Honrath U, Chong C K, Melo L G, Sonnenberg H
Department of Physiology, University of Toronto, ON, Canada.
Can J Physiol Pharmacol. 1999 Jun;77(6):454-7.
Atrial natriuretic peptide (ANP) is thought to play a role in renal regulation of salt balance by reducing tubular reabsorption of sodium and chloride. Therefore, in the chronic absence of this hormone, a defect of salt excretion should be evident. We used an ANP gene deletion model to test this premise. F2 homozygous mutant mice (-/-) and their wild-type littermates (+/+) were fed an 8% NaCl diet prior to an acute infusion of isotonic saline. Arterial blood pressures, renal excretions of salt and water, as well as collecting duct transport of fluid and electrolytes were measured. Pressures were significantly higher in -/- compared with +/+ mice (139 +/- 4 vs. 101 +/- 2 mmHg; 1 mmHg = 133.3 Pa). There was no difference in glomerular filtration rate (-/- = 0.84 +/- 0.06; +/+ = 0.81 +/- 0.04 mL x min(-1) x g(-1) kidney weight). In the collecting duct, sodium and chloride reabsorptions were significantly higher in the -/- group than in the +/+ group. As a result, natriuresis and chloruresis were relatively reduced (U(Na)V: -/- = 8.6 +/- 1.1; +/+ = 14.0 +/- 1.1; U(Cl)V: -/- = 10.1 +/- 1.4; +/+ = 16.0 +/- 1.1 micromol x min(-1) x g(-1) kidney weight). We conclude that the absence of endogenous ANP activity in mice on a high-salt diet subjected to acute saline infusion causes inappropriately high reabsorption of sodium and chloride in the medullary collecting duct, resulting in a relative defect in renal excretory capacity for salt.
心房利钠肽（ANP）被认为通过减少肾小管对钠和氯的重吸收在肾脏盐平衡调节中发挥作用。因此，在长期缺乏这种激素的情况下，盐排泄缺陷应该很明显。我们使用ANP基因缺失模型来验证这一前提。在急性输注等渗盐水之前，给F2纯合突变小鼠（-/-）及其野生型同窝小鼠（+/+）喂食8%氯化钠饮食。测量动脉血压、肾脏的盐和水排泄以及集合管的液体和电解质转运。与+/+小鼠相比，-/-小鼠的血压显著更高（139±4 vs. 101±2 mmHg；1 mmHg = 133.3 Pa）。肾小球滤过率没有差异（-/- = 0.84±0.06；+/+ = 0.81±0.04 mL·min⁻¹·g⁻¹肾重）。在集合管中，-/-组的钠和氯重吸收显著高于+/+组。结果，尿钠排泄和尿氯排泄相对减少（尿钠排泄量：-/- = 8.6±1.1；+/+ = 14.0±1.1；尿氯排泄量：-/- = 10.1±1.4；+/+ = 16.0±1.1 μmol·min⁻¹·g⁻¹肾重）。我们得出结论，在接受急性盐水输注的高盐饮食小鼠中，内源性ANP活性的缺失导致髓质集合管中钠和氯的重吸收过高，从而导致肾脏对盐的排泄能力相对缺陷。
