PATHOLOGICAL CONSEQUENCES OF INCREASED ANGIOTENSIN-II ACTIVITY

Citation
Cm. Ferrario et Jm. Flack, PATHOLOGICAL CONSEQUENCES OF INCREASED ANGIOTENSIN-II ACTIVITY, Cardiovascular drugs and therapy, 10(5), 1996, pp. 511-518
Citations number
99
Categorie Soggetti
Pharmacology & Pharmacy","Cardiac & Cardiovascular System
ISSN journal
09203206
Volume
10
Issue
5
Year of publication
1996
Pages
511 - 518
Database
ISI
SICI code
0920-3206(1996)10:5<511:PCOIAA>2.0.ZU;2-R
Abstract
Advances in molecular medicine and pharmacology have allowed clinician s to critically reassess the renin-angiotensin system. Angiotensin II (AII) participates in the control of cardiovascular function and elect rolyte balance, and plays a part in the regulation of cellular oncogen es and the expression of growth factors. The expression of the protein s of the renin-angiotensin system in organs other than the kidneys sug gests that these diverse actions are associated with the peptide in th e local environment. Tissue renin-angiotensin activity has prompted th e investigation of alternate pathways for the production of AII and ch aracterization of novel forms of angiotensin peptides that counteract the vasoconstrictor and proliferative actions of AII. The heptapeptide angiotensin-(1-7) appears to be critically involved in regulating the angiotensinogen activity of AII through stimulation of vasodilator pr ostaglandins and release of nitric oxide. Study in this area has been accelerated by the identification of receptors that convey the actions of angiotensin peptides at the cellular level and the pharmacologic c haracterization of agents that inhibit the ability of AII to bind to t arget receptors. The introduction of a new class of orally active AII- receptor blockers has provided a specific test of the role of AII in t he development of essential hypertension and the potential for improve d therapy for hypertension and cardiac and vascular sequelae.