[Physiology and pathophysiology of renal circulation].
An estimate of renal blood flow in the human kidney is possible with PAH-clearance, radiologic and radioisotopic techniques. But even animal experiments with clearance- and flow-measurements usually allow only a coarse evaluation of the renal blood flow. In the past, glomerular filtration has been determined by micropuncture methods. From changes in glomerular filtration, intrarenal alterations of flow resistance have been calculated. Using this method, resistance at different vascular levels could not be measured because the vessels of the mammalian kidney, except peritubular capillaries, vasa recta and single capillaries of the glomerulum, are not accessible to micropuncture. The recently developed split hydronephrotic kidney model allows investigation of almost all renal vessels. Thus it could be demonstrated that regulation of the renal blood flow is mediated not only by afferent and efferent arterioles, but also by arcuate and interlobular arteries. In this model, the effects of systemic blood pressure changes and local drug application on the renal vascular resistance were measured. Angiotensin II elicited pre- as well as postglomerular vasoconstriction, of which only a minor part was due to elevation of systemic blood pressure by Angiotensin II. Dopamine at low concentrations dilated especially the larger preglomerular arteries and, at higher concentrations, caused a vasoconstriction of these vessels. The vasodilatory response could be blocked by haloperidol, whereas the vasoconstrictory effect was abolished by phentolamine and propranolol. Calcium-channel-blockade by nitrendipine exerted a dose-dependent preglomerular vasodilation. Atrial natriuretic peptide (ANP) also dilated preglomerular vessel segments, but at higher doses it additionally induced a postglomerular vasoconstriction. Thus, increments of glomerular filtration by ANP could be explained by its hemodynamic effects.(ABSTRACT TRUNCATED AT 250 WORDS)
Steinhausen
M
M
I. Physiologisches Institut, Universität Heidelberg.
D058186:Acute Kidney Injury / Q000503:physiopathology; D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D005919:Glomerular Filtration Rate; D006706:Homeostasis; D006869:Hydronephrosis / Q000503:physiopathology*; D007671:Kidney Concentrating Ability; D051381:Rats; D012077:Renal Artery / Q000503:physiopathology; D012079:Renal Circulation
D000804:Angiotensin II
Physiologie und Pathophysiologie der Nierendurchblutung.