Widimský J, Kuchel O, Tremblay J, Hamet P
Clinical Research Institute of Montreal, Hôtel-Dieu Hospital, Montreal, Quebec, Canada.
J Hypertens. 1991 Mar;9(3):241-7. doi: 10.1097/00004872-199103000-00008.
Five weeks of high (8%) sodium intake, resulting in a decline of plasma atrial natriuretic factor (ANF) in normotensive Wistar-Kyoto (WKY) and Wistar rats, did not affect plasma ANF in spontaneously hypertensive rats (SHR) which became severely hypertensive. Regardless of salt consumption, SHR presented more pronounced glomerular particulate guanylate cyclase activation after large ANF doses in vitro than normotensive rats. In response to salt loading, plasma renin activity (PRA) and plasma aldosterone unexpectedly increased in SHR, in contrast to their decrease in the normotensive strains. Thus, SHR fail to react to prolonged high-salt intake as do normotensive rats, i.e. by a fall in plasma ANF, PRA and plasma aldosterone, and have higher stimulated glomerular particulate guanylate cyclase activity. Thus, ANF and its target response in SHR, as well as the PRA-plasma aldosterone reaction to prolonged salt loading, are distinct from those in normotensive strains. Since the relatively increased ANF and its target action in SHR appear to be a reactive antihypertensive defense rather than a primary event, systems other than ANF probably play an important role in the high salt-induced accelerated hypertension of SHR.
五周的高钠（8%）摄入，导致正常血压的Wistar-Kyoto（WKY）大鼠和Wistar大鼠血浆心房利钠因子（ANF）下降，但对已发生严重高血压的自发性高血压大鼠（SHR）的血浆ANF没有影响。无论盐摄入量如何，在体外给予大剂量ANF后，SHR的肾小球颗粒型鸟苷酸环化酶激活比正常血压大鼠更明显。与正常血压品系盐负荷后血浆肾素活性（PRA）和血浆醛固酮下降相反，SHR的PRA和血浆醛固酮在盐负荷后意外升高。因此，SHR不像正常血压大鼠那样对长期高盐摄入产生反应，即通过血浆ANF、PRA和血浆醛固酮的下降来反应，并且具有更高的刺激肾小球颗粒型鸟苷酸环化酶活性。因此，SHR中ANF及其靶反应，以及PRA-血浆醛固酮对长期盐负荷的反应，与正常血压品系不同。由于SHR中相对增加的ANF及其靶作用似乎是一种反应性的抗高血压防御而非原发性事件，因此除ANF外的其他系统可能在SHR高盐诱导的加速性高血压中起重要作用。
