Vascular smooth muscle reactivity to norepinephrine in ovariectomized rats: Relationship to vascular PGE2/PGF2α ratio

Zamorano, B; Bruzzone, M. E.; Martı́nez, Jorge

doi:10.1016/0306-3623(95)00060-7

Cited by 10 publications

(7 citation statements)

References 26 publications

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“…These findings corroborate previous data that show a potentiation of the vasoconstrictor response in castrated male rats (Stallone 1994;Glenn et al 1997;Cignarella et al 2000). Moreover, estrogen deprivation also increases the vascular reactivity of female animals to vasoconstrictor agents (Zamorano et al 1995;Nevala et al 1996;Minshall et al 1998;Ma et al 2000;Khalil 2005). The hyperreactivity to vasoconstrictor agents induced by gonadectomy could be explained by different cellular events, e.g.…”

Section: Discussionsupporting

confidence: 91%

Differential vascular adaptive response to stress exposure in male and female rats: Role of gonadal hormones and endothelial cells

Júnior

Cordellini

2007

Stress

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Section: Discussionsupporting

confidence: 91%

Differential vascular adaptive response to stress exposure in male and female rats: Role of gonadal hormones and endothelial cells

Júnior

Cordellini

2007

Stress

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“…These results are in agreement with the results of previous studies that used several vasoconstrictors and different time points after OVX, norepinephrine and rats treated 8 days after OVX in the study of Zamorano et al [13] and phenylephrine and rats treated 8 weeks after OVX in that of Crews and Khalil [14]. These results demonstrate that ovarian hormones modulate the contractility that is induced by adrenergic agonists [7,13,15,16]. It is widely accepted that agonist-induced vascular smooth muscle contraction is mediated by Ca 2+ release from intracellular stores and Ca 2+ entry from the extracellular space [17].…”

Section: The Effects Of Ovx On Phenylephrine-and Ca 2+ -Induced Aortisupporting

confidence: 83%

The Effects of 17�-Oestradiol on Increased a₁-Adrenergic Vascular Reactivity Induced by Prolonged Ovarian Hormone Deprivation: The Role of Voltage-Dependent L-type Ca²⁺Channels

Valencia-Hernández

Reyes-Ramírez²,

Urquiza-Marín³

et al. 2012

Pharmacology

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The present study investigated the hypothesis that the duration of ovarian hormone deprivation before reintroduction of oestrogen affects the role of oestrogen as a mediator of the contractile function of α₁-adrenergic receptors. Rats underwent ovariectomy (OVX) or were sham-operated, and the OVX rats were treated with vehicle (corn oil) or 17β-oestradiol (E₂) for 5 days either 10, 28 or 60 days after OVX. The OVX increased phenylephrine- and Ca²⁺-induced contractions. Interestingly, the phenylephrine-induced contractions were increased at each of the three time points, whereas the Ca²⁺-induced contractions were only increased in the 60-day group. E₂ had biphasic effects on phenylephrine- and Ca²⁺-induced contractility. Indeed, E₂ increased contractions in the 10-day group and diminished contractions in the other groups (the increased contractions were avoided by verapamil). These results indicate that E₂ controls α₁-adrenergic receptor-mediated contractility through effects on L-type Ca²⁺ channels in a way that depends on the timing in which the treatment with E₂ is initiated.

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“…In support of this view, it has been shown that PGF 2 α is one of the primary products of AA formed in most cardiovascular tissues in response to adrenergic stimuli (Malik, 1988). Moreover, in rat aortic rings, constrictor responses to NA were associated to an increased PGF 2 α vascular synthesis (Zamorano, Bruzzone & Martínez, 1995). Furthermore, PGF 2 α was the main prostanoid produced by rat endothelial cells in culture (Kis et al , 1999).…”

Section: Discussionmentioning

confidence: 99%

Effects of eicosanoids and nitric oxide on the noradrenaline‐induced contractions in the rat mesenteric bed

Peredo

Adler‐Graschinsky

2000

J. Autonom. Pharmacol.

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1. The effects of the inhibition of the metabolism of arachidonic acid (AA) on the constrictor responses to noradrenaline (NA) were studied in the rat perfused mesenteric bed. The inhibitor of all the pathways of AA metabolism, 10 microM eicosatetraynoic acid (ETYA), reduced the constrictor responses to all the concentrations of NA assayed. 2. The constrictor responses to NA were also reduced by the cyclooxygenase (COX) inhibitor, indomethacin (10 microM), as well as by the lipoxygenase inhibitor, nordihidroguaiaretic acid (1 microM; NDGA), whereas they were unmodified by the cytochrome P450 monooxigenase inhibitors, clotrimazole (10 microM), metyrapone (10 microM) and proadifen (10 microM). 3. The reduction in NA contractility induced by indomethacin was reverted with a decreasing order of potency by the thromboxane A2 analogue, U-46619 > prostaglandin (PG) E2 > PGF2alpha. The exposure of the mesenteric bed to NA increased the production of PGF2alpha, whereas it did not modify the production of the remaining AA metabolites. 4. The increase in the NA-induced contractions caused by endothelium removal, as well as by the inhibition of nitric oxide synthase (NOs) with NG-nitro-L-arginine methyl ester (400 microM; L-NAME), was suppressed by indomethacin but not by NDGA. These observations suggest that the lipoxygenase-derived metabolites are formed in the endothelium, whereas the COX-derived metabolites are formed in the vascular smooth muscle. 5. The TP receptor antagonist, SQ29548, did not modify the NA-induced contractions, either in the presence or in the absence of the endothelium. 6. Contractions elicited by KCI (60-100 mM) were unmodified by the AA metabolism inhibitors, ETYA, NDGA and indomethacin. 7. In summary, these results show that metabolites of AA, through both the COX and the lipoxygenase pathways, are involved in the NA-induced contractions in the rat mesenteric bed. The lipoxygenase metabolites are likely to be formed in the vascular endothelium, whereas the COX metabolite, which could be PGF2alpha, is apparently formed within the vascular smooth muscle.

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Vascular smooth muscle reactivity to norepinephrine in ovariectomized rats: Relationship to vascular PGE2/PGF2α ratio

Cited by 10 publications

References 26 publications

Differential vascular adaptive response to stress exposure in male and female rats: Role of gonadal hormones and endothelial cells

Differential vascular adaptive response to stress exposure in male and female rats: Role of gonadal hormones and endothelial cells

The Effects of 17�-Oestradiol on Increased a₁-Adrenergic Vascular Reactivity Induced by Prolonged Ovarian Hormone Deprivation: The Role of Voltage-Dependent L-type Ca²⁺Channels

Effects of eicosanoids and nitric oxide on the noradrenaline‐induced contractions in the rat mesenteric bed

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Vascular smooth muscle reactivity to norepinephrine in ovariectomized rats: Relationship to vascular PGE2/PGF2α ratio

Cited by 10 publications

References 26 publications

Differential vascular adaptive response to stress exposure in male and female rats: Role of gonadal hormones and endothelial cells

Differential vascular adaptive response to stress exposure in male and female rats: Role of gonadal hormones and endothelial cells

The Effects of 17�-Oestradiol on Increased a1-Adrenergic Vascular Reactivity Induced by Prolonged Ovarian Hormone Deprivation: The Role of Voltage-Dependent L-type Ca2+Channels

Effects of eicosanoids and nitric oxide on the noradrenaline‐induced contractions in the rat mesenteric bed

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The Effects of 17�-Oestradiol on Increased a₁-Adrenergic Vascular Reactivity Induced by Prolonged Ovarian Hormone Deprivation: The Role of Voltage-Dependent L-type Ca²⁺Channels