Nitric oxide accounts for histamine-induced increases in macromolecular extravasation

Research output: Contribution to journalArticle

94 Citations (Scopus)

Abstract

The goal of this study was to determine the role of nitric oxide in histamine-induced increases in macromolecular extravasation in the hamster cheek pouch in vivo. We used intravital fluorescent microscopy and fluorescein isothiocyanate dextran (FITC-dextran; mol wt = 70,000 K) to examine extravasation from postcapillary venules in response to histamine before and after application of an enzymatic inhibitor of nitric oxide, N(G)- monomethyl-L-arginine (L-NMMA; 1.0 μM). Increases in extravasation of macromolecules were quantitated counting the number of venular leaky sites. Histamine (1.0 and 5.0 μM) increased the number of venular leaky sites from zero (basal conditions) to 11 ± 1 and 21 ± 2/0.11 cm2, respectively. Superfusion of L-NMMA (1.0 μM) and LY-83583 (1.0 μM) significantly decreased histamine-induced formation of venular leaky sites, whereas L- arginine (100 μM) potentiated histamine-induced formation of venular leaky sites. In contrast, superfusion of N(G)-monomethyl-D-arginine (1.0 μM) did not inhibit the formation of venular leaky sites in response to histamine. Thus the findings of the present study suggest that production of nitric oxide, and subsequent activation of guanylate cyclase, plays an important role in macromolecular efflux in vivo in response to histamine.

Original languageEnglish (US)
Pages (from-to)H2369-H2373
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume266
Issue number6 35-6
StatePublished - Jan 1 1994

Fingerprint

histamine
Histamine
nitric oxide
Nitric Oxide
omega-N-Methylarginine
arginine
dextran
Arginine
6-anilino-5,8-quinolinedione
guanylate cyclase
Venules
Cheek
Guanylate Cyclase
isothiocyanates
fluorescein
pouches
hamsters
Cricetinae
microscopy

Keywords

  • L-arginine
  • LY-83583
  • N(G)- monomethyl-D-arginine
  • N(G)-monomethyl-L-arginine
  • endothelium-derived relaxing factor
  • fluorescein isothiocyanate dextran
  • hamsters
  • permeability
  • venules

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Nitric oxide accounts for histamine-induced increases in macromolecular extravasation. / Mayhan, W. G.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 266, No. 6 35-6, 01.01.1994, p. H2369-H2373.

Research output: Contribution to journalArticle

@article{12f3722bbef64117849ab6a4245fa33a,
title = "Nitric oxide accounts for histamine-induced increases in macromolecular extravasation",
abstract = "The goal of this study was to determine the role of nitric oxide in histamine-induced increases in macromolecular extravasation in the hamster cheek pouch in vivo. We used intravital fluorescent microscopy and fluorescein isothiocyanate dextran (FITC-dextran; mol wt = 70,000 K) to examine extravasation from postcapillary venules in response to histamine before and after application of an enzymatic inhibitor of nitric oxide, N(G)- monomethyl-L-arginine (L-NMMA; 1.0 μM). Increases in extravasation of macromolecules were quantitated counting the number of venular leaky sites. Histamine (1.0 and 5.0 μM) increased the number of venular leaky sites from zero (basal conditions) to 11 ± 1 and 21 ± 2/0.11 cm2, respectively. Superfusion of L-NMMA (1.0 μM) and LY-83583 (1.0 μM) significantly decreased histamine-induced formation of venular leaky sites, whereas L- arginine (100 μM) potentiated histamine-induced formation of venular leaky sites. In contrast, superfusion of N(G)-monomethyl-D-arginine (1.0 μM) did not inhibit the formation of venular leaky sites in response to histamine. Thus the findings of the present study suggest that production of nitric oxide, and subsequent activation of guanylate cyclase, plays an important role in macromolecular efflux in vivo in response to histamine.",
keywords = "L-arginine, LY-83583, N(G)- monomethyl-D-arginine, N(G)-monomethyl-L-arginine, endothelium-derived relaxing factor, fluorescein isothiocyanate dextran, hamsters, permeability, venules",
author = "Mayhan, {W. G.}",
year = "1994",
month = "1",
day = "1",
language = "English (US)",
volume = "266",
pages = "H2369--H2373",
journal = "American Journal of Physiology - Renal Physiology",
issn = "0363-6127",
publisher = "American Physiological Society",
number = "6 35-6",

