Angiotensin-converting enzyme inhibition in patients with essential hypertension.
The antihypertensive action of angiotensin-converting enzyme (ACE) inhibitors may be related to inhibition of systemic and local vascular angiotensin-II formation, to a potentiation of the local vascular kinin system with secondary stimulation of prostacyclin synthesis, and also to their effects on the central nervous system as well as on renal hemodynamics and excretory function. More detailed studies in patients with severe hypertension, previously not adequately controlled by conventional therapy with a diuretic, a beta-blocking agent and a vasodilator dihydralazine, showed that addition of the ACE inhibitor ramipril normalized systolic and diastolic blood pressure (BP) without hypotensive episodes or reflex tachycardia. ACE inhibition caused a change in the baroreceptor set point as we had previously demonstrated in healthy subjects, but baroreceptor sensitivity was not affected and the pressure response to exogenous norepinephrine remained unchanged by ACE inhibition. Despite the significant reduction in BP in our patients, endogenous creatinine clearance remained unaltered. Furthermore, the decrease in BP is accompanied by an initial natriuresis probably contributing to the BP-lowering effect of ACE inhibitors. Decreased proximal tubular reabsorption may include enhanced urate clearance reflected by a decrease in serum urate concentration which we observed despite continuous diuretic treatment. ACE inhibition also prevents secondary aldosteronism and thereby avoids renal potassium loss. In our patients this resulted in a 10% decrease in urinary potassium excretion and a small rise in serum potassium concentration. Redistribution of intrarenal blood flow with increased medullary flow, in addition, will antagonize the hydroosmotic effect of vasopressin, thus resulting in a rise in free-water clearance.(ABSTRACT TRUNCATED AT 250 WORDS)
Kramer
H J
HJ
Medizinische Poliklinik, University of Bonn, FRG.
Predel
H G
HG
Meyer-Lehnert
H
H
D000136:Acid-Base Equilibrium / Q000187:drug effects; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D007684:Kidney Tubules / Q000187:drug effects / Q000503:physiopathology; D011311:Pressoreceptors / Q000187:drug effects / Q000502:physiology; D012079:Renal Circulation / Q000187:drug effects
D000806:Angiotensin-Converting Enzyme Inhibitors