RAA system and cardiovascular control in normal subjects, hypertensives and patients with congestive heart failure

G. Seravalle, B. M. Cattaneo, C. Giannattasio, R. Perondi, A. Saino, G. Grassi, G. Mancia

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The involvement of the renin-angiotensin-aldosterone (RAA) system, particularly angiotensin II, in the pathogenesis of hypertension is widely acknowledged and is supported by several observations: the RAA system has been shown to be critically involved in the development of some experimental hypertensions; activation of the RAA system appears to be the crucial factor involved in the maintenance of the BP elevation in some antihypertensive patients; while drugs which interfere with the production of angiotensin II reduce BP in a large number of hypertensive patients. It is now clear that the chronic BP elevations caused by circulating (and perhaps locally produced) angiotensin II may have adverse effects on organ function and protection: for example, induction of cardiac hypertrophy and vascular hypertrophy and/or hyperplasia, reduction of arterial compliance and reduction in vagal tone and facilitation of sympathetic activity on cardiac and vascular targets. At the cardiac level, the renin-angiotensin sympathetic interaction may enhance electrical instability, thereby favouring arrhythmias and increasing mortality after a myocardial infarction. It finally enhances coronary vasoconstriction in man, producing or favouring myocardial ischaemia.

Original languageEnglish
JournalJournal of Human Hypertension
Volume7
Issue numberSUPPL. 2
Publication statusPublished - 1993

Fingerprint

Renin-Angiotensin System
Angiotensin II
Heart Failure
Blood Vessels
Hypertension
Angiotensins
Cardiomegaly
Vasoconstriction
Renin
Hypertrophy
Antihypertensive Agents
Compliance
Hyperplasia
Myocardial Ischemia
Cardiac Arrhythmias
Myocardial Infarction
Maintenance
Mortality
Pharmaceutical Preparations

Keywords

  • Cardiovascular control
  • Congestive heart failure
  • RAA system

ASJC Scopus subject areas

  • Internal Medicine

Cite this

RAA system and cardiovascular control in normal subjects, hypertensives and patients with congestive heart failure. / Seravalle, G.; Cattaneo, B. M.; Giannattasio, C.; Perondi, R.; Saino, A.; Grassi, G.; Mancia, G.

In: Journal of Human Hypertension, Vol. 7, No. SUPPL. 2, 1993.

Research output: Contribution to journalArticle

Seravalle, G. ; Cattaneo, B. M. ; Giannattasio, C. ; Perondi, R. ; Saino, A. ; Grassi, G. ; Mancia, G. / RAA system and cardiovascular control in normal subjects, hypertensives and patients with congestive heart failure. In: Journal of Human Hypertension. 1993 ; Vol. 7, No. SUPPL. 2.
@article{69c4133af8ac4c759ccd33e23540c4da,
title = "RAA system and cardiovascular control in normal subjects, hypertensives and patients with congestive heart failure",
abstract = "The involvement of the renin-angiotensin-aldosterone (RAA) system, particularly angiotensin II, in the pathogenesis of hypertension is widely acknowledged and is supported by several observations: the RAA system has been shown to be critically involved in the development of some experimental hypertensions; activation of the RAA system appears to be the crucial factor involved in the maintenance of the BP elevation in some antihypertensive patients; while drugs which interfere with the production of angiotensin II reduce BP in a large number of hypertensive patients. It is now clear that the chronic BP elevations caused by circulating (and perhaps locally produced) angiotensin II may have adverse effects on organ function and protection: for example, induction of cardiac hypertrophy and vascular hypertrophy and/or hyperplasia, reduction of arterial compliance and reduction in vagal tone and facilitation of sympathetic activity on cardiac and vascular targets. At the cardiac level, the renin-angiotensin sympathetic interaction may enhance electrical instability, thereby favouring arrhythmias and increasing mortality after a myocardial infarction. It finally enhances coronary vasoconstriction in man, producing or favouring myocardial ischaemia.",
keywords = "Cardiovascular control, Congestive heart failure, RAA system",
author = "G. Seravalle and Cattaneo, {B. M.} and C. Giannattasio and R. Perondi and A. Saino and G. Grassi and G. Mancia",
year = "1993",
language = "English",
volume = "7",
journal = "Journal of Human Hypertension",
issn = "0950-9240",
publisher = "Nature Publishing Group",
number = "SUPPL. 2",

}

TY - JOUR

T1 - RAA system and cardiovascular control in normal subjects, hypertensives and patients with congestive heart failure

AU - Seravalle, G.

AU - Cattaneo, B. M.

AU - Giannattasio, C.

AU - Perondi, R.

AU - Saino, A.

AU - Grassi, G.

AU - Mancia, G.

PY - 1993

Y1 - 1993

N2 - The involvement of the renin-angiotensin-aldosterone (RAA) system, particularly angiotensin II, in the pathogenesis of hypertension is widely acknowledged and is supported by several observations: the RAA system has been shown to be critically involved in the development of some experimental hypertensions; activation of the RAA system appears to be the crucial factor involved in the maintenance of the BP elevation in some antihypertensive patients; while drugs which interfere with the production of angiotensin II reduce BP in a large number of hypertensive patients. It is now clear that the chronic BP elevations caused by circulating (and perhaps locally produced) angiotensin II may have adverse effects on organ function and protection: for example, induction of cardiac hypertrophy and vascular hypertrophy and/or hyperplasia, reduction of arterial compliance and reduction in vagal tone and facilitation of sympathetic activity on cardiac and vascular targets. At the cardiac level, the renin-angiotensin sympathetic interaction may enhance electrical instability, thereby favouring arrhythmias and increasing mortality after a myocardial infarction. It finally enhances coronary vasoconstriction in man, producing or favouring myocardial ischaemia.

AB - The involvement of the renin-angiotensin-aldosterone (RAA) system, particularly angiotensin II, in the pathogenesis of hypertension is widely acknowledged and is supported by several observations: the RAA system has been shown to be critically involved in the development of some experimental hypertensions; activation of the RAA system appears to be the crucial factor involved in the maintenance of the BP elevation in some antihypertensive patients; while drugs which interfere with the production of angiotensin II reduce BP in a large number of hypertensive patients. It is now clear that the chronic BP elevations caused by circulating (and perhaps locally produced) angiotensin II may have adverse effects on organ function and protection: for example, induction of cardiac hypertrophy and vascular hypertrophy and/or hyperplasia, reduction of arterial compliance and reduction in vagal tone and facilitation of sympathetic activity on cardiac and vascular targets. At the cardiac level, the renin-angiotensin sympathetic interaction may enhance electrical instability, thereby favouring arrhythmias and increasing mortality after a myocardial infarction. It finally enhances coronary vasoconstriction in man, producing or favouring myocardial ischaemia.

KW - Cardiovascular control

KW - Congestive heart failure

KW - RAA system

UR - http://www.scopus.com/inward/record.url?scp=0027200448&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027200448&partnerID=8YFLogxK

M3 - Article

VL - 7

JO - Journal of Human Hypertension

JF - Journal of Human Hypertension

SN - 0950-9240

IS - SUPPL. 2

ER -