Endogenous Vasoactive Systems and the Pressor Effect of Acute N ω-Nitro-L-Arginine Methyl Ester Administration

Nafrialdi, Nafrialdi; Jover, Bernard; Mimran, A

doi:10.1097/00005344-199405000-00011

Cited by 28 publications

(24 citation statements)

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“…The acute pressor effect induced by inhibition of nitric oxide synthesis was not changed by pretreatment of rats with captopril (11,12) or enalapril (13). However, in dogs the hypertensive effect of L-NAME is reduced by captopril Table 1 -Effect of captopril and HOE 140 on L-NAME-induced hypertension.…”

Section: Intravenous Effect Of Bradykinin Before and After Hoe 140 (Pmentioning

confidence: 98%

Participation of kinins in the inhibitory action of captopril on acute hypertension induced by L-NAME in anesthetized rats

Moura

Leão

1997

Braz J Med Biol Res

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The aim of the present study was to investigate the role of bradykinin in the inhibitory action of captopril in hypertension induced by L-NAME in anesthetized rats. Male Wistar rats (260-320 g) were anesthetized with chloralose and arterial blood pressure was recorded with a polygraph pressure transducer. The hypertensive effect of L-NAME was studied in rats pretreated with saline, captopril or HOE 140 plus captopril. The effect of captopril was also studied during the sustained pressor effect of L-NAME. The acute pressor effect of L-NAME (10 mg/kg, iv) was significantly reduced by iv pretreatment with 2 mg/kg captopril (∆ increase of 49 ± 4.9 mmHg reduced to 20 ± 5.4 mmHg, P = 0.01). The pressor effect of L-NAME (∆ increase of 38 ± 4.8 mmHg) observed in rats pretreated with captopril and HOE 140 (0.1 mg/kg, iv) was not significantly different from that induced by L-NAME in rats pretreated with saline (P = 0.09). During the sustained pressor effect induced by L-NAME (∆ increase of 49 ± 4.9 mmHg) captopril induced a significant (P<0.05) reduction in arterial blood pressure (∆ decrease of 22 ± 3.0 mmHg). The present results demonstrate that the acute pressor effect of L-NAME is reduced by captopril and this inhibitory effect may be partly dependent on the potentiation of the vasodilator actions of bradykinin.

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Section: Intravenous Effect Of Bradykinin Before and After Hoe 140 (Pmentioning

confidence: 98%

Participation of kinins in the inhibitory action of captopril on acute hypertension induced by L-NAME in anesthetized rats

Moura

Leão

1997

Braz J Med Biol Res

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“…For instance, there are several reports demonstrating that Ang II stimulates endothelin-1 release from endothelial and mesangial cells (Emori et al, 1991;Imai et al, 1992;Kohno et al, 1992). Moreover, it has been documented that the potentiation by L-NAME of the effect of endogenous endothelium-derived endothelin, could be an important contributor to the pressure eect of NO synthesis inhibition (Ito et al, 1991;Nafrialdi et al, 1994;Qiu et al, 1995). Clearly, further studies are needed to elucidate which of these observations are valid in the present study.…”

Section: Blockade Of the No/cgmp Pathway Enhances Vasoconstrictor Resmentioning

confidence: 99%

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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“…Although the hypertension following the acute inhibition of NO synthesis is not generally considered to be driven by changes in the RAS (Lahera et al, 1991;Baylis et al, 1993;Nafrialdi et al, 1994), the accompanying increase of BP variability occurs in a frequency area which is partly dependent upon this humoral system (Ponchon & Elghozi, 1996). To investigate the contribution of the RAS to BP variability changes Brifish Journal of Pharmacology (1996) 119, [1085][1086][1087][1088][1089][1090][1091][1092] encountered during acute NO synthesis inhibition, we infused two doses of L-NAME and assessed the effects on BP and HR variabilities after blockade of the RAS by losartan.…”

