Brain renin-angiotensin system in cognitive function: pre-clinical findings and implications for prevention and treatment of dementia.

Biochemical, physiological and functional studies suggest that the brain renin-angiotensin system (RAS) is regulated independently of the peripheral RAS. Also, all enzymes and peptides necessary for the biosynthesis of various angiotensins have been recognized within the central nervous system. There are divergent opinions concerning the localization of the different components of this system which is not fully understood.

Angiotensin peptides and their pleiotropic actions.

The concept of tissue renin-angiotensin systems (RAS) is now well established and it is now usual to think in terms of renal and tissue systems. At the same time it has emerged that angiotensin II (Ang II) is not the only biologically active peptide generated by the RAS. At least three others have been identified: the heptapeptide Ang III, the hexapeptide Ang IV and Ang 1-7.

Comparative study of the inhibitory effects of adrenomedullin on angiotensin II contraction in rat conductance and resistance arteries.

Adrenomedullin (ADM), a ubiquitous vasoactive peptide, has been the target of a multitude of studies concerning its effect on the vascular tone. The present work aims at clarifying a series of its interactions with the renin-angiotensin system. The study uses the rat aorta ring as a model of conductance vessels, with or without vascular endothelium, and the second order branch of rat mesenteric arteries as a model of resistance arteries.

Biphasic effects of angiotensin (1-7) and its interactions with angiotensin II in rat aorta.

Using isolated rat aortic rings perfused with Krebs-Henseleit saline, the vascular effects of angiotensin (1-7) (Ang [1-7]) and its interactions with angiotensin II (Ang II) were investigated. Ang (1-7) induced endothelium-dependent relaxation and vasodilating effects in preparations precontracted with phenylephrine. Without preconstriction, Ang (1-7) at high doses (10(-6) 10(-5) M) produced either a significant inhibition of Ang II-induced vasoconstriction or a non-tachyphylactic vasopressor response.