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Hyporesponsiveness to Ca2+ of aortic smooth muscle in endotoxin-treated rats: no-dependent and -independent in vitro mechanisms.
Res Commun Mol Pathol Pharmacol. 1996 Jun; 92(3):275-84.RC

Abstract

The aim of this study was to assess the nature of vascular hyporeactivity to vasopressor agents in rats with endotoxemia. Endotoxemia was induced in rats by bacterial endotoxin (E. Coli lipopolysaccaharide, LPS). In LPS-treated rats, the reactivity of endothelium-denuded aortic rings to phenylephrine (PE) and potassium chloride (KCl) was characterized by a decreased magnitude of contraction, a slower onset of contraction and a faster rate of relaxation when compared to the control aortic rings. Addition of L-arginine (L-arg), the substrate of nitric oxide synthase (NOS), but not D-arginine (D-arg), reduced further PE-induced contraction in rings from LPS-treated rats. Inhibition of contraction in rings of LPS-treated rats was partially antagonized by the inhibitor of NOS, N omega-nitro-L-arginine methyl ester (L-NAME). Thus, production of non-endothelial nitric oxide (NO) was in part responsible for the hyporesponsiveness to PE. Rings from LPS-treated rats also displayed hyporeactivity and decreased sensitivity to Ca2+ in depolarizing medium (60 mM K+). Hyporeactivity and hyposensitivity to Ca2+ could only be partially reversed by L-NAME. The inhibitory effects of LPS-treatment on both PE-and KCl-induced aortic responses and the reversal effects of L-NAME confirm the contention that NO formation is involved in vascular hyporesponsiveness in endotoxic shock. The partial reversal by L-NAME of the hyporesponsiveness to KCl- and PE-induced contraction, and hyposensitivity to Ca2+ in depolarized aorta suggest that factors other than the action of nonendothelial source of NO formation in vitro from L-arg also contribute to endotoxin-induced vascular hyporesponsiveness to vasopressor agents.

Authors+Show Affiliations

Department of Physiology, Faculty of Medicine, University of Hong Kong, Hong Kong.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8827826

Citation

Ho, K H., et al. "Hyporesponsiveness to Ca2+ of Aortic Smooth Muscle in Endotoxin-treated Rats: No-dependent and -independent in Vitro Mechanisms." Research Communications in Molecular Pathology and Pharmacology, vol. 92, no. 3, 1996, pp. 275-84.
Ho KH, Kwan CY, Bourreau JP. Hyporesponsiveness to Ca2+ of aortic smooth muscle in endotoxin-treated rats: no-dependent and -independent in vitro mechanisms. Res Commun Mol Pathol Pharmacol. 1996;92(3):275-84.
Ho, K. H., Kwan, C. Y., & Bourreau, J. P. (1996). Hyporesponsiveness to Ca2+ of aortic smooth muscle in endotoxin-treated rats: no-dependent and -independent in vitro mechanisms. Research Communications in Molecular Pathology and Pharmacology, 92(3), 275-84.
Ho KH, Kwan CY, Bourreau JP. Hyporesponsiveness to Ca2+ of Aortic Smooth Muscle in Endotoxin-treated Rats: No-dependent and -independent in Vitro Mechanisms. Res Commun Mol Pathol Pharmacol. 1996;92(3):275-84. PubMed PMID: 8827826.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hyporesponsiveness to Ca2+ of aortic smooth muscle in endotoxin-treated rats: no-dependent and -independent in vitro mechanisms. AU - Ho,K H, AU - Kwan,C Y, AU - Bourreau,J P, PY - 1996/6/1/pubmed PY - 1996/6/1/medline PY - 1996/6/1/entrez SP - 275 EP - 84 JF - Research communications in molecular pathology and pharmacology JO - Res Commun Mol Pathol Pharmacol VL - 92 IS - 3 N2 - The aim of this study was to assess the nature of vascular hyporeactivity to vasopressor agents in rats with endotoxemia. Endotoxemia was induced in rats by bacterial endotoxin (E. Coli lipopolysaccaharide, LPS). In LPS-treated rats, the reactivity of endothelium-denuded aortic rings to phenylephrine (PE) and potassium chloride (KCl) was characterized by a decreased magnitude of contraction, a slower onset of contraction and a faster rate of relaxation when compared to the control aortic rings. Addition of L-arginine (L-arg), the substrate of nitric oxide synthase (NOS), but not D-arginine (D-arg), reduced further PE-induced contraction in rings from LPS-treated rats. Inhibition of contraction in rings of LPS-treated rats was partially antagonized by the inhibitor of NOS, N omega-nitro-L-arginine methyl ester (L-NAME). Thus, production of non-endothelial nitric oxide (NO) was in part responsible for the hyporesponsiveness to PE. Rings from LPS-treated rats also displayed hyporeactivity and decreased sensitivity to Ca2+ in depolarizing medium (60 mM K+). Hyporeactivity and hyposensitivity to Ca2+ could only be partially reversed by L-NAME. The inhibitory effects of LPS-treatment on both PE-and KCl-induced aortic responses and the reversal effects of L-NAME confirm the contention that NO formation is involved in vascular hyporesponsiveness in endotoxic shock. The partial reversal by L-NAME of the hyporesponsiveness to KCl- and PE-induced contraction, and hyposensitivity to Ca2+ in depolarized aorta suggest that factors other than the action of nonendothelial source of NO formation in vitro from L-arg also contribute to endotoxin-induced vascular hyporesponsiveness to vasopressor agents. SN - 1078-0297 UR - https://www.unboundmedicine.com/medline/citation/8827826/Hyporesponsiveness_to_Ca2+_of_aortic_smooth_muscle_in_endotoxin_treated_rats:_no_dependent_and__independent_in_vitro_mechanisms_ DB - PRIME DP - Unbound Medicine ER -