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Autoregulation and vasoconstriction in the intestine during acute renal hypertension.
Author(s) -
G. A. Meininger,
L K Routh,
Harris J. Granger
Publication year - 1985
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.7.3.364
Subject(s) - sma* , medicine , superior mesenteric artery , vasoconstriction , cardiology , renal artery , vascular resistance , renal artery stenosis , renal blood flow , kidney , blood pressure , endocrinology , mathematics , combinatorics
SUMMARY The purpose of this study was to investigate whether local mechanisms of blood flow autoregulation mediate vasoconstriction during the early development of renal hypertension. Anes- thetized rats were instrumented with Doppler flow probes on the celiac (CA), superior mesenteric (SMA), and renal arteries to measure flow velocity in these vessels. Acute two-kidney, one clip renal hypertension was produced by inflating a pneumatic occluder on the left renal artery to reduce flow velocity by 50%. Two hours after renal artery stenosis (RAS), femoral artery pressure (AP) was increased by 35 %, CA resistance by 45 %, and SMA resistance by 57 %. No increases were observed in AP or in CA and SMA resistances for sham-operated, control rats. To determine if autoregulation contributed to the increase in SMA resistance, we protected the SMA vasculature from the increased arterial pressure by servocontrolled inflation of a pneumatic cuff implanted around the SMA. Al- though normalizing SMA pressure with the protective cuff significantly reduced (p < 0.05) the increase in SMA resistance that occurred after RAS, SMA resistance remained elevated above control levels. These results suggest that (1) reduced intensity of SMA constriction produced by protection of the SMA is due to inhibition of a local autoregulatory mechanism that is contributing to the increase in SMA resistance during the acute development of renal hypertension, and (2) maintenance of ele- vated SMA resistance during protection from increased AP is the result of pressure-independent mechanisms that are activated subsequent to renal artery stenosis. (Hypertension 7: 364-373, 1985)

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