Pharmacological interferences with the renin-angiotensin system.
The important role of the renin-angiotensin system (RAS) in the maintenance of high blood pressure in certain forms of hypertension is well established. Inhibition of the RAS has therefore been studied with the aim to develop antihypertensive agents. Pharmacologic interferences with the RAS are possible at all steps of the formation, action and degradation of angiotensin II (ANG II). Renin activity can be inhibited by peptide analogues of angiotensinogen, peptides derived from the amino terminal sequence of pro-renin, inhibitors of acid proteases (pepstatin) and by specific renin antibodies. Inhibitors of the converting enzyme also prevent the formation of ANG II. ANG II receptor blockers (saralasin) prevent the action of the effector peptide of the RAS at the target cells. While some modes of intervention are still theoretical or experimental possibilities, others, e.g. inhibition of converting enzyme, are already used clinically for antihypertensive treatment.
D000806:Angiotensin-Converting Enzyme Inhibitors; D000808:Angiotensinogen / Q000494:pharmacology; D000818:Animals; D000906:Antibodies / Q000032:analysis; D004792:Enzyme Precursors / Q000378:metabolism; D006801:Humans; D010436:Pepstatins / Q000494:pharmacology; D012083:Renin / Q000276:immunology / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000187:drug effects*
D000806:Angiotensin-Converting Enzyme Inhibitors; D000906:Antibodies; D004792:Enzyme Precursors; D010436:Pepstatins; D000808:Angiotensinogen; C014195:Streptomyces pepsin inhibitor; D012083:Renin; C031375:pepstatin