Regional Renal Haemodynamics of Angiotensin II Infusion under Prostaglandin, Kinin or Converting Enzyme Inhibition in the Wistar Rat

Rudenstam, J.; Creutz, Jan; Göthberg, G; Karlström, Gunnar; Bergström, Göran

doi:10.1080/080370500453528

Cited by 5 publications

(4 citation statements)

References 7 publications

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“…However, in a later study they found that angiotensin converting enzyme inhibition (CEI) increased GFR in deep, but not in superficial glomeruli (Göransson & Sjöquist, 1985), and also increased free flow pressure in the loops of Henle but not in superficial proximal tubules (Göransson et al 1986). That is opposite to the relative fall in inner cortical filtration rate induced by losartan in the present study, possibly due to increased kinin formation induced by inhibition of converting enzyme (Nobes et al 1991; Rudenstam et al 2000) and not by losartan.…”

Section: Discussioncontrasting

confidence: 99%

Effect of exogenous and endogenous angiotensin II on intrarenal distribution of glomerular filtration rate in rats

Treeck

Roald

Tenstad

et al. 2002

The Journal of Physiology

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Exogenous angiotensin II (AngII) has a marked vasoconstrictor effect on most vascular beds, including the kidney. More important, a constant intrarenal formation of AngII, regulated mainly through renin release by the juxtaglomerular apparatus, provides a sustained contribution to vascular tone and resistance. A large number of studies have shown that AngII infusion causes relatively greater reduction of renal blood flow (RBF) than of glomerular filtration rate (GFR) and an increase in the filtration fraction, suggesting a preferential vasoconstriction in postglomerular resistance vessels (Navar et al. 1996). More conflicting results have been obtained on a possible preferential reduction of RBF in deep or superficial cortical layers, possibly due to a variable counter-regulation by prostaglandins or nitric oxide (NO) formation (Aiken & Vane, 1973;Aukland, 1976;Mattson & Roman, 1991;Hura & Stein, 1992;Pallone, 1994;Navar et al. 1996).In the 1970s many GFR distribution studies were performed using the Hanssen ferrocyanide technique (Hanssen, 1963) to test the hypothesis that renal sodium chloride excretion could be determined by the relative filtration rate in deep and superficial cortex. As summarized by Lameire et al. (1977) the results obtained in rats on varying salt intake Different changes in glomerular filtration rates (GFR) in deep and superficial glomeruli have been suggested to influence renal NaCl excretion and concentrating ability. Angiotensin II (AngII) has been implicated in such changes, but the experimental evidence has been conflicting, probably because of the methodological limitation of just one 'snapshot' measurement of local GFR per kidney. We have therefore studied the effect of AngII and AT 1 -receptor blockade on glomerular filtration in outer, middle and inner cortex (OC, MC and IC, respectively) in pentobarbitoneanaesthetised rats using the aprotinin (Ap) method, providing control and experimental measurements in the same kidney. Glomerular filtration rate per gram cortical tissue was measured based on 'free' glomerular filtration of Ap followed by complete tubular uptake and a 20 min sojourn in the proximal tubular cells before breakdown and incipient return to the plasma. Effect of exogenous and endogenous angiotensin II on intrarenal distribution of glomerular filtration rate in rats 125I-labelled Ap was injected I.V. to determine control Ap clearance, followed after 13 min by injection of AngII or the A1 type AngII receptor blocker losartan and 2 min thereafter by 131 Ilabelled Ap to determine clearance in the experimental period. Tracer activity in frequent blood samples and in tissue samples allowed calculation of GFR in the two periods. Mean GFR control values were: 1.13 ml min _1 in whole kidney and 1.44, 1.27 and 0.76 ml min _1 per gram cortical tissue in OC, MC and IC, respectively. The most sensitive and comprehensive measure of altered GFR distribution is the ratio between the relative filtration change in inner versus that in outer cortex, F = (IC E /IC C )/(OC E /OC C ), w...

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Section: Discussioncontrasting

confidence: 99%

Effect of exogenous and endogenous angiotensin II on intrarenal distribution of glomerular filtration rate in rats

Treeck

Roald

Tenstad

et al. 2002

The Journal of Physiology

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“…Intravenous administration of ANG II did not affect inner medullary blood flow in control rats and those pretreated with L-NAME but decreased it in indomethacin-pretreated rats, indicating that within the inner medulla, PGs, but not NO, seem to counteract the vasopressor effect of circulating ANG II (Badzynska et al, 2003). Rudenstam et al (2000) provided evidence suggesting that the increase in papillary blood flow in rats to ANG II seen after enalapril treatment is mediated possibly via effects of the ACE inhibitor on kinin breakdown and NO formation. In SHR, low-dose ANG II reduced renal medullary blood flow, and this effect was abolished by L-arginine given into the renal medulla; in SHR treated with enalapril for 10 weeks, ANG II did not alter the blood flow, but sensitivity to ANG II was unmasked after L-NAME was infused into the renal medulla ).…”

