Dendroaspis natriuretic peptide relaxes isolated human arteries and veins

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

Background: Dendroaspis natriuretic peptide (DNP) is the newest member of the natriuretic peptide family and is a circulating peptide in humans. The effects of DNP on the human vasculature are unknown. Since other natriuretic peptides are known to cause vasorelaxation, we determined the response to DNP on human blood vessels in vitro. We also investigated the mechanism of DNP mediated vasorelaxation. Methods: Rings of human internal mammary artery and saphenous vein were suspended in an organ bath. The response to cumulative concentrations of DNP was obtained. Inhibiting agents were used to determine the mechanism of this vasorelaxation. Results: DNP caused dose-dependent relaxation, with a greater effect on the internal mammary arteries (relaxation from 10-7 mol/l DNP: 80.6±4.1%) than the saphenous veins (33.4±4.1%). At 10-7 mol/l, DNP resulted in less arterial relaxation compared with atrial and C-type natriuretic peptides and similar relaxation to brain natriuretic peptide. In veins, DNP caused the greatest relaxation of the natriuretic peptides. DNP increased tissue cyclic guanosine monophosphate (cGMP) determined by radioimmunoassay by over 7-fold. Barium chloride and indomethacin attenuated DNP mediated vasorelaxation. However, glibenclamide, charydotoxin, apamin, tetraethyl-ammonium chloride and diisothiocyanato-stilbene-2,2′-disulfonic acid did not. DNP mediated vasorelaxation was mildly attenuated with removal of the endothelium. DNP immunoreactivity was identified in both arteries and veins. Conclusions: The current study demonstrates that DNP is an endogenous human natriuretic peptide that relaxes human arteries more than veins. Furthermore, DNP mediated vasorelaxation involves the inward rectifying potassium channels, prostaglandins, and cGMP. This newest member of the natriuretic peptide family may have an important physiologic role in the human vasculature.

Original languageEnglish (US)
Pages (from-to)375-384
Number of pages10
JournalCardiovascular Research
Volume55
Issue number2
DOIs
StatePublished - 2002

Fingerprint

Veins
Arteries
Natriuretic Peptides
Vasodilation
Mammary Arteries
Cyclic GMP
Saphenous Vein
Dendroaspis natriuretic peptide
C-Type Natriuretic Peptide
Apamin
Stilbenes
Ammonium Chloride
Glyburide
Brain Natriuretic Peptide
Potassium Channels
Atrial Natriuretic Factor
Baths
Indomethacin
Prostaglandins
Endothelium

Keywords

  • K-channel
  • Natriuretic peptide
  • Prostaglandins
  • Vasoactive agents

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Dendroaspis natriuretic peptide relaxes isolated human arteries and veins. / Best, Patricia; Burnett, John C Jr.; Wilson, Stephanie H.; Holmes, David; Lerman, Amir.

In: Cardiovascular Research, Vol. 55, No. 2, 2002, p. 375-384.

Research output: Contribution to journalArticle

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abstract = "Background: Dendroaspis natriuretic peptide (DNP) is the newest member of the natriuretic peptide family and is a circulating peptide in humans. The effects of DNP on the human vasculature are unknown. Since other natriuretic peptides are known to cause vasorelaxation, we determined the response to DNP on human blood vessels in vitro. We also investigated the mechanism of DNP mediated vasorelaxation. Methods: Rings of human internal mammary artery and saphenous vein were suspended in an organ bath. The response to cumulative concentrations of DNP was obtained. Inhibiting agents were used to determine the mechanism of this vasorelaxation. Results: DNP caused dose-dependent relaxation, with a greater effect on the internal mammary arteries (relaxation from 10-7 mol/l DNP: 80.6±4.1{\%}) than the saphenous veins (33.4±4.1{\%}). At 10-7 mol/l, DNP resulted in less arterial relaxation compared with atrial and C-type natriuretic peptides and similar relaxation to brain natriuretic peptide. In veins, DNP caused the greatest relaxation of the natriuretic peptides. DNP increased tissue cyclic guanosine monophosphate (cGMP) determined by radioimmunoassay by over 7-fold. Barium chloride and indomethacin attenuated DNP mediated vasorelaxation. However, glibenclamide, charydotoxin, apamin, tetraethyl-ammonium chloride and diisothiocyanato-stilbene-2,2′-disulfonic acid did not. DNP mediated vasorelaxation was mildly attenuated with removal of the endothelium. DNP immunoreactivity was identified in both arteries and veins. Conclusions: The current study demonstrates that DNP is an endogenous human natriuretic peptide that relaxes human arteries more than veins. Furthermore, DNP mediated vasorelaxation involves the inward rectifying potassium channels, prostaglandins, and cGMP. This newest member of the natriuretic peptide family may have an important physiologic role in the human vasculature.",
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T1 - Dendroaspis natriuretic peptide relaxes isolated human arteries and veins

AU - Best, Patricia

AU - Burnett, John C Jr.

