and inotropic responses to catecholamines in isolated mammalian hearts (10 13). In the isolated, perfused dog atrium, parasympathetic nerve stimulation attenuated both chronotropic and inotropic responses to norepinephrine but not those to Bay k 8644 (14), and adenosine attenu ated both cardiac responses to norepinephrine and Bay k 8644 (15). However, little is known about the interaction between the activation of K+ATP channels and the sym pathetic nervous system in the heart, although the interac tions between the K+ATP channel opener cromakalim and the sympathetic nervous system at the systemic and regional vascular levels have been reported in sponta neously hypertensive rats (16,17).…”

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confidence: 99%

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Pinacidil Attenuates Positive Inotropic but Not Chronotropic Responses to Norepinephrine in Isolated Dog Atrial and Ventricular Preparations

Takayama

Furukawa

Murakami

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-We investigated whether pinacidil, a K+ATP channel opener like acetylcholine and adenosine, attenuated the positive chronotropic and inotropic responses to norepinephrine in isolated, blood-perfused dog atrial and ventricular preparations. Pinacidil (0.01 -0.3 pmol) decreased atrial and ventricular contrac tile force to a much greater extent than sinus rate in a dose-related manner. Pinacidil dose-dependently attenuated increases in atrial and ventricular forces induced by norepinephrine but not increases in sinus rate. Pinacidil similarly attenuated the positive atrial and ventricular inotropic responses to Bay k 8644 and CaC12. The pinacidil doses producing a fifty percent decrease (ED50) of the atrial and ventricular contractile force were not significantly different from the respective pinacidil doses producing a fifty percent inhibition (ID50) of the positive inotropic responses to norepinephrine, Bay k 8644 and CaC12. Ouabain (5 and 15 nmol) did not affect the decreases in atrial and ventricular contractile force in response to pinacidil. These results suggest that the K+ATP-channel activator pinacidil, unlike acetylcholine or adenosine, functionally attenuates increases in ventricular and atrial contractile force in the responses to norepinephrine and other cardiotonics due to shortening of the action potential duration induced by K+ATP-channel activation in the dog heart.

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