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Release of the free nitric oxide radical (NO) and EDRF from endothelial cells

Release of the free nitric oxide radical (NO) and EDRF from endothelial cells
Release of the free nitric oxide radical (NO) and EDRF from endothelial cells
Release of nitric oxide (NO) from cultured macrovascular endothelial cells (EC) and from isolated perfused guinea pig hearts was measured with a specific spectrophotometric assay. Under basal conditions NO was continuously released from cultured cells and from isolated hearts into the coronary effluent perfusate. Bradykinin (10(-7) M) increased rate of NO release maximally two- to three-fold in both experimental models. Onset of NO release always preceded start of vasodilation (less than 15 s). Our results provide evidence that under basal and bradykinin-stimulated conditions. 1) endothelial cells release nitric oxide as a free radical, 2) NO is solely responsible for the vasodilatory properties of EDRF and, 3) under in vivo conditions the endogenous formation of NO is quantitatively sufficient to influence the coronary vascular tone and thus, may play an important role in the regulation of coronary vascular resistance.
0300-5860
70-74
Kelm, M.
d3823c15-6836-4780-8335-014aef2ec23f
Feelisch, Martin
8c1b9965-8614-4e85-b2c6-458a2e17eafd
Schrader, J.
d0a8ddf0-2c0e-46af-b164-5f4554696b14
Kelm, M.
d3823c15-6836-4780-8335-014aef2ec23f
Feelisch, Martin
8c1b9965-8614-4e85-b2c6-458a2e17eafd
Schrader, J.
d0a8ddf0-2c0e-46af-b164-5f4554696b14

Kelm, M., Feelisch, Martin and Schrader, J. (1989) Release of the free nitric oxide radical (NO) and EDRF from endothelial cells. Zeitschrift für Kardiologie, 78, supplement 6, 70-74. (PMID:2618132)

Record type: Article

Abstract

Release of nitric oxide (NO) from cultured macrovascular endothelial cells (EC) and from isolated perfused guinea pig hearts was measured with a specific spectrophotometric assay. Under basal conditions NO was continuously released from cultured cells and from isolated hearts into the coronary effluent perfusate. Bradykinin (10(-7) M) increased rate of NO release maximally two- to three-fold in both experimental models. Onset of NO release always preceded start of vasodilation (less than 15 s). Our results provide evidence that under basal and bradykinin-stimulated conditions. 1) endothelial cells release nitric oxide as a free radical, 2) NO is solely responsible for the vasodilatory properties of EDRF and, 3) under in vivo conditions the endogenous formation of NO is quantitatively sufficient to influence the coronary vascular tone and thus, may play an important role in the regulation of coronary vascular resistance.

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Published date: 1989
Organisations: Clinical & Experimental Sciences

Identifiers

Local EPrints ID: 337918
URI: http://eprints.soton.ac.uk/id/eprint/337918
ISSN: 0300-5860
PURE UUID: 6d6b4fc8-8598-4f2e-a31d-f337c1e290a1
ORCID for Martin Feelisch: ORCID iD orcid.org/0000-0003-2320-1158

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Date deposited: 14 Jun 2012 10:52
Last modified: 15 Mar 2024 03:42

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Contributors

Author: M. Kelm
Author: Martin Feelisch ORCID iD
Author: J. Schrader

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