King K A, Ledsome J R, Courneya C A
Department of Physiology, University of British Columbia, Vancouver, Canada.
Can J Physiol Pharmacol. 1992 Sep;70(9):1280-5. doi: 10.1139/y92-177.
Atrial natriuretic factor (ANF) is present in high concentration in atria but in very low concentration in the ventricles. Under conditions of haemodynamic overload ventricular gene expression may become activated, but it is not clear if ventricular ANF can be released through a regulated or constitutive pathway. The purpose of this study was to determine whether basal and stimulated release of ANF are increased in perinephritic rabbits with mild hypertension. Six rabbits were rendered hypertensive by wrapping both kidneys in cellophane, and six sham-operated rabbits were used as controls. Eight weeks after renal wrapping, mean arterial pressure was approximately 20 mmHg higher in the experimental group. After anaesthesia, the renal-wrapped group had a higher vascular resistance. Right and left atrial wall stress was measured using sonomicrometry. Volume expansion by 30% of blood volume, using donor blood, caused a small increase in right and left atrial diastolic and systolic wall stress but did not significantly increase plasma ANF. Pacing the heart at 6 Hz caused increases in systolic but not diastolic wall stress and caused a significant increase in plasma ANF; the increase was larger after volume expansion. There were no significant differences between the responses of the experimental and control groups. It is concluded that mild hypertension, in the rabbit, does not lead to changes in atrial wall stress or either basal or stimulated release of ANF.
心房利钠因子(ANF)在心房中的浓度很高,但在心室中的浓度极低。在血流动力学过载的情况下,心室基因表达可能会被激活,但尚不清楚心室ANF是否可以通过调节途径或组成型途径释放。本研究的目的是确定轻度高血压的肾周围性兔心房利钠因子的基础释放和刺激释放是否增加。六只兔子通过用玻璃纸包裹双侧肾脏而使其患高血压,六只假手术兔子用作对照。肾包裹八周后,实验组的平均动脉压大约高20 mmHg。麻醉后,肾包裹组的血管阻力更高。使用超声测微仪测量右心房和左心房壁应力。用供血者血液使血容量扩张30%,导致右心房和左心房舒张期和收缩期壁应力略有增加,但并未显著增加血浆ANF。以6 Hz频率起搏心脏导致收缩期壁应力增加,但舒张期壁应力未增加,并导致血浆ANF显著增加;血容量扩张后增加幅度更大。实验组和对照组的反应之间没有显著差异。得出的结论是,在兔中,轻度高血压不会导致心房壁应力或心房利钠因子的基础释放或刺激释放发生变化。