[Acute hypocapnia attenuates phosphaturic effect of atrial natriuretic peptide in rats].

Y Mimura
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Abstract

This study evaluated phosphate excretion in response to atrial natriuretic peptide during acute hypocapnia in the presence or absence of the renal nerves in rats. To achieve a hypocapnic state, rats were mechanically hyperventilated with room air. As mechanical ventilation per se has been reported to affect renal excretory functions depending on the ventilatory conditions, this study was designed to examine renal functions during acute hypocapnia as compared with those during normocapnia produced by normal and/or hyperventilation. Rats were divided into three experimental groups: 1) a normally ventilated normocapnic (control) group (n = 8), 2) a hyperventilated normocapnic group (n = 8), and 3) a hyperventilated hypocapnic group (n = 8). The innervated right kidney served as a control for the contralateral denervated kidney. Acute renal denervation produced a greater phosphaturia compared to the innervated kidney during the control period in the two normocanic groups but not in the hypocapnic group. Infusion of ANP 12 micrograms/kg/h produced a remarkable increase in phosphate excretion in either kidney in the normocapnic groups. The degree of the phosphaturia (delta FEPi%) during infusion of ANP was similar between the normally ventilated and hyperventilated normocapnic groups both in innervated (10.6 +/- 2.4% and 7.4 +/- 1.2%) and denervated (14.0 +/- 3.0% and 13.5 +/- 2.2%) kidneys. In contrast to both normocapnic groups, the hypocapnic group had a greater hypophosphaturia during the control and ANP infusion periods in either kidney. The increase in fractional excretion of phosphate was smaller both in innervated (0.34 +/- 0.34% delta FEPi) and denervated (0.72 +/- 0.69% delta FEPi) kidneys than that in the other two normocapnic groups.(ABSTRACT TRUNCATED AT 250 WORDS)

急性低碳酸血症减弱大鼠心房利钠肽的磷酸化作用。
本研究评估了在肾神经存在或不存在的情况下,大鼠急性低碳酸血症时,心房利钠肽对磷酸盐排泄的反应。为了达到低碳酸血症状态,用室内空气对大鼠进行机械过度通气。据报道,机械通气本身会根据通气条件影响肾脏排泄功能,因此本研究旨在检查急性低碳酸血症期间的肾功能,并与正常和/或过度通气引起的正常碳酸血症期间的肾功能进行比较。将大鼠分为3个实验组:1)正常通气正碳酸组(对照组)(n = 8), 2)正碳酸过度通气组(n = 8), 3)低碳酸过度通气组(n = 8)。以神经支配的右肾为对照,对侧失神经支配的肾为对照。与对照组相比,在两个高负荷组中,急性肾去神经支配产生了更大的磷尿,但在低碳酸血症组中没有。ANP输注12微克/千克/小时可显著增加正常代谢组任一肾脏的磷酸盐排泄量。ANP输注时,正常通气和过度通气的正肌酸组中神经支配肾(10.6 +/- 2.4%和7.4 +/- 1.2%)和去神经支配肾(14.0 +/- 3.0%和13.5 +/- 2.2%)的磷尿程度(δ FEPi%)相似。与两组相比,低碳酸组在对照组和ANP输注期间双肾有更大的低磷尿。神经支配肾(0.34 +/- 0.34% δ FEPi)和去神经支配肾(0.72 +/- 0.69% δ FEPi)的磷排泄量的增加均小于其他两组。(摘要删节250字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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