}

TY - JOUR

T1 - Nitric oxide accounts for histamine-induced increases in macromolecular extravasation

AU - Mayhan, W. G.

PY - 1994/1/1

Y1 - 1994/1/1

N2 - The goal of this study was to determine the role of nitric oxide in histamine-induced increases in macromolecular extravasation in the hamster cheek pouch in vivo. We used intravital fluorescent microscopy and fluorescein isothiocyanate dextran (FITC-dextran; mol wt = 70,000 K) to examine extravasation from postcapillary venules in response to histamine before and after application of an enzymatic inhibitor of nitric oxide, N(G)- monomethyl-L-arginine (L-NMMA; 1.0 μM). Increases in extravasation of macromolecules were quantitated counting the number of venular leaky sites. Histamine (1.0 and 5.0 μM) increased the number of venular leaky sites from zero (basal conditions) to 11 ± 1 and 21 ± 2/0.11 cm2, respectively. Superfusion of L-NMMA (1.0 μM) and LY-83583 (1.0 μM) significantly decreased histamine-induced formation of venular leaky sites, whereas L- arginine (100 μM) potentiated histamine-induced formation of venular leaky sites. In contrast, superfusion of N(G)-monomethyl-D-arginine (1.0 μM) did not inhibit the formation of venular leaky sites in response to histamine. Thus the findings of the present study suggest that production of nitric oxide, and subsequent activation of guanylate cyclase, plays an important role in macromolecular efflux in vivo in response to histamine.

AB - The goal of this study was to determine the role of nitric oxide in histamine-induced increases in macromolecular extravasation in the hamster cheek pouch in vivo. We used intravital fluorescent microscopy and fluorescein isothiocyanate dextran (FITC-dextran; mol wt = 70,000 K) to examine extravasation from postcapillary venules in response to histamine before and after application of an enzymatic inhibitor of nitric oxide, N(G)- monomethyl-L-arginine (L-NMMA; 1.0 μM). Increases in extravasation of macromolecules were quantitated counting the number of venular leaky sites. Histamine (1.0 and 5.0 μM) increased the number of venular leaky sites from zero (basal conditions) to 11 ± 1 and 21 ± 2/0.11 cm2, respectively. Superfusion of L-NMMA (1.0 μM) and LY-83583 (1.0 μM) significantly decreased histamine-induced formation of venular leaky sites, whereas L- arginine (100 μM) potentiated histamine-induced formation of venular leaky sites. In contrast, superfusion of N(G)-monomethyl-D-arginine (1.0 μM) did not inhibit the formation of venular leaky sites in response to histamine. Thus the findings of the present study suggest that production of nitric oxide, and subsequent activation of guanylate cyclase, plays an important role in macromolecular efflux in vivo in response to histamine.

KW - L-arginine

KW - LY-83583

KW - N(G)- monomethyl-D-arginine

KW - N(G)-monomethyl-L-arginine

KW - endothelium-derived relaxing factor

KW - fluorescein isothiocyanate dextran

KW - hamsters

KW - permeability

KW - venules

UR - http://www.scopus.com/inward/record.url?scp=0028001931&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028001931&partnerID=8YFLogxK

M3 - Article

C2 - 7912900

AN - SCOPUS:0028001931

VL - 266

SP - H2369-H2373

JO - American Journal of Physiology - Renal Physiology

JF - American Journal of Physiology - Renal Physiology

SN - 0363-6127

IS - 6 35-6

ER -