Renal microvascular actions of angiotensin II fragments

Rodijnen, William F. van; Lambalgen, Ton A. van; Wijhe, Michiel H. van; Tangelder, G. J.; Wee, Piet M. ter

doi:10.1152/ajprenal.00121.2001

Cited by 28 publications

(41 citation statements)

References 32 publications

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“…Whereas it is accepted that renal infusion of Ang II produces an increase in BP with decreased cortical blood flow and natriuresis, there is controversy on the renal effect of Ang IV. It has been reported that high concentrations of Ang IV are able to activate the AT 1 receptor, inducing renal microvascular constriction which suggest that AT 4 do not exert a vasodilator action in the kidney [30]. In contrast, other authors have reported that infusion of Ang IV increased natriuresis and renal cortical blood flow.…”

Section: Discussionmentioning

confidence: 97%

Angiotensinase activities in the kidney of renovascular hypertensive rats

et al. 2003

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In spite of the well-known contribution of angiotensin II (Ang II) in the pathogenesis of Goldblatt two-kidney one clip (G2K1C) hypertension, the importance of other Ang peptides, such as Ang III, Ang IV or Ang 2-10, is scarcely understood. The functional status of these peptides depends on the action of several aminopeptidases called angiotensinases. The metabolism of Ang III to Ang IV by aminopeptidase M (AlaAP) and of Ang I to Ang 2-10 by aspartyl aminopeptidase (AspAP) was evaluated in the renal cortex and medulla of normotensive (Sham-operated) and hypertensive (G2K1C) rats, treated or not with the AT 1 receptor antagonist valsartan. The results demonstrated a highly significant increase of membrane-bound (MEMB) AlaAP in the cortex of the non-ischemic kidney of G2K1C rats compared with the kidney of normal rats and with the clipped kidney of G2K1C rats. This suggests an increased formation of Ang IV in the non-clipped kidney of G2R1C rats. Valsartan reduced MEMB AlaAP and AspAP activities in the renal cortex of normotensive and in the clipped kidney of hypertensive rats. The reduced metabolism of Ang III may prolong its half-life in valsartan-treated animals. These results suggest a role for AlaAP in renovascular hypertension. In addition, the higher AspAP activity of the renal cortex compared to medulla reflects its relative functional difference between both locations.

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Section: Discussionmentioning

confidence: 97%

Angiotensinase activities in the kidney of renovascular hypertensive rats

et al. 2003

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“…25 for an extensive description). Briefly, the rat was anesthetized with a combination of pentobarbital sodium (50 mg/kg ip, Sanofi Sante, Maassluis, The Netherlands) and ketamine (25 mg/kg im, Kombivet, Etten-Leur, The Netherlands).…”

Section: Methodsmentioning

confidence: 99%

Direct vasoconstrictor effect of prostaglandin E₂on renal interlobular arteries: role of the EP3 receptor

Rodijnen¹,

Korstjens²,

Legerstee³

et al. 2007

American Journal of Physiology-Renal Physiology

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van Rodijnen WF, Korstjens IJ, Legerstee N, ter Wee PM, Tangelder GJ. Direct vasoconstrictor effect of prostaglandin E 2 on renal interlobular arteries: role of the EP3 receptor. Am J Physiol Renal Physiol 292: F1094 -F1101, 2007. First published December 5, 2006; doi:10.1152/ajprenal.00351.2005.-Evidence indicates that prostaglandin E2 (PGE2) preferentially affects preglomerular renal vessels. However, whether this is limited to small-caliber arterioles or whether larger vessels farther upstream also respond to PGE2 is currently unclear. In the present study, we first investigated the effects of PGE 2 along the preglomerular vascular tree and subsequently focused on proximal interlobular arteries (ILAs). Proximal ILAs in hydronephrotic rat kidneys as well as isolated vessels from normal kidneys constricted in response to PGE2, both under basal conditions and after the induction of vascular tone. By contrast, smaller vessels, i.e., distal ILAs and afferent arterioles, exhibited PGE2-induced vasodilation. Endothelium removal and pretreatment of single, isolated proximal ILAs with an EP1 receptor blocker (SC51322, 1 mol/l) or a thromboxane A2 receptor blocker (SQ29548, 1 mol/l) did not prevent vasoconstriction to PGE2. Furthermore, in the presence of SC51322, responses of these vessels to PGE2 and the EP1/EP3 agonist sulprostone were superimposable, indicating that PGE2-induced vasoconstriction is mediated by EP3 receptors on smooth muscle cells. Immunohistochemical staining of proximal ILAs confirmed the presence of EP3 receptor protein on these cells and the endothelium. Adding PGE2 to normal isolated kidneys induced a biphasic flow response, i.e., an initial flow increase at PGE2 concentrations Յ0.1 mol/l followed by a flow decrease at 1 mol/l PGE2. Thus our results demonstrate that PGE2 affects multiple segments of the preglomerular vascular tree in a different way. At the level of the proximal ILAs, PGE2 had a direct vasoconstrictor action mediated by EP3 receptors. interlobular arteries; vasoconstriction PGE 2 IS ONE OF the major cyclooxygenase-derived products produced by the kidney (17). The actions of PGE 2 intrarenally include both tubular and vascular effects (2). The latter are important for regulating renal function under various circumstances. So far, the effects of PGE 2 on smaller pre-and postglomerular arterioles have mainly received attention. The postglomerular efferent arterioles were found to be insensitive to PGE 2 (4, 23), while for the preglomerular afferent arterioles (AAs) and distal interlobular arteries (ILAs) most studies indicated vasodilation (4,8,23), although vasoconstriction in certain instances has been reported as well (9, 23). Whether larger vessels further upstream of the glomerulus are also sensitive to PGE 2 is currently unknown. Previous studies have demonstrated that larger preglomerular vessels constrict in response to inflammatory mediators, such as serotonin and leukotrienes (5, 19), suggesting a similar mode of action for PGE 2 .In general, the actions of PGE 2 are m...

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“…27 Dose-dependent biphasic effects were also observed on BP in rats, as well as in rabbit aorta rings 28 and rat renal vessels. 29 In the light of these controversial data, we studied the interactions at the arterial level between the two vasoactive angiotensin peptides, emphasising the biphasic properties of Ang (1-7) and its influence on the vasoconstricting effects of Ang II.…”

Section: Introductionmentioning

confidence: 99%