CAPTOPRIL ENHANCES RENAL RESPONSIVENESS TO ANF IN DOGS WITH COMPENSATED HIGH-OUTPUT HEART-FAILURE

被引:42
作者
VILLARREAL, D
FREEMAN, RH
JOHNSON, RA
机构
[1] UNIV MISSOURI,SCH MED,DEPT MED,COLUMBIA,MO 65212
[2] HARRY S TRUMAN MEM VET HOSP,COLUMBIA,MO 65212
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1992年 / 262卷 / 03期
关键词
ARTERIOVENOUS FISTULA; RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM; URINARY SODIUM EXCRETION; ATRIAL NATRIURETIC FACTOR;
D O I
10.1152/ajpregu.1992.262.3.R509
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The systemic hemodynamic, hormonal, and renal effects of chronic angiotensin-converting enzyme inhibition (CEI) with captopril and the responses to synthetic atrial natriuretic factor (ANF) infusions in the presence and absence of captopril were examined in normal dogs (n = 6) and in dogs with an arteriovenous (AV) fistula and compensated high-output heart failure (n = 6). This experimental model is characterized by normalization of the circulating renin-angiotensin-aldosterone system (RAAS) and persistent elevations in central filling pressures and plasma ANF. In both normal and AV-fistula dogs, oral captopril for 1 wk at 35 mg.kg-1.day-1 in three divided doses produced progressive reductions in arterial and atrial pressures (P < 0.05), plasma ANF (P < 0.05), and aldosterone (P < 0.05). After 1-2 days of a modest increase in urinary sodium excretion (U(Na)V) (P < 0.05), all of the dogs regained and maintained sodium balance during captopril administration. On the 8th day of the captopril regimen, synthetic ANF was infused at 15 and 30 ng.kg-1.min-1 for 75-min periods each. Control infusion experiments were performed in the same animals before captopril administration. The normal dogs exhibited dose-related elevations in U(Na)V (P < 0.05) that were not augmented with captopril (P > 0.05). In contrast, in the AV-fistula dogs the observed renal unresponsiveness to synthetic ANF in the control experiments was reversed with chronic CEI, and ANF-induced U(Na)V achieved levels comparable to those obtained in the normal animals. The enhanced natriuresis occurred despite marked reductions in baseline arterial pressure produced by captopril. In both normal and AV-fistula dogs, the increases in urinary guanosine 3',5'-cyclic monophosphate were similar with and without captopril administration. It is suggested that in the AV-fistula dogs a normal level of activity of the circulating RAAS and perhaps also an enhanced generation of intrarenal angiotensin II markedly antagonize the natriuretic actions of ANF; and this renal excretory unresponsiveness is reversed with the chronic blockade of the renal-adrenal hormonal axis.
引用
收藏
页码:R509 / R516
页数:8
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