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Cardiovascular Research 1998 38(3):782-787; doi:10.1016/S0008-6363(98)00046-7
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Permissive effect of nitric oxide in arachidonic acid induced dilation in isolated rat arterioles

Erik N.T.P. Bakker* and Pieter Sipkema

Laboratory for Physiology, Institute for Cardiovascular Research (ICaR-VU), Vrije Universiteit, Van der Boechorststraat 7, 1081 BT Amsterdam, Netherlands

* Corresponding author. Tel.: +31 (20) 444-8113; Fax: +31 (20) 444-8255.

Objective: Prostaglandins and nitric oxide play an important role in the regulation of arteriolar tone. L-Arginine analogues inhibit nitric oxide formation, but may also inhibit arachidonic-acid induced dilation. Nitric oxide was found to stimulate cyclooxygenase activity in cultured endothelial cells. Therefore, we hypothesized that the non-specific inhibition of prostaglandin-related dilation by L-arginine analogues is a consequence of the absence of nitric oxide. Methods: To test this hypothesis, arteriolar segments from rat cremaster muscle were studied in a pressure myograph at 75 mmHg. Segments developed spontaneous tone, the diameter reduced from 179±3 to 98±3 µm (n=41). In this condition, responses to exogenous arachidonic acid (1 µM) were recorded and compared with responses after addition of L-NNA, and addition of either SNAP, nitroprusside or 8-Br-cGMP in the presence of L-NNA. Results: Inhibition of basal nitric oxide production with L-NNA (0.1 mM) reduced arachidonic acid-induced dilation (from 52±9 to 31±6 µm). In the presence of L-NNA, responses to arachidonic acid were augmented when exogenous nitric oxide was also present (SNAP, 31±6 µm vs. 75±5 µm; nitroprusside, 31±8 µm vs. 42±7 µm). Responses were not augmented with the second messenger of nitric oxide-mediated dilation 8-Br-cGMP (37±9 µm vs. 32±9 µm). Conclusions: These results indicate that nitric oxide directly increases arachidonic acid-induced dilation. Thus, the non-specific effect of L-arginine analogues can be explained by a permissive effect of nitric oxide on endothelial arachidonic acid metabolism.

KEYWORDS Artery; Endothelial factor; Nitric oxide; Prostaglandin; Vasoconstriction; Vasodilation


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