Background |
Angiotensin II is the biologically active product of the renin-angiotensin system. The octapeptide angiotensin II (molecular weight 1046) is the strongest physiological vasoconstrictor known. From a large protein precursor (preproangiontesinogen) synthesized in the liver it is liberated in a series of proteolytic steps catalyzed by enzymes from various tissues. Angiotensin II is very shortlived in the plasma: Once generated from angiotensin I, it is degraded further into physiologically inactive peptides by various plasma peptidases, at a plasma half life of less than a minute. Since the generation of angiotensin II from angiotensinogen via angiotensin I is strongly affected by changes of the renin activity, all external factors influencing renin activity are to be carefully considered: renin activity is elevated during pregnancy, after sodium depletion, in upright position, and under the influence of a range of drugs, e.g. oral contraceptives, adrenalin, antihypertensive vasodilatators, diuretics, high doses of spironalactone and progesterone. Factors decreasing renin activity are: horizontal position, increased sodium uptake, a-methyl-DOPA, L-DOPA, propranolol, reserpin, clonidin and old age. Renin activity is also subject to a diurnal rhythm with peak values in the morning. |
