Dagnino L, Lavigne J P, Nemer M
Institut de recherches cliniques de Montréal, Canada.
Hypertension. 1992 Nov;20(5):690-700. doi: 10.1161/01.hyp.20.5.690.
The cardiac natriuretic peptide family includes atrial natriuretic factor and brain or B-type natriuretic peptide, also known as iso-atrial natriuretic factor (isoANF). Although these peptides contribute to cardiovascular homeostasis, their respective roles remain unclear. To study regulation of atrial natriuretic factor and isoANF gene expression during progression of hypertension, we developed a quantitative polymerase chain reaction protocol to measure their transcript level in spontaneously hypertensive rat (SHR) hearts. At the onset of hypertension, atrial natriuretic factor transcripts in 5-week-old SHR were 50% of those of age-matched Wistar-Kyoto (WKY) rats, whereas the level of isoANF transcripts was similar in atria and twofold higher in ventricles. Because atria are the major sites of atrial natriuretic factor gene expression and ventricles contribute predominantly to cardiac isoANF synthesis, total atrial natriuretic factor messenger RNA (mRNA) in the hearts of 5-week-old SHR was about 50% of that in WKY rats, and total isoANF mRNA content was already higher than in control rats. In left ventricles and ventricular septa, progression of hypertension led to a maximal increase of twofold and fourfold in atrial natriuretic factor and isoANF mRNA levels, respectively, with no detectable change in right ventricles. In the atria of older SHR, atrial natriuretic factor and isoANF mRNA levels were comparable to those of age-matched controls. These data indicate that, although increased blood pressure stimulates both atrial natriuretic factor and isoANF gene expression, regulation of the two natriuretic peptide genes is not temporally coordinated in all cardiac compartments. Furthermore, isoANF mRNA is already induced in the ventricles at the onset of the hypertensive stage, and in older SHR, the isoANF gene is hyperresponsive to progression of hypertension compared with atrial natriuretic factor. Thus, isoANF might represent a very sensitive marker of cardiac changes in hypertension.
心脏利钠肽家族包括心房利钠因子和脑钠肽或B型利钠肽,也称为异心房利钠因子(isoANF)。尽管这些肽有助于心血管稳态,但其各自的作用仍不清楚。为了研究高血压进展过程中心房利钠因子和isoANF基因表达的调控,我们开发了一种定量聚合酶链反应方案,以测量自发性高血压大鼠(SHR)心脏中它们的转录水平。在高血压发作时,5周龄SHR的心房利钠因子转录本是年龄匹配的Wistar-Kyoto(WKY)大鼠的50%,而异位ANF转录本水平在心房中相似,在心室中高出两倍。由于心房是心房利钠因子基因表达的主要部位,而心室主要参与心脏isoANF的合成,5周龄SHR心脏中的总心房利钠因子信使核糖核酸(mRNA)约为WKY大鼠的50%,总isoANF mRNA含量已经高于对照大鼠。在左心室和室间隔中,高血压进展导致心房利钠因子和isoANF mRNA水平分别最大增加两倍和四倍,右心室无明显变化。在老年SHR的心房中,心房利钠因子和isoANF mRNA水平与年龄匹配的对照组相当。这些数据表明,尽管血压升高会刺激心房利钠因子和isoANF基因表达,但这两种利钠肽基因的调控在所有心脏腔室中并非在时间上协调一致。此外,在高血压阶段开始时,心室中isoANF mRNA就已被诱导,在老年SHR中,与心房利钠因子相比,isoANF基因对高血压进展的反应更强烈。因此,isoANF可能是高血压心脏变化的一个非常敏感的标志物。