Endothelium-Dependent Relaxation in the Isolated Rat Kidney

Stephan, Dominique; Billing, Alain; Krieger, Jean-Paul; Grima, Michèle; Fabre, M; Hofner, Maurice; Imbs, Jean-Louis; Barthelmebs, Mariette

doi:10.1097/00005344-199512000-00003

Cited by 42 publications

(24 citation statements)

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“…Thus, a tonic release of NO contributed to the basal relaxed state and exerted a direct vasodilator eect in the in vitro perfused kidney. This ®nding was consistent with those reported by most of the authors using the isolated perfused rat kidney (Radermacher et al, 1990;Gardes et al, 1994;Bryant et al, 1995;Kaufmann et al, 1995;Stephan et al, 1995). None of the AT-R antagonists used, under any experimental conditions, was able to signi®-cantly aect basal vascular resistance.…”

Section: Blockade Of the No/cgmp Pathway Increases Basal Vascular Ressupporting

confidence: 91%

AT₂‐antagonist sensitive potentiation of angiotensin II‐induced vasoconstrictions by blockade of nitric oxide synthesis in rat renal vasculature

Muller

Endlich

Barthelmebs

et al. 1997

British J Pharmacology

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1 Although the actions of angiotensin II (Ang II) on renal haemodynamics appear to be mediated by activation of the AT 1 receptor subtype, AT 2 binding sites have also been evidenced in the adult kidney vasculature. As NO is known to mask part of the renal eects of vasoconstrictor drugs, we queried whether the Ang II-induced vasoconstrictions could occur via multiple receptor subtypes during inhibition of NO synthesis. We explored the eect of AT 1 and AT 2 receptor (AT-R) antagonists on Ang II-induced pressure increases during NO synthase or soluble guanylyl cyclase inhibition in rat isolated kidneys perfused in the presence of indomethacin at constant¯ow in a single-pass circuit. 2 In the absence of NO blockade, the AT 1 -R antagonist L-158809 (500 nM) antagonized the Ang IIinduced vasoconstrictions, while the AT 2 -R antagonist PD-123319 (500 nM) had no eect. 3 Perfusing kidneys in the presence of either NO synthase inhibitors, L-NAME (100 mM) or L-NOARG (1 mM), or soluble guanylyl cyclase inhibitor, LY-83583 (10 mM), signi®cantly increased both molar pD 2 (from 9.40+0.25 to 10.36+0.11) and E max values (from 24.9+3.1 to 79.9+4.9 mmHg) of the concentration ± response curve for Ang II-induced vasoconstriction. 4 In the presence of L-NAME, 500 nM L158809 abolished the Ang II-induced vasoconstrictions whatever the concentration tested. On the other hand, 500 nM PD-123319 reversed the left shift of the concentration ± response curve for Ang II (molar pD 2 value 9.72+0.13) leaving E max value unaected (91.3+7.6 mmHg). 5 In the presence of L-NAME, the potentiated vasoconstriction induced by 0.1 nM and the augmented vasoconstriction induced by 10 nM Ang II were fully inhibited in a concentration-dependent manner by L-158809 (0.05 ± 500 nM). By contrast, PD-123319 (0.5 ± 500 nM) did not aect the 10 nM Ang II-induced vasoconstriction and concentration-dependently decreased the 0.1 nM Ang II-induced vasoconstriction plateauing at 65% inhibition above 5 nM antagonist. 6 Similar to PD-123319, during NO blockade the AT 2 -R antagonist CGP-42112A at 5 nM decreased by 50% the 0.1 nM Ang II-induced vasoconstriction and at 500 nM had no eect on 10 nM Ang II-induced vasoconstriction. 7 In conclusion, the renal Ang II-induced vasoconstriction, which is antagonized only by AT 1 -R antagonist in the presence of endogenous NO, becomes sensitive to both AT 1 -and AT 2 -R antagonists during NO synthesis inhibition. While AT 1 -R antagonist inhibited both L-NAME-potentiated and -augmented components of Ang II-induced vasoconstriction, AT 2 -R antagonists inhibited only the L-NAME-potentiated component.

