Angiotensin II-stimulated nitric oxide release from porcine pulmonary endothelium is mediated by angiotensin IV

Nathalie S Hill-kapturczak, Matthias H. Kapturczak, Edward R. Block, Jawaharlal M. Patel, Tadeusz Malinski, Kirsten M. Madsen, C. Craig Tisher

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

In this study, a nitric oxide (NO) sensor was used to examine the ability of angiotensin II (AngII), AngIV, and bradykinin (Bk) to stimulate NO release from porcine pulmonary artery (PPAE) and porcine aortic endothelial (PAE) cells and to explore the mechanism of the AngII-stimulated NO release. Physiologic concentrations of AngII, but not Bk, caused release of NO from PPAE cells. In contrast, Bk, but not AngII, stimulated NO release from PAE cells, AngII-stimulated NO release from PPAE cells required extracellular L- arginine and was inhibited by L-nitro-arginine methyl ester. AT1 and AT2 receptor inhibition had no affect on AngII-mediated NO release or activation of NO synthase (NOS). AngIV, an AngII metabolite with binding sites that are pharmacologically distinct from the classic AngII receptors, stimulated considerably greater NO release and greater endothelial-type constitutive NOS activity than the same amount of AngII. The AngIV receptor antagonist, divalinal AngIV, blocked both AngII- and AngIV-mediated NO release as well as NOS activation. The results demonstrate that AngIV and the AngIV receptor are responsible, at least in part, for AngII-stimulated NO release and the associated endothelium-dependent vasorelaxation. Furthermore, these results suggest that differences exist in both AngII- and Bk-mediated NO release between PPAE and PAE cells, which may reflect important differences in response to these hormones between vascular beds.

Original languageEnglish (US)
Pages (from-to)481-491
Number of pages11
JournalJournal of the American Society of Nephrology
Volume10
Issue number3
StatePublished - Mar 1999
Externally publishedYes

Fingerprint

Angiotensin II
Endothelium
Nitric Oxide
Swine
Lung
Bradykinin
Nitric Oxide Synthase
Pulmonary Artery
Endothelial Cells
des-Asp(1)-des-Arg(2)-Ile(5)-angiotensin II
Angiotensin Receptors
Vasodilation
Blood Vessels
Arginine
Binding Sites
Hormones

ASJC Scopus subject areas

  • Nephrology

Cite this

Hill-kapturczak, N. S., Kapturczak, M. H., Block, E. R., Patel, J. M., Malinski, T., Madsen, K. M., & Tisher, C. C. (1999). Angiotensin II-stimulated nitric oxide release from porcine pulmonary endothelium is mediated by angiotensin IV. Journal of the American Society of Nephrology, 10(3), 481-491.

Angiotensin II-stimulated nitric oxide release from porcine pulmonary endothelium is mediated by angiotensin IV. / Hill-kapturczak, Nathalie S; Kapturczak, Matthias H.; Block, Edward R.; Patel, Jawaharlal M.; Malinski, Tadeusz; Madsen, Kirsten M.; Tisher, C. Craig.

In: Journal of the American Society of Nephrology, Vol. 10, No. 3, 03.1999, p. 481-491.

Research output: Contribution to journalArticle

Hill-kapturczak, NS, Kapturczak, MH, Block, ER, Patel, JM, Malinski, T, Madsen, KM & Tisher, CC 1999, 'Angiotensin II-stimulated nitric oxide release from porcine pulmonary endothelium is mediated by angiotensin IV', Journal of the American Society of Nephrology, vol. 10, no. 3, pp. 481-491.
Hill-kapturczak NS, Kapturczak MH, Block ER, Patel JM, Malinski T, Madsen KM et al. Angiotensin II-stimulated nitric oxide release from porcine pulmonary endothelium is mediated by angiotensin IV. Journal of the American Society of Nephrology. 1999 Mar;10(3):481-491.
Hill-kapturczak, Nathalie S ; Kapturczak, Matthias H. ; Block, Edward R. ; Patel, Jawaharlal M. ; Malinski, Tadeusz ; Madsen, Kirsten M. ; Tisher, C. Craig. / Angiotensin II-stimulated nitric oxide release from porcine pulmonary endothelium is mediated by angiotensin IV. In: Journal of the American Society of Nephrology. 1999 ; Vol. 10, No. 3. pp. 481-491.
@article{0459e304ae444400bdcd08d964ae3d0d,
title = "Angiotensin II-stimulated nitric oxide release from porcine pulmonary endothelium is mediated by angiotensin IV",
abstract = "In this study, a nitric oxide (NO) sensor was used to examine the ability of angiotensin II (AngII), AngIV, and bradykinin (Bk) to stimulate NO release from porcine pulmonary artery (PPAE) and porcine aortic endothelial (PAE) cells and to explore the mechanism of the AngII-stimulated NO release. Physiologic concentrations of AngII, but not Bk, caused release of NO from PPAE cells. In contrast, Bk, but not AngII, stimulated NO release from PAE cells, AngII-stimulated NO release from PPAE cells required extracellular L- arginine and was inhibited by L-nitro-arginine methyl ester. AT1 and AT2 receptor inhibition had no affect on AngII-mediated NO release or activation of NO synthase (NOS). AngIV, an AngII metabolite with binding sites that are pharmacologically distinct from the classic AngII receptors, stimulated considerably greater NO release and greater endothelial-type constitutive NOS activity than the same amount of AngII. The AngIV receptor antagonist, divalinal AngIV, blocked both AngII- and AngIV-mediated NO release as well as NOS activation. The results demonstrate that AngIV and the AngIV receptor are responsible, at least in part, for AngII-stimulated NO release and the associated endothelium-dependent vasorelaxation. Furthermore, these results suggest that differences exist in both AngII- and Bk-mediated NO release between PPAE and PAE cells, which may reflect important differences in response to these hormones between vascular beds.",
author = "Hill-kapturczak, {Nathalie S} and Kapturczak, {Matthias H.} and Block, {Edward R.} and Patel, {Jawaharlal M.} and Tadeusz Malinski and Madsen, {Kirsten M.} and Tisher, {C. Craig}",
year = "1999",
month = "3",
language = "English (US)",
volume = "10",
pages = "481--491",
journal = "Journal of the American Society of Nephrology",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "3",

