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Surgical Reversal of Twohyphenkidney One Clip Hypertension During Inhibition of the Reninhyphenangiotensin System

 

作者: GAVIN RUSSELL,   ROBERT BING,   HERBERT THURSTON,   JOHN SWALES,  

 

期刊: Hypertension  (OVID Available online 1982)
卷期: Volume 4, issue 1  

页码: 69-76

 

ISSN:0194-911X

 

年代: 1982

 

出版商: OVID

 

数据来源: OVID

 

摘要:

Conscious rats with twohyphenkidney one dip Goldblatt hypertension had the constricting dip removed during continuous infusion of either dextrose, saralasin, or captopril. Other dextrosehypheninfused animals underwent removal of the ischemic kidney or a sham procedure. Direct arterial blood pressure (BP) was recorded throughout the 15-hour preoperative and subsequent 24-hour postoperative period. Rats were studied in the “early” phase (1–3 weeks duration) or “chronic” phase (> 4 months) of hypertension. Animals subjected to a sham procedure returned to preoperative BP values. The BP of animals undipped or nephrectomlzed did not return to previous hypertensive levels. Instead, a biphasic response was seen where BP partially recovered from an operative fall and then slowly declined to normal at 24 hours; this effect occurred in both stages of hypertension. At 24 hours, removal of the ischeraic kidney was as effective as removal of the constricting dip in the correction of both eariy and chronic phase hypertension. Rats infused with saralasin or captopril demonstrated an acute (within 2 hours) and sustained fall in BP, but not to nonnotensive levels. This fall was significant In all animals (p< 0.01) apart from chronic phase rats infused with saralasin where no significant fall was seen. Although animals infused with saralasin or captopril commenced at a lower preoperative BP, the biphasic pattern of response to undipping was identical to that of dextrosehypheninfused undipped rats. Thus, sustained inhibition of the reninhyphenangiotensin system did not modify the correction of hypertension produced by removal of the constricting clip, and the response to surgical correction did not appear to be entirely mediated by changes in the activity of the reninhyphenangiotensin system, particularly in the chronic stage. Equally, the rapidity of correction is not consistent with a role for vascular hypertrophy. (Hypertension 4: 69–76, 1982)

 

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