Induction of nitric oxide synthase in human mammary arteries in vitro

Berrazueta, JoséR.; Salas, Eduardo; Amado, J A; Vega, María J. Sánchez de; Poveda, J J

doi:10.1016/0014-2999(94)90414-6

Cited by 12 publications

(4 citation statements)

References 13 publications

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“…It has been described that LPS decreases vascular resistance, produces vascular hyporeactivity to different vasoconstrictors and potentiates the inhibitory effect of L ‐Arg by overproduction of NO mediated by activation of iNOS ( Ueno & Lee, 1993 ; Berrazueta et al ., 1994 ; Brian et al ., 1995 ; Villamor et al ., 1995 ; Alonso et al ., 1998 ). In our study, LPS inhibited the vasoconstrictor responses induced by PGF 2α and the effect of dexamethasone and polymyxin B on basal tone, the contraction induced by PGF 2α and on the L ‐Arg‐induced vasodilatation.…”

Section: Discussionmentioning

confidence: 99%

“…This reduction could be due to an induction of iNOS because it was potentiated by LPS. Similar results have been obtained in the porcine basilar artery ( Ueno & Lee, 1993 ), the rat aorta ( Rees et al ., 1990 ) and the human mammary artery ( Berrazueta et al ., 1994 ) in normotension. The participation of iNOS in this time‐dependent reduction of PGF 2α contraction was also supported by the fact that in the presence of dexamethasone or polymyxin B, such a reduction was transformed in an increase of contraction that was antagonized by LPS.…”

Section: Discussionmentioning

confidence: 99%

“…The participation of iNOS in this time‐dependent reduction of PGF 2α contraction was also supported by the fact that in the presence of dexamethasone or polymyxin B, such a reduction was transformed in an increase of contraction that was antagonized by LPS. An inhibition by dexamethasone and polymyxin B of the time‐dependent loss of agonist‐induced tone has been reported ( Rees et al ., 1990 ; Berrazueta et al ., 1994 ). The presence of gentamycin plus ampicillin did not alter the contractile response reduction which indicates that this reduction is not due to the presence of bacterial contaminant in the medium.…”

Section: Discussionmentioning

confidence: 99%

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Role of iNOS in the vasodilator responses induced by L‐arginine in the middle cerebral artery from normotensive and hypertensive rats

Briones

Alonso

Marı́n

et al. 1999

British J Pharmacology

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1 The substrate of nitric oxide synthase (NOS), L-arginine (L-Arg, 0.01 mM71 mM), induced endothelium-independent relaxations in segments of middle cerebral arteries (MCAs) from normotensive Wistar-Kyoto (WKY) and hypertensive rats (SHR) precontracted with prostaglandin F 2a (PGF 2a ). These relaxations were higher in SHR than WKY arteries. 2 L-N G -nitroarginine methyl ester (L-NAME) and 2-amine-5,6-dihydro-6-methyl-4H-1,3-tiazine (AMT), unspeci®c and inducible NOS (iNOS) inhibitors, respectively, reduced those relaxations, specially in SHR.3 Four-and seven-hours incubation with dexamethasone reduced the relaxations in MCAs from WKY and SHR, respectively. 4 Polymyxin B and calphostin C, protein kinase C (PKC) inhibitors, reduced the L-Arg-induced relaxation. 5 Lipopolysaccharide (LPS, 7 h incubation) unaltered and inhibited these relaxations in WKY and SHR segments, respectively. LPS antagonized the e ect polymyxin B in WKY and potentiated LArg-induced relaxations in SHR in the presence of polymyxin B. 6 The contraction induced by PGF 2a was greater in SHR than WKY arteries. This contraction was potentiated by dexamethasone and polymyxin B although the e ect of polymyxin B was higher in SHR segments. LPS reduced that contraction and antagonized dexamethasone-and polymyxin Binduced potentiation, these e ects being greater in arteries from SHR. 7 These results suggest that in MCAs: (1) the induction of iNOS participates in the L-Arg relaxation and modulates the contraction to PGF 2a ; (2) that induction is partially mediated by a PKC-dependent mechanism; and (3) the involvement of iNOS in such responses is greater in the hypertensive strain.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Role of iNOS in the vasodilator responses induced by L‐arginine in the middle cerebral artery from normotensive and hypertensive rats

Briones

Alonso

Marı́n

et al. 1999

British J Pharmacology

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“…20 In early reports, the presence of a constitutive NOS in vascular smooth muscle cells has been suggested, 175,176 but these observations were probably related to the induction of iNOS during the isolation and manipulation of the cells or tissue. 172,177,178…”

Section: Atherosclerosis and Inducible Nitric Oxide Synthase Expressionmentioning

confidence: 99%

Nitric oxide function in atherosclerosis

Matthys

Bult

1997

Mediators of Inflammation

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Atherosclerosis is a chronic inflammatory process in the intima of conduit arteries, which disturbs the endothelium-dependent regulation of the vascular tone by the labile liposoluble radical nitric oxide (NO) formed by the constitutive endothelial nitric oxide synthase (eNOS). This defect predisposes to coronary vasospasm and cardiac ischaemia, with anginal pain as the typical clinical manifestation. It is now appreciated that endothelial dysfunction is an early event in atherogenesis and that it may also involve the microcirculation, in which atherosclerotic lesions do not develop. On the other hand, the inflammatory environment in atherosclerotic plaques may result in the expression of the inducible NO synthase (iNOS) isozyme. Whether the dysfunction in endothelial NO production is causal to, or the result of, atherosclerotic lesion formation is still highly debated. Most evidence supports the hypothesis that constitutive endothelial NO release protects against atherogenesis e.g. by preventing smooth muscle cell proliferation and leukocyte adhesion. Nitric oxide generated by the inducible isozyme may be beneficial by replacing the failing endothelial production but excessive release may damage the vascular wall cells, especially in combination with reactive oxygen intermediates.

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Vessel and Inflammation

Bernard

Basic Science for the Cardiologist

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Induction of nitric oxide synthase in human mammary arteries in vitro

Cited by 12 publications

References 13 publications

Role of iNOS in the vasodilator responses induced by L‐arginine in the middle cerebral artery from normotensive and hypertensive rats

Role of iNOS in the vasodilator responses induced by L‐arginine in the middle cerebral artery from normotensive and hypertensive rats

Nitric oxide function in atherosclerosis

Vessel and Inflammation

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