Selective Inhibition of Pressor and Haemodynamic Effects of NG-Nitro-L-Arginine by Halothane

Wang, Yong Xiang; Abdelrahman, Aly M.; Pang, Catherine C.Y.

doi:10.1097/00005344-199310000-00010

Cited by 19 publications

(8 citation statements)

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“…Similar observations of the effects of L-NAME and L-NOARG on CO and TPR have been reported (Gardiner et al, 1990;Bower & Law, 1993;Wang et al, 1993a;Herity et al, 1994). L-NOARG was found to cause generalized peripheral vasoconstriction, as vascular conductances in all beds, which include the lungs, heart, liver, stomach, intestine, colon, kidneys, spleen, muscle skin, testes and brain, were reduced (Wang et al, 1993a). The greatest vasoconstrictor influence was in the bronchial bed whereas the least was in the hepatic arterial bed.…”

Section: Discussionsupporting

confidence: 82%

Increase by N^G‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

Wang

Lim

Pang

1995

British J Pharmacology

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1 The effects of the nitric oxide (NO) synthase inhibitor, N0-nitro-L-arginine methyl ester (L-NAME), on mean circulatory filling pressure (MCFP), total peripheral resistance (TPR), cardiac output (CO) and resistance to venous return (Rv) were studied in rats.2 In conscious, unrestrained rats, L-NAME (0.5-16mgkg-') dose-dependently increased mean arterial pressure (MAP) but not MCFP, an inverse index of venous compliance, either in the absence or presence of the ganglionic blocker mecamylamine (10mgkg-'). 3 In pentobarbitone-anaesthetized rats, L-NAME (2, 4, 8 mg kg-') increased MAP and reduced CO in a dose-related manner but did not change MCFP. TPR (+ 84, + 140 and + 192%) as well as R, (+ 62, +72, +110%) were dose-dependently increased by L-NAME. 4 Our results show that L-NAME reduces CO by increasing arterial as well as venous resistances. L-NAME does not affect MCFP.

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Section: Discussionsupporting

confidence: 82%

Increase by N^G‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

Wang

Lim

Pang

1995

British J Pharmacology

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“…Hypertension with bradycardia has been obtained with other acute NO synthase inhibitors (Rees et al, 1989;Nafrialdi et al, 1994;Richard et al, 1995). L-NAME was shown to increase BP by elevating total peripheral resistance rather than cardiac output, the latter being dose-dependently decreased by L-NAME (Gardiner et al, 1990;Wang et al, 1993;. Furthermore, acute administration of Larginine analogues were shown to increase splanchnic (Gardiner et al, 1990) and renal vascular resistances (Baylis et al, 1990;Zatz & De Nucci, 1991).…”

Section: Discussionmentioning

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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“…To investigate a possible role of NO in buffering of renal vasoconstrictor responses to ET-1 and/or in the effects of ET B receptor antagonism, NOS was inhibited by N -nitro-L-arginine methyl ester (L-NAME, 25 mg/kg bolus iv in 1 ml/kg saline) 35 min after the first injection of ET-1. This dose of L-NAME was chosen on the basis of our preliminary experiments and the literature to exceed the 10 mg/kg known to produce maximum effects on AP and RBF (2,9,28,46). To minimize the vasoconstrictor and pressor effects of L-NAME and to maintain constant ambient levels of NO, the NO donor nitroprusside (NP, 1 mg ⅐ kg Ϫ1 ⅐ ml Ϫ1 ) was infused intravenously.…”

Section: Experimental Groupsmentioning

confidence: 99%

NO and NO-independent mechanisms mediate ET_Breceptor buffering of ET-1-induced renal vasoconstriction in the rat

Just¹,

Olson²,

Falck

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Vascular endothelin (ET) type B (ET(B)) receptors exert dilator and constrictor actions in a complex interaction with ET(A) receptors. We aimed to clarify the presence and relative importance of nitric oxide (NO) and other mechanisms underlying the dilator effects of ET(B) receptors in rat kidneys. Complete inhibition of NO production with Nomega-nitro-L-arginine methyl ester (L-NAME, 25 mg/kg iv) enhanced the renal vasoconstriction elicited by ET-1 injected into the renal artery from -15 to -30%. Additional infusion of the NO donor nitroprusside (NP) into the renal artery did not reverse this effect (-29%) but effectively buffered ANG II-mediated vasoconstriction. Similarly, ET-1 responses were enhanced after a smaller intrarenal dose of L-NAME (-22 vs. -15%) and were unaffected by subsequent NP infusion (-21%). These results indicate that the responsiveness to ET-1 is buffered by ET(B) receptor-stimulated phasic release of NO, rather than its static mean level. Infusion of the ET(B) receptor antagonist BQ-788 into the renal artery further enhanced the ET-1 constrictor response to NP+L-NAME (-92 vs. -49%), revealing an NO-independent dilator component. In controls, vasoconstriction to ET-1 was unaffected by vehicle (-27 vs. -20%) and markedly enhanced by BQ-788 (-70%). The same pattern was observed when indomethacin (Indo) was used to inhibit cyclooxygenase (-20% for control, -22% with Indo, and -56% with ET(B) antagonist) or methylsulfonyl-6-(2-propargyloxyphenyl)-hexanamide (MS-PPOH) or miconazole+Indo was used to inhibit epoxygenase alone (-10% for control, -11% with MS-PPOH, and -35% with ET(B) antagonist) or in combination (-14% for control, -20% with Indo + miconazole, and -43% with ET(B) antagonist). We conclude that phasic release of NO, but not its static level, mediates part of the dilator effect of ET(B) receptors and that an NO-independent mechanism, distinct from prostanoids and epoxyeicosatetraenoic acids, perhaps ET(B) receptor clearance of ET-1, plays a major buffering role.

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Selective Inhibition of Pressor and Haemodynamic Effects of NG-Nitro-L-Arginine by Halothane

Cited by 19 publications

References 0 publications

Increase by N^G‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

Increase by N^G‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

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

NO and NO-independent mechanisms mediate ET_Breceptor buffering of ET-1-induced renal vasoconstriction in the rat

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Selective Inhibition of Pressor and Haemodynamic Effects of NG-Nitro-L-Arginine by Halothane

Cited by 19 publications

References 0 publications

Increase by NG‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

Increase by NG‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

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

NO and NO-independent mechanisms mediate ETBreceptor buffering of ET-1-induced renal vasoconstriction in the rat

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Increase by N^G‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

Increase by N^G‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

NO and NO-independent mechanisms mediate ET_Breceptor buffering of ET-1-induced renal vasoconstriction in the rat