Selective inhibition of pressor and haemodynamic effects of ng-nitro-l-arginine by halothane

Yong Xiang Wang, Aly Abdelrahman, Catherine C Y Pang

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

We investigated the characteristics of inhibition by halothane of the pressor responses to NG-substituted L-arginine derivatives, nitric oxide (NO) synthase inhibitors. Intravenous (i.v.) bolus injections of NG-nitro-L-arginine (L-NNA, 1–32 mg/kg), NG-nitro-L-arginine methyl ester (L-NAME, 0.4–12.8 mg/kg), norepinephrine (NE, 0.25–8 (μg/kg) and angiotensin II (AH, 0.02–0.64 μg/kg) each caused dose-dependent pressor responses in conscious rats. Halothane attenuated responses to the highest dose of NE and AH by 18% but completely abolished responses to L-NNA and L-NAME. The haemodynamic effects of L-NNA were further examined by the microsphere technique in two groups of conscious rats and two groups of halothane-anaesthetized rats. An i.v. bolus injection of L-NNA (16 mg/kg) in conscious rats increased mean arterial pressure (MAP) and total peripheral resistance (TPR) and reduced heart rate (HR) and cardiac output (CO). These changes were associated with reduced conductance in all vascular beds, with the greatest reduction in the lungs and the least in the liver. In halothane-anaesthetized rats, L-NNA caused significant but markedly less change in MAP, HR, TPR, and CO as compared with those in conscious rats. The vasoconstrictor effects of L-NNA were attenuated by halothane in all beds except liver and spleen, with the greatest inhibition in heart. Our results suggest that NO plays a role in maintenance of peripheral vascular resistance and that halothane selectively and “noncompetitively” inhibits the vasoconstrictor effects of NO synthase inhibitors.

Original languageEnglish
Pages (from-to)577-578
Number of pages2
JournalJournal of Cardiovascular Pharmacology
Volume22
Issue number4
Publication statusPublished - 1993

Fingerprint

Halothane
Arginine
Hemodynamics
Vascular Resistance
NG-Nitroarginine Methyl Ester
Vasoconstrictor Agents
Nitric Oxide Synthase
Intravenous Injections
Cardiac Output
Arterial Pressure
Heart Rate
Nitroarginine
Liver
Microspheres
Angiotensin II
Blood Vessels
Norepinephrine
Nitric Oxide
Spleen
Maintenance

Keywords

  • Blood pressure
  • Haemo-dynamics
  • Halothane
  • Ng-nitro-l-arginine
  • Ng-nitro-l-arginine methyl ester
  • Nitric oxide
  • Rat
  • Vascular conductance

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

Selective inhibition of pressor and haemodynamic effects of ng-nitro-l-arginine by halothane. / Wang, Yong Xiang; Abdelrahman, Aly; Pang, Catherine C Y.

In: Journal of Cardiovascular Pharmacology, Vol. 22, No. 4, 1993, p. 577-578.

Research output: Contribution to journalArticle

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N2 - We investigated the characteristics of inhibition by halothane of the pressor responses to NG-substituted L-arginine derivatives, nitric oxide (NO) synthase inhibitors. Intravenous (i.v.) bolus injections of NG-nitro-L-arginine (L-NNA, 1–32 mg/kg), NG-nitro-L-arginine methyl ester (L-NAME, 0.4–12.8 mg/kg), norepinephrine (NE, 0.25–8 (μg/kg) and angiotensin II (AH, 0.02–0.64 μg/kg) each caused dose-dependent pressor responses in conscious rats. Halothane attenuated responses to the highest dose of NE and AH by 18% but completely abolished responses to L-NNA and L-NAME. The haemodynamic effects of L-NNA were further examined by the microsphere technique in two groups of conscious rats and two groups of halothane-anaesthetized rats. An i.v. bolus injection of L-NNA (16 mg/kg) in conscious rats increased mean arterial pressure (MAP) and total peripheral resistance (TPR) and reduced heart rate (HR) and cardiac output (CO). These changes were associated with reduced conductance in all vascular beds, with the greatest reduction in the lungs and the least in the liver. In halothane-anaesthetized rats, L-NNA caused significant but markedly less change in MAP, HR, TPR, and CO as compared with those in conscious rats. The vasoconstrictor effects of L-NNA were attenuated by halothane in all beds except liver and spleen, with the greatest inhibition in heart. Our results suggest that NO plays a role in maintenance of peripheral vascular resistance and that halothane selectively and “noncompetitively” inhibits the vasoconstrictor effects of NO synthase inhibitors.

AB - We investigated the characteristics of inhibition by halothane of the pressor responses to NG-substituted L-arginine derivatives, nitric oxide (NO) synthase inhibitors. Intravenous (i.v.) bolus injections of NG-nitro-L-arginine (L-NNA, 1–32 mg/kg), NG-nitro-L-arginine methyl ester (L-NAME, 0.4–12.8 mg/kg), norepinephrine (NE, 0.25–8 (μg/kg) and angiotensin II (AH, 0.02–0.64 μg/kg) each caused dose-dependent pressor responses in conscious rats. Halothane attenuated responses to the highest dose of NE and AH by 18% but completely abolished responses to L-NNA and L-NAME. The haemodynamic effects of L-NNA were further examined by the microsphere technique in two groups of conscious rats and two groups of halothane-anaesthetized rats. An i.v. bolus injection of L-NNA (16 mg/kg) in conscious rats increased mean arterial pressure (MAP) and total peripheral resistance (TPR) and reduced heart rate (HR) and cardiac output (CO). These changes were associated with reduced conductance in all vascular beds, with the greatest reduction in the lungs and the least in the liver. In halothane-anaesthetized rats, L-NNA caused significant but markedly less change in MAP, HR, TPR, and CO as compared with those in conscious rats. The vasoconstrictor effects of L-NNA were attenuated by halothane in all beds except liver and spleen, with the greatest inhibition in heart. Our results suggest that NO plays a role in maintenance of peripheral vascular resistance and that halothane selectively and “noncompetitively” inhibits the vasoconstrictor effects of NO synthase inhibitors.

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