Section: In Vivo Study In Ratsmentioning

confidence: 99%

Interaction of Endothelial Nitric Oxide and Angiotensin in the Circulation

2007

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“…In rats and rabbits, infusions of angiotensin II reduce total renal blood flow (RBF) and cortical blood flow but have a lesser effect on medullary blood flow (MBF). [2][3][4][5] Angiotensin II can even increase MBF, especially when administered as a bolus. 6 -8 Nitric oxide synthase and/or cyclooxygenase blockade can enhance angiotensin II-induced reductions in MBF and abolish angiotensin II-induced increases in MBF, both of which are chiefly AT 1 mediated.…”

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confidence: 99%

Disparate Roles of AT ₂ Receptors in the Renal Cortical and Medullary Circulations of Anesthetized Rabbits

et al. 2003

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Abstract-The contributions of angiotensin II type 1 (AT 1 ) and type 2 (AT 2 ) receptors to the control of regional kidney blood flow were determined in pentobarbital-anesthetized rabbits. Intravenous candesartan (AT 1 antagonist; 10 g/kg plus 10 g · kg Ϫ1 · h Ϫ1) reduced mean arterial pressure (12%) and increased total renal blood flow (29%) and cortical laser-Doppler flux (18%) but not medullary laser-Doppler flux. Neither intravenous PD123319 (AT 2 antagonist; 1 mg/kg plus 1 mg · kg Ϫ1 · h Ϫ1 ) nor saline vehicle significantly affected these variables, and the responses to candesartan plus PD123319 were indistinguishable from those of candesartan alone. In vehicle-treated rabbits, renal-arterial infusions of angiotensin II (1 to 25 ng · kg Ϫ1 · min Ϫ1 ) and angiotensin III (5 to 125 ng · kg Ϫ1 · min Ϫ1) dose-dependently reduced renal blood flow (up to 51%) and cortical laser-Doppler flux (up to 50%) but did not significantly affect medullary laser-Doppler flux or arterial pressure. Angiotensin(1-7) (20 to 500 ng · kg Ϫ1 · min Ϫ1) had similar effects but of lesser magnitude. CGP42112A (20 to 500 ng · kg Ϫ1 · min Ϫ1) did not significantly affect these variables. After PD123319 administration, angiotensin II and angiotensin III dose-dependently increased medullary laser-Doppler flux (up to 84%), and reductions in renal blood flow in response to angiotensin II were enhanced. Candesartan abolished renal hemodynamic responses to the angiotensin peptides, even when given in combination with PD123319. We conclude that AT 2 receptor activation counteracts AT 1 -mediated vasoconstriction in the renal cortex but also counteracts AT 1 -mediated vasodilatation in vascular elements controlling medullary perfusion. These mechanisms might have an important effect on the control of medullary perfusion under conditions of activation of the renin-angiotensin system. Key Words: receptors, angiotensin Ⅲ kidney Ⅲ laser-Doppler flowmetry Ⅲ rabbits Ⅲ renal circulation T he medullary circulation contributes to the control of mean arterial pressure (MAP) and body fluid homeostasis. 1 However, the roles of angiotensin II type 1 (AT 1 ) and type 2 (AT 2 ) receptors in regulating regional kidney perfusion remain unclear. In rats and rabbits, infusions of angiotensin II reduce total renal blood flow (RBF) and cortical blood flow but have a lesser effect on medullary blood flow (MBF). [2][3][4][5] Angiotensin II can even increase MBF, especially when administered as a bolus. 6 -8 Nitric oxide synthase and/or cyclooxygenase blockade can enhance angiotensin II-induced reductions in MBF and abolish angiotensin II-induced increases in MBF, both of which are chiefly AT 1 mediated. 4,6 -12 However, the contributions of AT 2 receptors to these effects have received little attention, even though they are expressed in vessels that might contribute to MBF control (eg, afferent arterioles and vasa recta). 13 AT 2 -mediated counterregulatory vasodilatation can oppose AT 1 -mediated vasoconstriction. For example, in rat renalwrap hypertension, AT 2 re...

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Regional Renal Haemodynamics of Angiotensin II Infusion under Prostaglandin, Kinin or Converting Enzyme Inhibition in the Wistar Rat

Cited by 5 publications

References 7 publications

Effect of exogenous and endogenous angiotensin II on intrarenal distribution of glomerular filtration rate in rats

Effect of exogenous and endogenous angiotensin II on intrarenal distribution of glomerular filtration rate in rats

Interaction of Endothelial Nitric Oxide and Angiotensin in the Circulation

Disparate Roles of AT ₂ Receptors in the Renal Cortical and Medullary Circulations of Anesthetized Rabbits

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Regional Renal Haemodynamics of Angiotensin II Infusion under Prostaglandin, Kinin or Converting Enzyme Inhibition in the Wistar Rat

Cited by 5 publications

References 7 publications

Effect of exogenous and endogenous angiotensin II on intrarenal distribution of glomerular filtration rate in rats

Effect of exogenous and endogenous angiotensin II on intrarenal distribution of glomerular filtration rate in rats

Interaction of Endothelial Nitric Oxide and Angiotensin in the Circulation

Disparate Roles of AT 2 Receptors in the Renal Cortical and Medullary Circulations of Anesthetized Rabbits

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Disparate Roles of AT ₂ Receptors in the Renal Cortical and Medullary Circulations of Anesthetized Rabbits