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| Content Provider | PubMed Central |
|---|---|
| Author | Flitney, F. W. Megson, I. L. Thomson, J. L. Kennovin, G. D. Butler, A. R. |
| Abstract | 1. The vasodilator properties and photochemical decomposition of two synthetic iron-sulphur-nitrosyl clusters (cluster A: [Fe4S4(NO)4], tetranitrosyl-tetra-mu 3-sulphido-tetrahedro-tetrairon; and B:[Fe4S3 (NO)7]-1, heptanitrosyl-tri-mu 3-thioxotetraferrate(-1)) have been investigated. Experiments were carried out on isolated, internally-perfused segments of rat tail artery. 2. Bolus injections (10 microliters) of A or B ( > 0.25 mM) delivered into the internal perfusate generated sustained (or S-type) vasodilator responses, characterized by a persistent plateau of reduced tone due to NO released from clusters which enter and become trapped within endothelial cells. Clusters were therefore irradiated with visible laser light (lambda = 457.9 or 514.5 nm) either (a) in solution, while passing through a glass tube en route to the artery; or (b) when retained within the endothelium, by illuminating the artery directly during the plateau of an S-type response. Irradiation produced an additional vasodilator response, the magnitude of which depended upon wavelength and laser beam energy. 3. The nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (100 microM), had no effect on light-induced vasodilator responses. However, they were (a) blocked entirely by adding oxyhaemoglobin (5 microM) to the internal perfusate; and (b) greatly enhanced by the enzyme superoxide dismutase (150 u ml-1). 4. Photolysis of cluster B was measured by absorption spectroscopy and by detecting NO released with an electrochemical sensor. The photochemical reaction was found to be oxygen-dependent. The half-time for inactivation of cluster-derived NO was measured by interposing different lengths of tubing (i.e. time delays) between the photolysis tube and NO sensor. The steady-state probe current decayed exponentially with increasing delay time, with a t 1/2 of 21 s. The amplitudes of vasodilator responses of the tail artery also decreased exponentially by increasing the time delay (t 1/2 = 58 s). Superoxide dismutase (150 u ml-1) prevented this from happening, showing that "inactivation' of cluster-derived NO was caused by reaction with superoxide anions formed during photolysis. 5. We conclude that potentiation of vasodilator responses to iron-sulphur-nitrosyl clusters by visible light is due to an oxygen-dependent photochemical reaction which accelerates the release of ligated nitrosyl groups as free NO. Based on our measurements, we estimate that ca 100 pM NO is sufficient to produce a just-detectable additional vasodilatation and that the ED50 dose is ca 3.7 nM. |
| Starting Page | 1549 |
| File Format | |
| ISSN | 00071188 |
| Journal | British Journal of Pharmacology |
| Issue Number | 7 |
| Volume Number | 117 |
| Language | English |
| Publisher Date | 1996-04-01 |
| Access Restriction | Open |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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