Neither ventricles nor afterload relief influence the raised plasma atrial natriuretic factor induced by volume expansion in the spontaneously hypertensive rat.

STUDY OBJECTIVE

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.

DESIGN

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.

EXPERIMENTAL MATERIAL

All experiments were conducted on 15 week old SHR and WKY rats.

MEASUREMENTS AND MAIN RESULTS

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.

CONCLUSIONS

(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.