[The renal renin-angiotensin system and its contribution to the regulation of glomerular hemodynamics].

It has been demonstrated in whole kidney and micropuncture studies that angiotensin II, either delivered systemically or formed locally, has a crucial role in the regulation of both afferent and efferent arteriolar resistances throughout the cortex. The angiotensin induced constriction on preglomerular arterioles has been further confirmed by direct assessments of segmental vascular responses during systemic or topical administration of the peptide. The preglomerular vasoconstrictor effects of the peptide is not restricted only to the afferent arteriole. Angiotensin II formed even beyond the glomerular circulation in the postglomerular capillary and/or interstitial environment can reduce glomerular and proximal tubular function. Recent findings on intrarenal angiotensin formation i. e. the existence and response of angiotensinogen mRNA to different experimental and clinical conditions, the high intrarenal conversion of angiotensin I to II, the higher concentration of angiotensin I in the blood than that of angiotensin II etc., all support the idea that the effects of angiotensin II on the renal hemodynamics may be mainly due to the effects of the locally formed peptide. Therefore it is especially important to emphasize that there are some differences observed between the effects of angiotensin II formed intrarenally versus delivered systemically on renal hemodynamics.