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Section: Blockade Of the No/cgmp Pathway Increases Basal Vascular Ressupporting

confidence: 91%

AT₂‐antagonist sensitive potentiation of angiotensin II‐induced vasoconstrictions by blockade of nitric oxide synthesis in rat renal vasculature

Muller

Endlich

Barthelmebs

et al. 1997

British J Pharmacology

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“…Relaxation by EDHF seems more prominent in arteries with small diameter, unlike NO that plays a bigger role in large vessels (Hwa et al, 1994;Garland et al, 1995). A limited contribution of NO in vasodilation has previously been reported in the kidney for BK (Fulton et al, 1992) and for ACh (Stephan et al, 1995). The apparent predominance of EDHF in endothelium-dependent vasodilation in small resistance arteries is therefore not speci®c for an agonist.…”

Section: Discussionmentioning

confidence: 83%

“…Two concentrations of ACh (3 and 30 nM) were tested with the same time-interval as used for Tyr(Me) 8 BK. The highest concentrations tested (10 and 30 nM respectively) were previously shown to induce maximal renal vasodilator responses (BagateÂ et al, 1999;Stephan et al, 1995). A supramaximal concentration of SNP (10 mM) was administered at the end of the experiments.…”

Section: Experimental Protocolsmentioning

confidence: 99%

“…N G -nitro-L-arginine (L-NOARG, 100 mM) and indomethacin (30 mM) were added alone or together to the perfusate to inhibit NO synthase (NOS) and cyclo-oxygenase (COX) activity. A nonionic detergent, 3-[(3-cholamidopropyl)-dimethyl-ammonio]-1-propane sulphonate (CHAPS), was used to remove endothelial cells from intrarenal blood vessels as described by Bhardwaj & Moore (1988) and used before (Stephan et al, 1995). However, the usual dose of CHAPS (4.7 mg ml 71 , 30-s infusion) altered smooth muscle vascular reactivity in Tyrode-perfused kidneys as was obvious from hyporesponsiveness to prostaglandin F 2a and blunting of SNP-induced vasorelaxation.…”

Section: Experimental Protocolsmentioning

confidence: 99%

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Signal transduction pathways involved in kinin B₂ receptor‐mediated vasodilation in the rat isolated perfused kidney

Bagaté

Grima

Imbs

et al. 2001

British J Pharmacology

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1 The signal transduction pathways involved in kinin B 2 receptor-related vasodilation were investigated in rat isolated perfused kidneys. During prostaglandin F 2a or KCl-induced constriction, the vasodilator response to a selective B 2 receptor agonist, Tyr(Me) BK by more than 60%, while inhibition of the cannabinoid CB 1 receptor (SR 141716A) had only a moderate eect. 5 Acetylcholine induced a concentration-dependent relaxation with characteristics nearly similar to the response to Tyr(Me) 8 BK. In contrast, the relaxation elicited by sodium nitroprusside was potentiated in the absence of NO (L-NOARG or removal of endothelium) but remained unchanged otherwise. 6 These results indicate that the activation of kinin B 2 receptors in the rat isolated kidney elicits an endothelium-dependent vasorelaxation, mainly dependent on the activation of charybdotoxinsensitive Ca 2+ -activated K + channels. In addition, cytochrome P450 derivatives appear to be involved.

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“…7,8 L-arginine analogues such as N-nitro-Larginine (NOLA) can inhibit production of NO from L-arginine by competing for NO synthase. CsA exposure in vitro reduces endothelium-dependent vasorelaxation 5,9 attributed to decreased NO activity in resistance vessels 10 and decreased NO production. 4 Endothelin-1 (ET-1) is a potent vasoconstrictor acting via vascular smooth muscle ETA and ETB receptors.…”

Section: Introductionmentioning

confidence: 99%

Modulation of nitric oxide improves cyclosporin A-induced hypertension in rats and primates

et al. 1998

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Endothelium-Dependent Relaxation in the Isolated Rat Kidney

Cited by 42 publications

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AT₂‐antagonist sensitive potentiation of angiotensin II‐induced vasoconstrictions by blockade of nitric oxide synthesis in rat renal vasculature

AT₂‐antagonist sensitive potentiation of angiotensin II‐induced vasoconstrictions by blockade of nitric oxide synthesis in rat renal vasculature

Signal transduction pathways involved in kinin B₂ receptor‐mediated vasodilation in the rat isolated perfused kidney

Modulation of nitric oxide improves cyclosporin A-induced hypertension in rats and primates

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Endothelium-Dependent Relaxation in the Isolated Rat Kidney

Cited by 42 publications

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AT2‐antagonist sensitive potentiation of angiotensin II‐induced vasoconstrictions by blockade of nitric oxide synthesis in rat renal vasculature

AT2‐antagonist sensitive potentiation of angiotensin II‐induced vasoconstrictions by blockade of nitric oxide synthesis in rat renal vasculature

Signal transduction pathways involved in kinin B2 receptor‐mediated vasodilation in the rat isolated perfused kidney

Modulation of nitric oxide improves cyclosporin A-induced hypertension in rats and primates

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AT₂‐antagonist sensitive potentiation of angiotensin II‐induced vasoconstrictions by blockade of nitric oxide synthesis in rat renal vasculature

AT₂‐antagonist sensitive potentiation of angiotensin II‐induced vasoconstrictions by blockade of nitric oxide synthesis in rat renal vasculature

Signal transduction pathways involved in kinin B₂ receptor‐mediated vasodilation in the rat isolated perfused kidney