Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1982-4-20
pubmed:abstractText
This study is concerned with the mechanisms of human renovascular hypertension. Unilateral partial occlusion of a renal artery was accomplished using a balloon-tipped catheter for occlusive angiography in seven normotensive and 17 primary hypertensive subjects. The renin and circulatory responses were studied during a 60 min reduction of the renal perfusion pressure (RPP) by 50% of control. This stimulus was considered to be safe and strong enough to produce a three to four-fold rise in plasma renin activity. It was observed that: a) systemic (arterial) renin was significantly raised at 5 min, reached a peak at 15 min and continued to be significantly higher than the baseline until the occlusion was removed; b) venous renin and venous arterial difference on the occluded side became elevated after the stimulus and remained so for the duration of the occlusion; c) renin release from the contralateral kidney became partially inhibited; d) in no case did systemic arterial pressure, heart rate or cardiac output change during the studies; e) renin and circulatory patterns were similar in normotensive and hypertensive subjects. It is concluded that in humans unilateral RPP reduction duplicates the renin pattern of the Goldblatt kidney, but does not duplicate the circulatory response. This evidence applies to a 1 h renal artery occlusion and does not exclude the possibility that renin may have a role in a rise in blood pressure following renal artery stenosis of longer duration.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0008-6363
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
637-42
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
Circulatory and renin responses in man to unilateral reduction of the renal perfusion pressure.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't