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 language | English |
|---|---|
| Journal | Journal of Human Hypertension |
| Volume | 7 |
| Issue number | SUPPL. 2 |
| Publication status | Published - 1993 |
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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 journal › Article
}
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 -