Lachance D, Garcia R
Clinical Research Institute of Montreal, Quebec, Canada.
Cardiovasc Res. 1991 Jun;25(6):475-83. doi: 10.1093/cvr/25.6.475.
The aims were (1) to study the influence of afterload relief on the rise in atrial natriuretic factor (ANF) which occurs during acute volume expansion in the spontaneously hypertensive rat (SHR); (2) to assess the contribution of the atria and the ventricles to ANF release under these circumstances.
In the first series of experiments, SHR were treated with captopril (150 mg.kg-1.d-1) orally for 10 d. Untreated SHR and Wistar-Kyoto (WKY) rats served as controls. Volume expansion, equivalent to 10% of the total blood volume, was performed three times with human plasma protein fraction at 15 min intervals on conscious animals. Some haemodynamic variables and plasma ANF were measured. Tissue ANF measurements were conducted on another series of treated and control SHR not submitted to volume expansion. In another series of experiments, conscious SHR and WKY rats were submitted to repetitive 30% volume expansion (three times at 15 min intervals). Non-expanded animals served as controls. At the end of the experiments, tissue ANF measurements were performed.
All experiments were conducted on 15 week old SHR and WKY rats.
Captopril treatment reduced systolic blood pressure and cardiac hypertrophy in SHR. During volume expansion, changes in left ventricular end diastolic pressure were greater in control SHR than in treated SHR or WKY rats. Central venous pressure was affected similarly by volume expansion in both SHR groups. Plasma ANF rises induced by volume expansion were equal in all groups. Captopril treatment had no effect on right or left auricular ANF content prior to volume expansion. Repetitive 30% expansion reduced both right and left auricular ANF concentrations to the same extent (approximately 300-1500 ng.mg-1 protein) in SHR and WKY groups. Ventricular ANF was not affected by volume expansion in SHR, whereas volume expanded WKY rats had higher right and left ventricular ANF concentrations than their non-expanded controls.
(1) The increase in plasma ANF during volume expansion is not impaired in SHR with newly established hypertension; (2) captopril treatment decreases afterload and the changes in left ventricular end diastolic pressure during volume expansion in SHR, without affecting plasma ANF increases; (3) both the auricles, but not the ventricles, contribute to enhanced ANF secretion caused by acute volume expansion in SHR and WKY rats.
本研究旨在（1）探讨后负荷减轻对自发性高血压大鼠（SHR）急性容量扩张时心房利钠因子（ANF）升高的影响；（2）评估在此情况下心房和心室对ANF释放的贡献。
在第一组实验中，给SHR口服卡托普利（150mg·kg⁻¹·d⁻¹），持续10天。未治疗的SHR和Wistar-Kyoto（WKY）大鼠作为对照。对清醒动物每隔15分钟用人体血浆蛋白组分进行三次相当于总血容量10%的容量扩张。测量了一些血流动力学变量和血浆ANF。对另一组未进行容量扩张的经治疗和对照的SHR进行了组织ANF测量。在另一组实验中，对清醒的SHR和WKY大鼠进行重复30%的容量扩张（每隔15分钟进行三次）。未扩张的动物作为对照。实验结束时，进行了组织ANF测量。
所有实验均在15周龄的SHR和WKY大鼠上进行。
卡托普利治疗降低了SHR的收缩压和心脏肥大。在容量扩张期间，对照SHR的左心室舒张末期压力变化大于经治疗的SHR或WKY大鼠。两组SHR中容量扩张对中心静脉压的影响相似。容量扩张诱导的血浆ANF升高在所有组中是相等的。在容量扩张前，卡托普利治疗对右或左耳房ANF含量没有影响。在SHR和WKY组中，重复30%的扩张使右和左耳房ANF浓度降低到相同程度（约300 - 1500ng·mg⁻¹蛋白）。在SHR中，心室ANF不受容量扩张的影响，而容量扩张的WKY大鼠的右和左心室ANF浓度高于未扩张的对照。
（1）新发生高血压的SHR在容量扩张期间血浆ANF的升高未受损害；（2）卡托普利治疗降低了SHR容量扩张时的后负荷和左心室舒张末期压力变化，而不影响血浆ANF的升高；（3）在SHR和WKY大鼠中，急性容量扩张引起的ANF分泌增加是由心房而非心室导致的。
