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The release mechanism for atrial natriuretic factor during blood volume expansion and tachycardia in dogs.

作者信息

Christensen G, Ilebekk A, Aakeson I, Kiil F

机构信息

University of Oslo, Institute for Experimental Medical Research, Norway.

出版信息

Acta Physiol Scand. 1988 Oct;134(2):263-70. doi: 10.1111/j.1748-1716.1988.tb08487.x.

DOI:10.1111/j.1748-1716.1988.tb08487.x
PMID:2976238
Abstract

Atrial natriuretic factor (ANF) is released during blood volume expansion and tachycardia, but only blood volume expansion causes atrial distension, which presumably promotes ANF release. Our study was undertaken to search for a common release mechanism. In five anaesthetized, closed-chest dogs, plasma immunoreactive (IR) ANF was measured at three levels of blood volume, which were obtained by infusing a Ringer's solution. At each level of blood volume, plasma IR-ANF was measured at three pacing frequencies. Plasma IR-ANF increased as mean right atrial pressure (mRAP) was raised from 2 to 10 mmHg by volume expansion, whereas pacing tachycardia (at heart rates (HR) 50 +/- 3 and 98 +/- 1 beats min-1 above control) at each level of blood volume expansion increased plasma IR-ANF and systolic RAP (sRAP) at constant mRAP. Plasma IR-ANF was more strongly correlated to sRAP (r = 0.83) than to mRAP (r = 0.69), but the product sRAP x HR had the highest correlation coefficient (r = 0.86). According to the multiple regression equation: plasma IR-ANF = k1 + k2mRAP + k3sRAP + k4sRAP x HR, the product sRAP x HR had the highest coefficient of determination (r2 = 0.75) and was the only significant determinant. We conclude that atrial tension or stress, developing during each atrial systole, is an important determinant of ANF release. Since atrial diastolic and systolic dimensions do not increase during pacing tachycardia, ANF release is not dependent on atrial distension.

摘要

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