[Angiotensin-converting enzyme inhibition: direct and indirect mechanisms].
The introduction of angiotensin-converting-enzyme (ACE)-inhibitors into the analysis of the renin-angiotensin system (RAS) had broadened our knowledge of the integral role of renin and the kidney in circulatory homeostasis and has provided a pathophysiologically based concept for the treatment of hypertension. When the RAS is activated, as it is when sodium is restricted, the renal blood supply shows the most striking vasodilatation among vascular beds assessed after ACE-inhibition. Sodium excretion rises, there is a fall in blood-pressure, and plasma concentrations of angiotensin II (AII) and aldosterone are reduced. Conversely, with sodium loading the hemodynamic and hormonal effects of ACE-inhibitors are small. In 50-60% of normal or high-renin patients with essential hypertension ACE-inhibitors induce a potentiated acute renal response: renal blood flow and sodium excretion increase more than they do in the remainder of the hypertensives or in normal subjects. The responders of the hypertensive patients fail to increase renal blood flow or to enhance renal vascular responsiveness to infused AII when they shift from a low to a high sodium intake. The altered renal response of these "sodium-sensitive" hypertensives could be related to local activity of the RAS which is insufficiently suppressed by sodium loading. ACE-inhibition reverses this failure of the renal blood supply to respond to sodium loading. Kidneys of spontaneously hypertensive rats and the renin-rich kidney of Goldblatt-hypertensive rats show an increased tubulo glomerular (TG) feedback response as compared to normal kidneys. The change in TG-feedback response might be expected to contribute to the inability of the hypertensive kidney to respond adequately to sodium loading. ACE-inhibition reduces TG-feedback sensitivity. In renal artery stenosis glomerular capillary pressure tends to be maintained by an AII mediated rise in postglomerular resistance. Suppression of AII by ACE-inhibition reduces efferent vascular tone and thus filtration rate. There is a potential for interaction of ACE-inhibitors with the kallikrein and prostaglandin pathways as well as with the sympathetic nervous system and endogenous opioids. This may modify the renal and blood pressure responses to these compounds.
D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D002216:Captopril / Q000627:therapeutic use; D005246:Feedback; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D006978:Hypertension, Renovascular / Q000188:drug therapy; D007705:Kinins / Q000097:blood; D051381:Rats; D011918:Rats, Inbred SHR; D012079:Renal Circulation / Q000187:drug effects; D012084:Renin-Angiotensin System / Q000187:drug effects*; D012964:Sodium / Q000652:urine; D013318:Stroke Volume / Q000187:drug effects; D013722:Teprotide / Q000627:therapeutic use; D014655:Vascular Resistance / Q000187:drug effects; D014882:Water-Electrolyte Balance / Q000187:drug effects*
D000806:Angiotensin-Converting Enzyme Inhibitors; D007705:Kinins; D002216:Captopril; D012964:Sodium; D013722:Teprotide
Angiotensin-Conversions-Enzym-Hemmung: Direkte und indirekte renale Mechanismen.