The action of two natriuretic peptides (atrial natriuretic peptide and brain natriuretic peptide) in the human placental vasculature

Gershon Holcberg, Wilhelm Kossenjans, Anthony Brewer, Menachem Miodovnik, Leslie Myatt

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

OBJECTIVE: Our purpose was to compare the actions of atrial natriuretic peptide and brain natriuretic peptide in the human placental vasculature. STUDY DESIGN: Isolated placental cotyledons were dually perfused with fetal perfusion pressure used as an index of vascular response. The effect of angiotensin II (10-10 to 10-6 mol/L bolus injection) was established in the absence or presence of atrial natriuretic peptide (10-8 mo./L) or brain natriuretic peptide (10-8 mol/L final concentration). The role of nitric oxide as a mediator of natriuretic peptide action was investigated by perfusion of n-nitro-l-arginine (10-3 mol/L), an inhibitor of nitric oxide synthase. Attenuation of the action of atrial natriuretic peptide by placental peptidases was studied by perfusion with the peptidase inhibitor benzamidine (2 × 10-2 mol/L). Statistical significance was determined by analysis of variance and paired t test. RESULTS: Significant attenuation of vasoconstrictor responses to angiotensin II occurred within both atrial natriuretic peptide and brain natriuretic peptide; however, brain natriuretic peptide was more effective. n-Nitro-l-arginine did not affect the attenuation of angiotensin II-induced vasoconstriction by atrial or brain natriuretic peptides. In the presence of benzamidine atrial natriuretic peptide exerted a significantly greater vasodilator effect. CONCLUSION: Brain natriuretic peptide is a more potent vasodilator of the placental vasculature than is atrial natriuretic peptide. The low efficacy of atrial natriuretic peptide may be related to placental peptidases. Nitric oxide does not mediate the action of atrial natriuretic peptide or brain natriuretic peptide.

Original languageEnglish (US)
Pages (from-to)71-77
Number of pages7
JournalAmerican Journal of Obstetrics and Gynecology
Volume172
Issue number1 PART 1
DOIs
StatePublished - 1995
Externally publishedYes

Fingerprint

Natriuretic Peptides
Brain Natriuretic Peptide
Atrial Natriuretic Factor
Angiotensin II
Perfusion
Vasodilator Agents
Arginine
Nitric Oxide
Peptide Hydrolases
Cotyledon
Vasoconstrictor Agents
Vasoconstriction
Protease Inhibitors
Nitric Oxide Synthase
Blood Vessels
Analysis of Variance
Pressure
Injections

Keywords

  • angiotensin
  • Atrial natriuretic peptide
  • brain natriuretic peptide
  • nitric oxide
  • placenta

ASJC Scopus subject areas

  • Obstetrics and Gynecology
  • Medicine(all)

Cite this

The action of two natriuretic peptides (atrial natriuretic peptide and brain natriuretic peptide) in the human placental vasculature. / Holcberg, Gershon; Kossenjans, Wilhelm; Brewer, Anthony; Miodovnik, Menachem; Myatt, Leslie.

In: American Journal of Obstetrics and Gynecology, Vol. 172, No. 1 PART 1, 1995, p. 71-77.

Research output: Contribution to journalArticle

Holcberg, Gershon ; Kossenjans, Wilhelm ; Brewer, Anthony ; Miodovnik, Menachem ; Myatt, Leslie. / The action of two natriuretic peptides (atrial natriuretic peptide and brain natriuretic peptide) in the human placental vasculature. In: American Journal of Obstetrics and Gynecology. 1995 ; Vol. 172, No. 1 PART 1. pp. 71-77.
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T1 - The action of two natriuretic peptides (atrial natriuretic peptide and brain natriuretic peptide) in the human placental vasculature

AU - Holcberg, Gershon

AU - Kossenjans, Wilhelm

AU - Brewer, Anthony

AU - Miodovnik, Menachem

AU - Myatt, Leslie

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N2 - OBJECTIVE: Our purpose was to compare the actions of atrial natriuretic peptide and brain natriuretic peptide in the human placental vasculature. STUDY DESIGN: Isolated placental cotyledons were dually perfused with fetal perfusion pressure used as an index of vascular response. The effect of angiotensin II (10-10 to 10-6 mol/L bolus injection) was established in the absence or presence of atrial natriuretic peptide (10-8 mo./L) or brain natriuretic peptide (10-8 mol/L final concentration). The role of nitric oxide as a mediator of natriuretic peptide action was investigated by perfusion of n-nitro-l-arginine (10-3 mol/L), an inhibitor of nitric oxide synthase. Attenuation of the action of atrial natriuretic peptide by placental peptidases was studied by perfusion with the peptidase inhibitor benzamidine (2 × 10-2 mol/L). Statistical significance was determined by analysis of variance and paired t test. RESULTS: Significant attenuation of vasoconstrictor responses to angiotensin II occurred within both atrial natriuretic peptide and brain natriuretic peptide; however, brain natriuretic peptide was more effective. n-Nitro-l-arginine did not affect the attenuation of angiotensin II-induced vasoconstriction by atrial or brain natriuretic peptides. In the presence of benzamidine atrial natriuretic peptide exerted a significantly greater vasodilator effect. CONCLUSION: Brain natriuretic peptide is a more potent vasodilator of the placental vasculature than is atrial natriuretic peptide. The low efficacy of atrial natriuretic peptide may be related to placental peptidases. Nitric oxide does not mediate the action of atrial natriuretic peptide or brain natriuretic peptide.

AB - OBJECTIVE: Our purpose was to compare the actions of atrial natriuretic peptide and brain natriuretic peptide in the human placental vasculature. STUDY DESIGN: Isolated placental cotyledons were dually perfused with fetal perfusion pressure used as an index of vascular response. The effect of angiotensin II (10-10 to 10-6 mol/L bolus injection) was established in the absence or presence of atrial natriuretic peptide (10-8 mo./L) or brain natriuretic peptide (10-8 mol/L final concentration). The role of nitric oxide as a mediator of natriuretic peptide action was investigated by perfusion of n-nitro-l-arginine (10-3 mol/L), an inhibitor of nitric oxide synthase. Attenuation of the action of atrial natriuretic peptide by placental peptidases was studied by perfusion with the peptidase inhibitor benzamidine (2 × 10-2 mol/L). Statistical significance was determined by analysis of variance and paired t test. RESULTS: Significant attenuation of vasoconstrictor responses to angiotensin II occurred within both atrial natriuretic peptide and brain natriuretic peptide; however, brain natriuretic peptide was more effective. n-Nitro-l-arginine did not affect the attenuation of angiotensin II-induced vasoconstriction by atrial or brain natriuretic peptides. In the presence of benzamidine atrial natriuretic peptide exerted a significantly greater vasodilator effect. CONCLUSION: Brain natriuretic peptide is a more potent vasodilator of the placental vasculature than is atrial natriuretic peptide. The low efficacy of atrial natriuretic peptide may be related to placental peptidases. Nitric oxide does not mediate the action of atrial natriuretic peptide or brain natriuretic peptide.

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