Effects of Hydrogen Ion on the Changes in Adenosine Production in the Isolated Rat Heart Perfused at a Constant Flow System

Ochi, Toya; Tanaka, Toshiko; Yoshihara, Shingo; Fukumoto, Tazuru; Nakashima, Yasuhide; Kuroiwa, Akio

doi:10.1159/000174775

Cited by 2 publications

(2 citation statements)

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“…Our data support this earlier observation. In contrast, Ochi et al [17], who used a constant flow system similar to ours, reported that acidosis (pH 7.2) produced a small decrease in CPP, from 93.9 ± 8.5 to 84.8 ± 6.8mmHg. In their report, the precise timing of the decrease in CPP is not stated but the response is clearly different to that seen by us.…”

Section: Discussioncontrasting

confidence: 54%

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Acidosis-induced coronary constriction in the rat heart: Evidence for the activation of L-type calcium channels

Wilson

Woodward

1999

Heart Vessels

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Perfused rat hearts were used to study the effects of acidosis on coronary tone. When pH was decreased, over the range pH 7.4 to pH 6.2, by reducing perfusate bicarbonate levels, under constant flow conditions, there was a transient decrease in coronary perfusion pressure (CPP), followed by a sustained acidosis-dependent increase in CPP, which reversed when pH was returned to pH 7.4. This increase in CPP was seen at perfusion rates of 5, 10, and 20 ml/min(-1). When using constant pressure perfusion acidosis reduced coronary flow. In a HEPES-buffered bicarbonate-free solution, acidosis did not cause a transient fall in CPP but it did produce a sustained increase in CPP. Addition of ammonium chloride (10 mM) reduced CPP, while washout of ammonium chloride increased CPP. The acidosis-induced increase in CPP was not affected by indomethacin, nitro-L-arginine, the nonselective adenosine receptor antagonist, 8-phenyl theophylline, or the thromboxane receptor antagonist, ZD 1542. The acidosis-induced increase in CPP was independent of the myocardial depressant effects of acidosis, but was attenuated by three different L-type calcium channel blockers. These results demonstrate that the coronary circulation of the rat constricts in response to acidosis. Experiments performed with L-type calcium channel blockers, and the calcium channel activator BAY K8644, suggest that constriction occurs via activation of L-type calcium channels. This would not be expected on the basis of electrophysiological studies, which have shown an inhibition of L-type calcium channels by acidosis.

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Section: Discussioncontrasting

confidence: 54%

“…In contrast, a more recent study in the rat described an acidosis-induced coronary dilatation [17]. In view of these apparent contradictory reports we have reexamined the effect of acidosis on coronary resistance in the rat heart.…”

Section: Introductionmentioning

confidence: 88%