This chapter explains how the rennin-angiotensin system (RAS) plays an important role in the regulation of blood pressure under normal and pathophysiological conditions. The RAS interacts with the autonomic nervous system for blood pressure regulation, with angiotensin receptors localized to brain regions involved in modulation of both sympathetic and parasym-pathetic nervous system activity. Angiotensin converting enzyme (ACE), a lung-derived dipeptidyl carboxypeptidase, sub-sequently cleaves angiotensin I into angiotensin II, the main effector peptide of the RAS. Depending on the cell and tissue type, AT1 receptor activation is associated with inhibition of adenylyl cyclase, activation of phospholipase C or phosphoinositide hydrolysis. Angiotensin II stimulation of AT1 receptors induces vasoconstriction, sympathetic activation, suppression of baroreflex function, sodium and water reabsorption, cellular proliferation and hypertrophy, inflammation, oxidative stress and release of aldosterone, vasopressin and noradrenaline. The counterregulatory actions of angiotensin II and angiotensin-(1-7) suggest that the balance of these two peptides is important to cardiovascular physiology and pathophysiology.
|Original language||English (US)|
|Title of host publication||Primer on the Autonomic Nervous System|
|Number of pages||4|
|State||Published - Dec 1 2012|
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