Section: Introductionmentioning

confidence: 99%

Contribution of the renin‐angiotensin system to short‐term blood pressure variability during blockade of nitric oxide synthesis in the rat

Blanc

Gaudet

et al. 1996

British J Pharmacology

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1 The aim of this study was to investigate, by use of spectral analysis, (1) the blood pressure (BP) variability changes in the conscious rat during blockade of nitric oxide (NO) synthesis by the L-arginine analogue N0-nitro-L-arginine methyl ester (L-NAME); (2) the involvement of the renin-angiotensin system in these modifications, by use of the angiotensin II AT,-receptor antagonist losartan.2 Blockade of NO synthesis was achieved by infusion for 1 h of a low-dose (10 jug kg-' min-', i.v., n= 10) and high-dose (100 pg kg-' min-', i.v., n= 10) of L-NAME. The same treatment was applied in two further groups (2 x n = 10) after a bolus dose of losartan (10 mg kg-', i.v.). 3 Thirty minutes after the start of the infusion of low-dose L-NAME, systolic BP (SBP) increased (+ 10 + 3 mmHg, P< 0.01), with the effect being more pronounced 5 min after the end of L-NAME administration (+ 20 + 4 mmHg, P< 0.001). With high-dose L-NAME, SBP increased immediately (5 min: + 8+2 mmHg, P<0.05) and reached a maximum after 40 min (+ 53+4 mmHg, P<0.001); a bradycardia was observed (60 min: -44+ 13 beats min'-, P<0.01). 4 Low-dose L-NAME increased the low-frequency component (LF: 0.02-0.2 Hz) of SBP variability (50 min: 6.7+ 1.7 mmHg2 vs 3.4+0.5 mmHg2, P<0.05), whereas the high dose of L-NAME not only increased the LF component (40 min: 11.7 + 2 mmHg2 vs 2.7 + 0.5 mmHg2, P<0.001) but also decreased the mid frequency (MF: 0.2-0.6 Hz) component (60 min: 1.14+0.3 mmHg2 vs 1.7+0.1 mmHg2, P<0.05) of SBP. 5 Losartan did not modify BP levels but had a tachycardic effect (+45 beats min-'). Moreover, losartan increased MF oscillations of SBP (4.26 + 0.49 mmHg2 vs 2.43 + 0.25 mmHg2, P< 0.001), prevented the BP rise provoked by the low-dose of L-NAME and delayed the BP rise provoked by the high-dose of L-NAME. Losartan also prevented the amplification of the LF oscillations of SBP induced by L-NAME; the decrease of the MF oscillations of SBP induced by L-NAME was reinforced after losartan. 6 We conclude that the renin-angiotensin system is involved in the increase in variability of SBP in the LF range which resulted from the withdrawal of the vasodilating influence of NO. We propose that NO may counterbalance LF oscillations provoked by the activity of the renin-angiotensin system.

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Endogenous Vasoactive Systems and the Pressor Effect of Acute N ω-Nitro-L-Arginine Methyl Ester Administration

Cited by 28 publications

References 0 publications

Participation of kinins in the inhibitory action of captopril on acute hypertension induced by L-NAME in anesthetized rats

Participation of kinins in the inhibitory action of captopril on acute hypertension induced by L-NAME in anesthetized rats

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

Contribution of the renin‐angiotensin system to short‐term blood pressure variability during blockade of nitric oxide synthesis in the rat

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Endogenous Vasoactive Systems and the Pressor Effect of Acute N ω-Nitro-L-Arginine Methyl Ester Administration

Cited by 28 publications

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Participation of kinins in the inhibitory action of captopril on acute hypertension induced by L-NAME in anesthetized rats

Participation of kinins in the inhibitory action of captopril on acute hypertension induced by L-NAME in anesthetized rats

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

Contribution of the renin‐angiotensin system to short‐term blood pressure variability during blockade of nitric oxide synthesis in the rat

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