}

TY - JOUR

T1 - Angiotensin II-stimulated nitric oxide release from porcine pulmonary endothelium is mediated by angiotensin IV

AU - Hill-kapturczak, Nathalie S

AU - Kapturczak, Matthias H.

AU - Block, Edward R.

AU - Patel, Jawaharlal M.

AU - Malinski, Tadeusz

AU - Madsen, Kirsten M.

AU - Tisher, C. Craig

PY - 1999/3

Y1 - 1999/3

N2 - In this study, a nitric oxide (NO) sensor was used to examine the ability of angiotensin II (AngII), AngIV, and bradykinin (Bk) to stimulate NO release from porcine pulmonary artery (PPAE) and porcine aortic endothelial (PAE) cells and to explore the mechanism of the AngII-stimulated NO release. Physiologic concentrations of AngII, but not Bk, caused release of NO from PPAE cells. In contrast, Bk, but not AngII, stimulated NO release from PAE cells, AngII-stimulated NO release from PPAE cells required extracellular L- arginine and was inhibited by L-nitro-arginine methyl ester. AT1 and AT2 receptor inhibition had no affect on AngII-mediated NO release or activation of NO synthase (NOS). AngIV, an AngII metabolite with binding sites that are pharmacologically distinct from the classic AngII receptors, stimulated considerably greater NO release and greater endothelial-type constitutive NOS activity than the same amount of AngII. The AngIV receptor antagonist, divalinal AngIV, blocked both AngII- and AngIV-mediated NO release as well as NOS activation. The results demonstrate that AngIV and the AngIV receptor are responsible, at least in part, for AngII-stimulated NO release and the associated endothelium-dependent vasorelaxation. Furthermore, these results suggest that differences exist in both AngII- and Bk-mediated NO release between PPAE and PAE cells, which may reflect important differences in response to these hormones between vascular beds.

AB - In this study, a nitric oxide (NO) sensor was used to examine the ability of angiotensin II (AngII), AngIV, and bradykinin (Bk) to stimulate NO release from porcine pulmonary artery (PPAE) and porcine aortic endothelial (PAE) cells and to explore the mechanism of the AngII-stimulated NO release. Physiologic concentrations of AngII, but not Bk, caused release of NO from PPAE cells. In contrast, Bk, but not AngII, stimulated NO release from PAE cells, AngII-stimulated NO release from PPAE cells required extracellular L- arginine and was inhibited by L-nitro-arginine methyl ester. AT1 and AT2 receptor inhibition had no affect on AngII-mediated NO release or activation of NO synthase (NOS). AngIV, an AngII metabolite with binding sites that are pharmacologically distinct from the classic AngII receptors, stimulated considerably greater NO release and greater endothelial-type constitutive NOS activity than the same amount of AngII. The AngIV receptor antagonist, divalinal AngIV, blocked both AngII- and AngIV-mediated NO release as well as NOS activation. The results demonstrate that AngIV and the AngIV receptor are responsible, at least in part, for AngII-stimulated NO release and the associated endothelium-dependent vasorelaxation. Furthermore, these results suggest that differences exist in both AngII- and Bk-mediated NO release between PPAE and PAE cells, which may reflect important differences in response to these hormones between vascular beds.

UR - http://www.scopus.com/inward/record.url?scp=0033055979&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033055979&partnerID=8YFLogxK

M3 - Article

C2 - 10073598

AN - SCOPUS:0033055979

VL - 10

SP - 481

EP - 491

JO - Journal of the American Society of Nephrology

JF - Journal of the American Society of Nephrology

SN - 1046-6673

IS - 3

ER -