A carregar...

The pressor actions of noradrenaline and angiotension II in chronic autonomic failure treated with indomethacin.

1 Indomethacin treatment of postural hypotension in four patients with chronic autonomic failure increased their pressor supersensitivity to intravenous noradrenaline without causing fluid retention. 2 All patients were supersensitive to angiotensin II in spite of normal levels of plasma renin activ...

ver descrição completa

Na minha lista:
Detalhes bibliográficos
Main Authors: Davies, I B, Bannister, R, Hensby, C, Sever, P S
Formato: Artigo
Idioma:English
Publicado em: 1980
Assuntos:
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC1430064/
https://ncbi.nlm.nih.gov/pubmed/7437238
Tags: Adicionar Tag
Sem tags, seja o primeiro a adicionar uma tag!
id pubmed-1430064
record_format dspace
spelling pubmed-14300642008-01-14 The pressor actions of noradrenaline and angiotension II in chronic autonomic failure treated with indomethacin. Davies, I B Bannister, R Hensby, C Sever, P S Br J Clin Pharmacol Research Article 1 Indomethacin treatment of postural hypotension in four patients with chronic autonomic failure increased their pressor supersensitivity to intravenous noradrenaline without causing fluid retention. 2 All patients were supersensitive to angiotensin II in spite of normal levels of plasma renin activity in the supine position and therefore (by inference) of angiotensin II. This suggests that in autonomic failure, the degree of angiotensin receptor occupancy by endogenous angiotensin II is not important in determining pressor sensitivity to exogenous angiotensin II. Indomethacin increased the pressor supersensitivity to angiotensin II in all patients. 3 Indomethacin treatment decreased supine plasma renin activity to 50% of the level present before indomethacin treatment. 4 Indomethacin increased the lying but not the standing blood pressure. The failure to raise the standing pressure may be the result of the additional postural stress overcoming any vasoconstriction resulting from the increased sensitivity of vascular receptors to noradrenaline. The decrease in plasma renin activity could also contribute to the failure of indomethacin to prevent a fall in blood pressure on standing. 5 In our patients the excretion of the main urinary metabolite (PGFM) of prostaglandin F2 alpha was higher than recorded previously in normal controls. During treatment with indomethacin, plasma indomethacin levels were in the range at which inhibition of prostaglandin synthesis occurs and the excretion of PGFM was decreased. 6 Indomethacin was not effective in the treatment of postural hypotension in these patients with autonomic failure. 1980-09 /pmc/articles/PMC1430064/ /pubmed/7437238 Text en
institution US National Library of Medicine
collection PubMed Central
language English
format Article
topic Research Article
spellingShingle Research Article
Davies, I B
Bannister, R
Hensby, C
Sever, P S
The pressor actions of noradrenaline and angiotension II in chronic autonomic failure treated with indomethacin.
description 1 Indomethacin treatment of postural hypotension in four patients with chronic autonomic failure increased their pressor supersensitivity to intravenous noradrenaline without causing fluid retention. 2 All patients were supersensitive to angiotensin II in spite of normal levels of plasma renin activity in the supine position and therefore (by inference) of angiotensin II. This suggests that in autonomic failure, the degree of angiotensin receptor occupancy by endogenous angiotensin II is not important in determining pressor sensitivity to exogenous angiotensin II. Indomethacin increased the pressor supersensitivity to angiotensin II in all patients. 3 Indomethacin treatment decreased supine plasma renin activity to 50% of the level present before indomethacin treatment. 4 Indomethacin increased the lying but not the standing blood pressure. The failure to raise the standing pressure may be the result of the additional postural stress overcoming any vasoconstriction resulting from the increased sensitivity of vascular receptors to noradrenaline. The decrease in plasma renin activity could also contribute to the failure of indomethacin to prevent a fall in blood pressure on standing. 5 In our patients the excretion of the main urinary metabolite (PGFM) of prostaglandin F2 alpha was higher than recorded previously in normal controls. During treatment with indomethacin, plasma indomethacin levels were in the range at which inhibition of prostaglandin synthesis occurs and the excretion of PGFM was decreased. 6 Indomethacin was not effective in the treatment of postural hypotension in these patients with autonomic failure.
author Davies, I B
Bannister, R
Hensby, C
Sever, P S
author_facet Davies, I B
Bannister, R
Hensby, C
Sever, P S
author_sort Davies, I B
title The pressor actions of noradrenaline and angiotension II in chronic autonomic failure treated with indomethacin.
title_short The pressor actions of noradrenaline and angiotension II in chronic autonomic failure treated with indomethacin.
title_full The pressor actions of noradrenaline and angiotension II in chronic autonomic failure treated with indomethacin.
title_fullStr The pressor actions of noradrenaline and angiotension II in chronic autonomic failure treated with indomethacin.
title_full_unstemmed The pressor actions of noradrenaline and angiotension II in chronic autonomic failure treated with indomethacin.
title_sort pressor actions of noradrenaline and angiotension ii in chronic autonomic failure treated with indomethacin.
publishDate 1980
url https://ncbi.nlm.nih.gov/pmc/articles/PMC1430064/
https://ncbi.nlm.nih.gov/pubmed/7437238
_version_ 1760307785346580480