Acute responses of arterial pressure and plasma renin activity to converting enzyme inhibition (SQ 20,881) in serially studied dogs with Neonatally-Induced oarctation hypertension

Susan Bagby, Daniel K. Gray

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

In six inbred dogs with neonatally-induced coarctation hypertension, and in seven littermate controls, acute responses of proximal arterial pressure and plasma renln activity (PRA) to converting enzyme inhibitor (CEI; SQ 20,881, 0.5 rag/kg i.v.) were serially examined. Studies were performed at 2, 6, and 12 months post-aortic banding under sodium-replete and -deplete conditions. Both in normotensive controls and in coarcted dogs, depressor responses (pre- minus post-CEI values) were positively correlated, not only with initial (pre-CEI) PRA, but also independently with initial blood pressure. Although absolute depressor responses in coarcted dogs exceeded those of the control group, there were no significant group differences when, by analysis of covariance, depressor responses were adjusted for the physiologic influence of initial pressure. Similarly, depressor responses expressed as a percent of initial pressure were comparable in coarcted and control groups. Initial PRA and PRA response to CEI in coarcted dogs were also comparable to control dogs; the PRA response correlated with initial PRA in both groups. CEI did not significantly diminish the magnitude of blood-pressure difference between coarcted and control dogs. Thus, in neonatally-induced coarctation hypertension, under both sodium replete- and -deplete conditions: 1) acute depressor and PRA responses to CEI are modulated by the same factors that influence responses of normotensive controls; 2) larger absolute depressor responses to CEI appear to be a physiologic function of higher initial pressure; and 3) blood pressure excess over littermate controls is largely sustained by CEI-resistant factors, potentially including the known volume excess in coarcted dogs.

Original languageEnglish (US)
Pages (from-to)146-154
Number of pages9
JournalHypertension
Volume4
Issue number1
StatePublished - 1982

Fingerprint

Renin
Arterial Pressure
Dogs
Hypertension
Enzymes
Blood Pressure
Pressure
Sodium
Control Groups
Enzyme Inhibitors

Keywords

  • Extracellular volume
  • Thoracic aorta banding

ASJC Scopus subject areas

  • Internal Medicine

Cite this

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title = "Acute responses of arterial pressure and plasma renin activity to converting enzyme inhibition (SQ 20,881) in serially studied dogs with Neonatally-Induced oarctation hypertension",
abstract = "In six inbred dogs with neonatally-induced coarctation hypertension, and in seven littermate controls, acute responses of proximal arterial pressure and plasma renln activity (PRA) to converting enzyme inhibitor (CEI; SQ 20,881, 0.5 rag/kg i.v.) were serially examined. Studies were performed at 2, 6, and 12 months post-aortic banding under sodium-replete and -deplete conditions. Both in normotensive controls and in coarcted dogs, depressor responses (pre- minus post-CEI values) were positively correlated, not only with initial (pre-CEI) PRA, but also independently with initial blood pressure. Although absolute depressor responses in coarcted dogs exceeded those of the control group, there were no significant group differences when, by analysis of covariance, depressor responses were adjusted for the physiologic influence of initial pressure. Similarly, depressor responses expressed as a percent of initial pressure were comparable in coarcted and control groups. Initial PRA and PRA response to CEI in coarcted dogs were also comparable to control dogs; the PRA response correlated with initial PRA in both groups. CEI did not significantly diminish the magnitude of blood-pressure difference between coarcted and control dogs. Thus, in neonatally-induced coarctation hypertension, under both sodium replete- and -deplete conditions: 1) acute depressor and PRA responses to CEI are modulated by the same factors that influence responses of normotensive controls; 2) larger absolute depressor responses to CEI appear to be a physiologic function of higher initial pressure; and 3) blood pressure excess over littermate controls is largely sustained by CEI-resistant factors, potentially including the known volume excess in coarcted dogs.",
keywords = "Extracellular volume, Thoracic aorta banding",
author = "Susan Bagby and Gray, {Daniel K.}",
year = "1982",
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journal = "Hypertension",
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T1 - Acute responses of arterial pressure and plasma renin activity to converting enzyme inhibition (SQ 20,881) in serially studied dogs with Neonatally-Induced oarctation hypertension

AU - Bagby, Susan

AU - Gray, Daniel K.

PY - 1982

Y1 - 1982

N2 - In six inbred dogs with neonatally-induced coarctation hypertension, and in seven littermate controls, acute responses of proximal arterial pressure and plasma renln activity (PRA) to converting enzyme inhibitor (CEI; SQ 20,881, 0.5 rag/kg i.v.) were serially examined. Studies were performed at 2, 6, and 12 months post-aortic banding under sodium-replete and -deplete conditions. Both in normotensive controls and in coarcted dogs, depressor responses (pre- minus post-CEI values) were positively correlated, not only with initial (pre-CEI) PRA, but also independently with initial blood pressure. Although absolute depressor responses in coarcted dogs exceeded those of the control group, there were no significant group differences when, by analysis of covariance, depressor responses were adjusted for the physiologic influence of initial pressure. Similarly, depressor responses expressed as a percent of initial pressure were comparable in coarcted and control groups. Initial PRA and PRA response to CEI in coarcted dogs were also comparable to control dogs; the PRA response correlated with initial PRA in both groups. CEI did not significantly diminish the magnitude of blood-pressure difference between coarcted and control dogs. Thus, in neonatally-induced coarctation hypertension, under both sodium replete- and -deplete conditions: 1) acute depressor and PRA responses to CEI are modulated by the same factors that influence responses of normotensive controls; 2) larger absolute depressor responses to CEI appear to be a physiologic function of higher initial pressure; and 3) blood pressure excess over littermate controls is largely sustained by CEI-resistant factors, potentially including the known volume excess in coarcted dogs.

AB - In six inbred dogs with neonatally-induced coarctation hypertension, and in seven littermate controls, acute responses of proximal arterial pressure and plasma renln activity (PRA) to converting enzyme inhibitor (CEI; SQ 20,881, 0.5 rag/kg i.v.) were serially examined. Studies were performed at 2, 6, and 12 months post-aortic banding under sodium-replete and -deplete conditions. Both in normotensive controls and in coarcted dogs, depressor responses (pre- minus post-CEI values) were positively correlated, not only with initial (pre-CEI) PRA, but also independently with initial blood pressure. Although absolute depressor responses in coarcted dogs exceeded those of the control group, there were no significant group differences when, by analysis of covariance, depressor responses were adjusted for the physiologic influence of initial pressure. Similarly, depressor responses expressed as a percent of initial pressure were comparable in coarcted and control groups. Initial PRA and PRA response to CEI in coarcted dogs were also comparable to control dogs; the PRA response correlated with initial PRA in both groups. CEI did not significantly diminish the magnitude of blood-pressure difference between coarcted and control dogs. Thus, in neonatally-induced coarctation hypertension, under both sodium replete- and -deplete conditions: 1) acute depressor and PRA responses to CEI are modulated by the same factors that influence responses of normotensive controls; 2) larger absolute depressor responses to CEI appear to be a physiologic function of higher initial pressure; and 3) blood pressure excess over littermate controls is largely sustained by CEI-resistant factors, potentially including the known volume excess in coarcted dogs.

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