AU - Wilson, Stephanie H.

AU - Holmes, David

AU - Lerman, Amir

PY - 2002

Y1 - 2002

N2 - Background: Dendroaspis natriuretic peptide (DNP) is the newest member of the natriuretic peptide family and is a circulating peptide in humans. The effects of DNP on the human vasculature are unknown. Since other natriuretic peptides are known to cause vasorelaxation, we determined the response to DNP on human blood vessels in vitro. We also investigated the mechanism of DNP mediated vasorelaxation. Methods: Rings of human internal mammary artery and saphenous vein were suspended in an organ bath. The response to cumulative concentrations of DNP was obtained. Inhibiting agents were used to determine the mechanism of this vasorelaxation. Results: DNP caused dose-dependent relaxation, with a greater effect on the internal mammary arteries (relaxation from 10-7 mol/l DNP: 80.6±4.1%) than the saphenous veins (33.4±4.1%). At 10-7 mol/l, DNP resulted in less arterial relaxation compared with atrial and C-type natriuretic peptides and similar relaxation to brain natriuretic peptide. In veins, DNP caused the greatest relaxation of the natriuretic peptides. DNP increased tissue cyclic guanosine monophosphate (cGMP) determined by radioimmunoassay by over 7-fold. Barium chloride and indomethacin attenuated DNP mediated vasorelaxation. However, glibenclamide, charydotoxin, apamin, tetraethyl-ammonium chloride and diisothiocyanato-stilbene-2,2′-disulfonic acid did not. DNP mediated vasorelaxation was mildly attenuated with removal of the endothelium. DNP immunoreactivity was identified in both arteries and veins. Conclusions: The current study demonstrates that DNP is an endogenous human natriuretic peptide that relaxes human arteries more than veins. Furthermore, DNP mediated vasorelaxation involves the inward rectifying potassium channels, prostaglandins, and cGMP. This newest member of the natriuretic peptide family may have an important physiologic role in the human vasculature.

AB - Background: Dendroaspis natriuretic peptide (DNP) is the newest member of the natriuretic peptide family and is a circulating peptide in humans. The effects of DNP on the human vasculature are unknown. Since other natriuretic peptides are known to cause vasorelaxation, we determined the response to DNP on human blood vessels in vitro. We also investigated the mechanism of DNP mediated vasorelaxation. Methods: Rings of human internal mammary artery and saphenous vein were suspended in an organ bath. The response to cumulative concentrations of DNP was obtained. Inhibiting agents were used to determine the mechanism of this vasorelaxation. Results: DNP caused dose-dependent relaxation, with a greater effect on the internal mammary arteries (relaxation from 10-7 mol/l DNP: 80.6±4.1%) than the saphenous veins (33.4±4.1%). At 10-7 mol/l, DNP resulted in less arterial relaxation compared with atrial and C-type natriuretic peptides and similar relaxation to brain natriuretic peptide. In veins, DNP caused the greatest relaxation of the natriuretic peptides. DNP increased tissue cyclic guanosine monophosphate (cGMP) determined by radioimmunoassay by over 7-fold. Barium chloride and indomethacin attenuated DNP mediated vasorelaxation. However, glibenclamide, charydotoxin, apamin, tetraethyl-ammonium chloride and diisothiocyanato-stilbene-2,2′-disulfonic acid did not. DNP mediated vasorelaxation was mildly attenuated with removal of the endothelium. DNP immunoreactivity was identified in both arteries and veins. Conclusions: The current study demonstrates that DNP is an endogenous human natriuretic peptide that relaxes human arteries more than veins. Furthermore, DNP mediated vasorelaxation involves the inward rectifying potassium channels, prostaglandins, and cGMP. This newest member of the natriuretic peptide family may have an important physiologic role in the human vasculature.

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KW - Natriuretic peptide

KW - Prostaglandins

KW - Vasoactive agents

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