When is it useful to inhibit the renin-angiotensin system for treating hypertension?

The acute, 60 min blood pressure and plasma renin responses to an oral test dose of captopril given to a quietly seated patient can be used to gain information quickly on renin dependency or lack of it in a hypertensive situation. This information is verified by a baseline renin sodium profile test. These two diagnostic steps define either renin dependency or a sodium-volume mechanism involved in the vasoconstrictor. At the same time they also enable the complete diagnosis or exclusion of curable renovascular disease. For long-term therapy, pharmacologic inhibition of the renin-angiotensin system can be accomplished by or using converting enzyme inhibitors to block angiotensin II formation or beta receptor blocking drugs to block renin secretion and by combining the two. Inhibition of the renin-angiotensin system is the logical first step in antihypertensive drug therapy, both for acute hypertensive emergencies or chronic therapy, whenever the hypertension is largely or significantly renin dependent, i.e., in the high and normal renin forms of hypertension. This includes up to 70% of patients with essential hypertension. If converting enzyme inhibition or beta blockade is only partially effective, the two can be combined to achieve more complete blockade. A more popular alternative to this has been the addition of a diuretic as the second drug. However, this introduces well-known problems of diuretic therapy including dehydration, which eliminates the conceptual advantage of pure blockade of renin-mediated vasoconstriction, i.e., reducing pressure without reducing tissue flow.(ABSTRACT TRUNCATED AT 250 WORDS)