Ackermann U, Irizawa T G, Barber B
Department of Physiology, University of Toronto, Ont., Canada.
Can J Physiol Pharmacol. 1989 Jun;67(6):675-81. doi: 10.1139/y89-108.
The effect of atrial natriuretic factor (ANF) on baroreflex sensitivity was determined in unanesthetized normotensive (Wistar-Kyoto, WKY) or spontaneously hypertensive rats (SHR) during acute hypertensive stimuli (phenylephrine) or hypotensive stimuli (sodium nitroprusside). The i.v. dose of rat ANF [( Ser99,Tyr126]ANF) was 50 ng/min per rat, sufficient to decrease mean arterial blood pressure (ABP) by about 6 mmHg (1 mmHg = 133.3 Pa) in WKY. SHR showed no change in ABP with this ANF dose. During a control infusion of physiological saline, the mean heart rate (HR) response to increases in ABP was -1.30 +/- 0.27 beats/min (bpm)/mmHg in WKY and -0.37 +/- 0.22 in SHR (p less than 0.05). These values were not affected significantly by ANF. However, ANF blunted chronotropic responses to ABP decreases. The control values of the delta HR/delta ABP slope in WKY and SHR were -2.34 +/- 0.57 and -2.01 +/- 0.37 bpm/mmHg, respectively. In the presence of ANF, the slope changed to -0.36 +/- 0.43 (i.e., bradycardia in response to hypotension) in WKY and to +0.20 +/- 0.21 in SHR (p less than 0.005 for the difference from control for both). This ANF-induced loss of baroreflex sensitivity was reversed in WKY by the addition of angiotensin I (sufficient to increase ABP by 5 mmHg in control rats). Angiotensin did not restore baroreflex sensitivity in ANF-infused SHR, and ANF had no effect on the ABP increase caused by angiotensin in either group. The data suggest that ANF does not act on baroreceptor structures directly, but inhibits mechanisms involved in efferent sympathetic activation. Parasympathetic responses do not appear to be compromised.
在未麻醉的正常血压（Wistar - Kyoto，WKY）大鼠或自发性高血压大鼠（SHR）中，在急性高血压刺激（去氧肾上腺素）或低血压刺激（硝普钠）期间，测定了心房利钠因子（ANF）对压力反射敏感性的影响。大鼠ANF [（Ser99，Tyr126）ANF]的静脉注射剂量为每只大鼠50 ng/min，足以使WKY大鼠的平均动脉血压（ABP）降低约6 mmHg（1 mmHg = 133.3 Pa）。该ANF剂量下，SHR的ABP无变化。在生理盐水中进行对照输注期间，WKY大鼠对ABP升高的平均心率（HR）反应为-1.30±0.27次/分钟（bpm）/mmHg，SHR为-0.37±0.22（p<0.05）。这些值未受到ANF的显著影响。然而，ANF减弱了对ABP降低的变时反应。WKY和SHR中HR/ABP斜率的对照值分别为-2.34±0.57和-2.01±0.37 bpm/mmHg。在存在ANF的情况下，WKY大鼠的斜率变为-0.36±0.43（即对低血压的心动过缓），SHR变为+0.20±0.21（两者与对照相比差异p<0.005）。这种由ANF引起的压力反射敏感性丧失在WKY大鼠中通过添加血管紧张素I（足以使对照大鼠的ABP升高5 mmHg）得以逆转。血管紧张素未能恢复ANF输注的SHR中的压力反射敏感性，且ANF对两组中血管紧张素引起的ABP升高均无影响。数据表明，ANF不直接作用于压力感受器结构，而是抑制传出交感神经激活所涉及的机制。副交感神经反应似乎未受损害。
