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Role of nitric oxide in the regulation of coronary vascular tone in hearts from hypertensive rats. Maintenance of nitric oxide-forming capacity and increased basal production of nitric oxide

Role of nitric oxide in the regulation of coronary vascular tone in hearts from hypertensive rats. Maintenance of nitric oxide-forming capacity and increased basal production of nitric oxide
Role of nitric oxide in the regulation of coronary vascular tone in hearts from hypertensive rats. Maintenance of nitric oxide-forming capacity and increased basal production of nitric oxide
In arterial hypertension, coronary flow reserve, expressed by the difference between autoregulated and maximal coronary flow, is frequently impaired. Previous experimental and clinical investigations using acetylcholine as a stimulus for the production of endothelium-derived relaxing factor suggested that an impaired endothelium-dependent vasodilation, presumably caused by a decreased formation of nitric oxide (NO), may account for this microvascular dysfunction. However, so far no study has been performed that quantifies the formation of NO within the coronary circulation of hypertensive hearts to assess its role in setting coronary vascular tone in the hypertensive heart. We therefore quantified NO formation within the coronary circulation of constant flow-perfused, isolated hearts from spontaneously hypertensive rats (SHR, 16th to 26th week), as a model for hypertensive heart disease, and from the normotensive control strain (Wistar-Kyoto, WKY) using the oxyhemoglobin technique. Coronary perfusion pressure and vascular resistance were almost 30% higher in SHR compared with WKY hearts. Intracoronarily applied NO decreased coronary vascular resistance by maximally 45% of resting values in a concentration-dependent manner in both groups. The bradykinin-induced decrease in coronary vascular resistance and the parallel increase in NO release were comparable in SHR and WKY hearts and fell within the vasodilator range of exogenously applied NO. Moreover, basal release of NO normalized to heart wet weight was 50% higher in SHR compared with WKY hearts. Rates of basal NO release were correlated inversely with changes in coronary perfusion pressure and vascular resistance in both groups (r = -.85 and -.84, respectively, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
endothelium-derived relaxing factor, nitric oxide, hypertension, arterial, coronary circulation, bradykinin
0194-911X
186-93
Kelm, Malte
db2bb062-32d7-4b50-9f65-8ba89ffa5f42
Feelisch, Martin
8c1b9965-8614-4e85-b2c6-458a2e17eafd
Krebber, Thomas
7114f31f-154e-4bd0-ac27-b1439acb1f8b
Deußen, Andreas
0215a482-2e63-4c87-9a10-d2b932308d40
Motz, Wolfgang
1f23e8c8-e0b2-478b-bbbc-5b84be6f87d4
Strauer, Bodo E.
7343fe67-ccf3-4079-94a0-ea6238979951
Kelm, Malte
db2bb062-32d7-4b50-9f65-8ba89ffa5f42
Feelisch, Martin
8c1b9965-8614-4e85-b2c6-458a2e17eafd
Krebber, Thomas
7114f31f-154e-4bd0-ac27-b1439acb1f8b
Deußen, Andreas
0215a482-2e63-4c87-9a10-d2b932308d40
Motz, Wolfgang
1f23e8c8-e0b2-478b-bbbc-5b84be6f87d4
Strauer, Bodo E.
7343fe67-ccf3-4079-94a0-ea6238979951

Kelm, Malte, Feelisch, Martin, Krebber, Thomas, Deußen, Andreas, Motz, Wolfgang and Strauer, Bodo E. (1995) Role of nitric oxide in the regulation of coronary vascular tone in hearts from hypertensive rats. Maintenance of nitric oxide-forming capacity and increased basal production of nitric oxide. Hypertension, 25 (2), 186-93. (doi:10.1161/01.HYP.25.2.186). (PMID:7843768)

Record type: Article

Abstract

In arterial hypertension, coronary flow reserve, expressed by the difference between autoregulated and maximal coronary flow, is frequently impaired. Previous experimental and clinical investigations using acetylcholine as a stimulus for the production of endothelium-derived relaxing factor suggested that an impaired endothelium-dependent vasodilation, presumably caused by a decreased formation of nitric oxide (NO), may account for this microvascular dysfunction. However, so far no study has been performed that quantifies the formation of NO within the coronary circulation of hypertensive hearts to assess its role in setting coronary vascular tone in the hypertensive heart. We therefore quantified NO formation within the coronary circulation of constant flow-perfused, isolated hearts from spontaneously hypertensive rats (SHR, 16th to 26th week), as a model for hypertensive heart disease, and from the normotensive control strain (Wistar-Kyoto, WKY) using the oxyhemoglobin technique. Coronary perfusion pressure and vascular resistance were almost 30% higher in SHR compared with WKY hearts. Intracoronarily applied NO decreased coronary vascular resistance by maximally 45% of resting values in a concentration-dependent manner in both groups. The bradykinin-induced decrease in coronary vascular resistance and the parallel increase in NO release were comparable in SHR and WKY hearts and fell within the vasodilator range of exogenously applied NO. Moreover, basal release of NO normalized to heart wet weight was 50% higher in SHR compared with WKY hearts. Rates of basal NO release were correlated inversely with changes in coronary perfusion pressure and vascular resistance in both groups (r = -.85 and -.84, respectively, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

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Published date: February 1995
Keywords: endothelium-derived relaxing factor, nitric oxide, hypertension, arterial, coronary circulation, bradykinin
Organisations: Clinical & Experimental Sciences

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Local EPrints ID: 337900
URI: http://eprints.soton.ac.uk/id/eprint/337900
ISSN: 0194-911X
PURE UUID: dbf2cd93-d944-4581-ba7d-c6caecff97af
ORCID for Martin Feelisch: ORCID iD orcid.org/0000-0003-2320-1158

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Date deposited: 29 Jun 2012 15:55
Last modified: 15 Mar 2024 03:41

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Contributors

Author: Malte Kelm
Author: Martin Feelisch ORCID iD
Author: Thomas Krebber
Author: Andreas Deußen
Author: Wolfgang Motz
Author: Bodo E. Strauer

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