Sensitivity of norepinephrine-evoked vasoconstriction to pertussis toxin in the old rat

Robert, A.; Tran, Nguyen; Giummelly, Philippe; Atkinson, Jeffrey; Capdeville-Atkinson, Christine

doi:10.1152/ajpregu.1998.274.6.r1604

Cited by 8 publications

(9 citation statements)

References 21 publications

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“…Such a loss of agonistevoked contraction was not produced by endotoxin contamination, as treatment with polymixin B (which binds to the lipid A of bacterial endotoxin, and thus may inhibit endotoxin-induced changes in contraction) had no effect [19]. Taken together, our present and previous results suggest that in aortic rings incubated in DMEM alone -as with aging [16][17][18] -the reduction in agonistevoked contraction occurs at some site in the intracellular transduction pathway downstream of [Ca 2+ ] i mobilization.…”

Section: Discussionsupporting

confidence: 58%

“…during chronic hypertension and atherosclerosis). On the other hand, oxidative stress in vascular smooth muscle cells, especially during aging, leads to an increase in inducible nitric oxide synthase (iNOS) expression [13,14], with an increasing importance of NO‐mediated dilation [15] and thus to a fall in the sensitivity to vasoconstrictor agonists [16–18]. Similar mechanisms have been observed following 3 days of incubation of aortic rings from adult rats, which are susceptible to oxidative stress and increased iNOS expression [19].…”

Section: Introductionmentioning

confidence: 99%

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Melatonin counteracts the loss of agonist‐evoked contraction of aortic rings induced by incubation

Lartaud¹,

Faure²,

Tabellion³

et al. 2007

Fundamemntal Clinical Pharma

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Incubation of aortic rings in a culture medium produces phenomena similar to those observed with aging, i.e. oxidative stress and inflammation leading to increased nitric oxide (NO)‐mediated dilation and decreased arterial sensitivity to vasoconstrictor agents. We evaluated whether melatonin protects aortic rings from such a decrease in vasoreactivity. Two concentrations of melatonin were used: 10−8 m, EC50 for vascular MT1–MT2 receptors, and 10−5 m, reported as anti‐oxidant. Anti‐oxidant capacity, inducible nitric oxide synthase (iNOS) expression and isometric contraction of thoracic aorta rings (Wistar rats) evoked by norepinephrine (NE) were assessed. Three days of incubation of aortic rings induced iNOS expression and a fall in NE‐evoked contraction. When melatonin was added to the organ bath, it (10−5 m) increased (+96%, P < 0.05), but did not restore (compared with freshly isolated rings) NE‐evoked contraction. Three days of treatment with melatonin increased (10−8 m, +99%) or restored (10−5 m, +216%) NE‐evoked contraction (compared with freshly isolated rings). The beneficial effects of 10−8 and 10−5 m melatonin on NE‐evoked contraction were abolished in the presence of luzindole (2 × 10−6 m, a melatonin receptor antagonist). The incubation‐induced increase in iNOS expression was reduced following 3 days of melatonin administration (10−8 and 10−5 m). Melatonin (10−5 m) increased catalase activity (6550 ± 256, P < 0.05 vs. nontreated fresh aortic rings 5554 ± 444 nmol min−1 mg protein−1). In conclusion, melatonin counteracts the incubation‐induced loss of agonist‐evoked contraction of aortic rings by a specific receptor‐mediated phenomenon involving iNOS expression; at higher melatonin concentrations, an anti‐oxidant effect is probably also involved.

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Section: Discussionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 99%

Melatonin counteracts the loss of agonist‐evoked contraction of aortic rings induced by incubation

Lartaud¹,

Faure²,

Tabellion³

et al. 2007

Fundamemntal Clinical Pharma

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“…In our laboratory's experiments on the rat, intracellular calcium is some 100,000 lower than total arterial calcium content (calculated from data in Refs. 17,60,100,119). Furthermore, it is uncertain whether changes in vascular wall intracellular calcium with age could be physiologically relevant.…”

