Role of the Renin-Angiotensin System in Renal Hypertension. An Experimental Approach

Einflu� von Indometacin auf den Blutdruck in Ratten mit renovascul�rer Hypertonie: Abh�ngigkeit von der Plasmareninaktivit�t

“…The predominant function of the reninangiotensin axis in sustaining both normal and elevated PB in volume depleted rats is demonstrated by the finding that indomethacin decreased systolic blood pressure by decreasing elevated plasma renin levels. This supports the theory that maintenance of blood pressure in renovascular hypertension under conditions of volume depletion is dependent on a functioning renin-angiotensinsystem (Helmchen and Kneissler 1976;Helmchen et al 1978 ;Freeman et al 1979).…”

Endotheliotropic (hemolytic) nephroangiopathy and its various manifestation forms (thrombotic microangiopathy, primary malignant nephrosclerosis, hemolytic-uremic syndrome)

“…It is difficult to decide to what extent these consecutive arterial lesions are the immediate result of the initial endothelial or intimal lesion and to what extent they are the consequence of developing malignant hypertension; it can be shown in the Goldblatt experiment that malignant hypertension alone can induce similar nephroangiopathic lesions [21,40]. The influence of malignent hypertension on the arterial lesion is therefore doubtless significant.…”

Structural analysis of the formation of glomerular microaneurysms in the Habu venom model

“…If the capillary blood pressure rises above a certain level the mesangial cell -GBM connections may burst [39]. As seen in desoxycorticosterone acetate (DOCA) hypertension [9,18] and in the "one clip -two kidney" model of hypertension [10] sudden, as well as gradual but persistent, rise in capillary pressure may result in disconnections of the GBM from the mesangium. In both models glomerular microaneurysms develop.…”

“…Although lysis of the mesangial matrix is most probably the main causative factor in the IPK [37], the lack of microaneurysms (despite widespread capillary ballooning) may also be explained by the short duration of the experiments (maximum 2 h). The high pressure models (uninephrectomised-DOCA-hypertension, one clip-two kidneys model [9,10,39]) and especially the removal of the clip in the latter model associated with the sudden rise of blood pressure in the formerly clipped kidney are different, since the mesangium may be expected to be intact (or even hypertrophied as has been shown in the DOCA model [18]). The lesions probably result from excessive mechanical load at the mesangium by elevated distending forces.…”

“…Many other reports have followed [6,24,25,35] and identical or similar lesions have been observed after poisoning with other snake venoms [31,32,38] or various chemicals and drugs [1, S. Uiker • W. Kriz (~) Institute of Anatomy and Cell Biology I, University of Heidelberg, Im Neuenheimer Feld 307, D-69120 Heidelberg, Germany 14,42], after temporary glomerular ischaemia [39], systemic hypertension [9,10,18], after intravenous injection of anti-Thy 1-1 antibodies [2,12,40,44] and in certain types of glomerulonephritis including diabetic glomerulosclerosis [5,11,27,30,34,43].…”