Bianchi C, Thibault G, Wrobel-Konrad E, De Léan A, Genest J, Cantin M
Laboratory of Pathobiology, Clinical Research Institute of Montreal, Quebec, Canada.
Am J Physiol. 1989 Oct;257(4 Pt 2):F515-23. doi: 10.1152/ajprenal.1989.257.4.F515.
A quantitative in vitro autoradiographic study was performed on the aorta, renal glomeruli, and adrenal cortex of cardiomyopathic hamsters in various stages of heart failure and correlated, in some instances, with in vivo autoradiography. The results indicate virtually no correlation between the degree of congestive heart failure and the density of 125I-labeled atrial natriuretic factor [(Ser99, Tyr126)ANF] binding sites (Bmax) in the tissues examined. Whereas the Bmax was increased in the thoracic aorta in moderate and severe heart failure, there were no significant changes in the zona glomerulosa. The renal glomeruli Bmax was lower in mild and moderate heart failure compared with control and severe heart failure. The proportion of ANF B- and C-receptors was also evaluated in sections of the aorta, adrenal, and kidney of control and cardiomyopathic hamsters with severe heart failure. (Arg102, Cys121)ANF [des-(Gln113, Ser114, Gly115, Leu116, Gly117) NH2] (C-ANF) at 10(-6) M displaced approximately 505 of (Ser99, Tyr126)125I-ANF bound in the aorta and renal glomeruli and approximately 20% in the adrenal zona glomerulosa in both series of animals. These results suggest that ANF may exert a buffering effect on the vasoconstriction of heart failure and to a certain extent may inhibit aldosterone secretion. The impairment of renal sodium excretion does not appear to be related to glomerular ANF binding sites at any stage of the disease.
对处于心力衰竭不同阶段的心肌病仓鼠的主动脉、肾小球和肾上腺皮质进行了定量体外放射自显影研究,在某些情况下还与体内放射自显影相关联。结果表明,在所检查的组织中,充血性心力衰竭的程度与125I标记的心房利钠因子[(Ser99,Tyr126)ANF]结合位点(Bmax)的密度之间几乎没有相关性。虽然在中度和重度心力衰竭时胸主动脉中的Bmax增加,但球状带没有显著变化。与对照组和重度心力衰竭相比,轻度和中度心力衰竭时肾小球Bmax较低。还评估了对照组和重度心力衰竭心肌病仓鼠的主动脉、肾上腺和肾脏切片中ANF B和C受体的比例。在两个系列的动物中,10(-6)M的(Arg102,Cys121)ANF [des-(Gln113,Ser114,Gly115,Leu116,Gly117)NH2](C-ANF)取代了主动脉和肾小球中约50%的(Ser99,Tyr126)125I-ANF结合,在肾上腺球状带中约取代20%。这些结果表明,ANF可能对心力衰竭的血管收缩发挥缓冲作用,并在一定程度上可能抑制醛固酮分泌。在疾病的任何阶段,肾钠排泄受损似乎与肾小球ANF结合位点无关。