Section: Balance Between Promoters and Inhibitors Of Calcificationmentioning

confidence: 99%

Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences

Atkinson¹

2008

Journal of Applied Physiology

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Atkinson J. Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences. J Appl Physiol 105: 1643-1651, 2008. First published September 4, 2008 doi:10.1152/japplphysiol.90476.2008.-With age, the calcium content of the arterial wall increases. Calcification occurs at two main levels: intimal plaques and the medial elastic fiber network. The latter has been referred to as medial elastocalcinosis and is the subject of this review. The mechanisms involved in elastocalcinosis are complex and involve polar, apolar, and active processes. Vascular calcification may be species specific to humans. As laboratory animals, such as the rat, grow old, they suffer from only very mild arterial calcification. Different animal models of induction of massive arterial calcification by pharmacological and other means exist. Although extrapolation from such models to the clinical situation in terms of etiology is difficult, such models could be useful in the nonclinical study of the pathophysiological consequences of vascular calcification. Vascular calcification modifies arterial wall stiffness, and this could have clinically significant consequences on cardiac function and downstream circulatory control.artery; calcium; wall stiffness; aging Development of the Concept of ElastocalcinosisSeveral recent reviews deal with the subject of elastocalcinosis (1,21,25,41,54,56,82,108).Age-linked vascular calcification has been known since the nineteenth century (85,122). It appears to be "specific" in that vascular wall calcium and phosphorus contents increase with age, whereas there are no significant increases in the aortic content of most other elements, such as sodium, potassium, and magnesium (128). Vascular calcification linked to age is also specific for arteries and does not involve other soft tissues, such as veins (57,60,117). Vascular calcification is associated with hypertension. Blumenthal et al. (9) showed that the onset of arterial calcification occurs at an earlier age in hypertensive subjects. The association in humans between arterial calcification and hypertension has since been reported by many investigators (75). The etiology of the complex multifactorial interactions, however, between hypertension (and associated changes in vascular wall mechanics) and amplification of calcification remains obscure.Vascular calcification can occur in localized intimal plaques and in a diffuse fashion in the media (53), and often there is no indication in published reports of where samples were taken. Méndez and Tejada (76) reported that the calcium content of plaques is 10-fold higher than that of "plaque-free" artery. Thus "contamination" of samples with plaque material could mask medial, diffuse elastocalcinosis. It is to be noted that the calcium content of "normal" intima (i.e., free of plaques and fatty streaks) is low and shows only a slight increase with age (6, 29). Medial elastocalcinosis independent of atheroma-associated calcification has been demonstrated by Elliot and McGra...

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“…Speculation on how that mechanism might work includes the following: (i) a study comparing epinephrine and prazosin binding in rat parotid cell preparations indicates a naturally occurring, post-alpha 1 adrenoreceptor defect in signal transduction (Ishikawa et al, 1989); (ii) agerelated impairments in alpha 1 adrenergic responsiveness could be partially caused by alterations in the coupling of alpha adrenergic receptors with G proteins (Myamoto et al 1992); (iii) another study indicated a decline in the G protein amplification of constriction (Robert et al 1998). …”

Section: Mean ± Sementioning

confidence: 99%

Alpha 1 adrenergic receptor control of renal blood vessels during aging

Passmore¹,

Rowell²,

Joshua³

et al. 2005

Can. J. Physiol. Pharmacol.

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Aging humans and rats have a reduced renal vascular constriction response to stress, change in posture, or exercise. In this study, renal interlobar arteries from 9- (intermediate age) to 15-month-old (aging) male Wistar rats constricted less to alpha-adrenergic agonists than those of 4-month-old (young adult) rats. The reduced contraction to A61603 (alpha 1 A agonist) was similar to that to norepinephrine and phenylephrine. Therefore, it appears that the reduction in constriction is primarily related to alpha 1 A receptor stimulation. GeneChip microarray hybridization analysis of the interlobar arteries with the RAE 230A GeneChip indicated that there were no significant differences in gene expression for alpha 1 A/C, 1B, or 1D receptors between 4-month-old (young adult) and 1-year-old (aging) male Wistar rats. Competitive binding experiments (prazosin) revealed that maximal binding (Bmax, fmol/mg protein) of the alpha 1 receptors of interlobar arteries was reduced 25% by 10 months of age and 50% by 18+ months of age. Alpha 1 receptor-induced arterial constriction and prazosin binding were both down-regulated. The loss of receptor-initiated constriction likely includes down-regulation of maximum agonist binding by alpha 1 adrenergic receptors.

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Sensitivity of norepinephrine-evoked vasoconstriction to pertussis toxin in the old rat

Cited by 8 publications

References 21 publications

Melatonin counteracts the loss of agonist‐evoked contraction of aortic rings induced by incubation

Melatonin counteracts the loss of agonist‐evoked contraction of aortic rings induced by incubation

Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences

Alpha 1 adrenergic receptor control of renal blood vessels during aging

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