Physiological Modulation of α-Adrenoceptor and 5HT Receptor Expression in Blood Vessels

McGrath, J.C.; Dunn, William R.; Templeton, A.G.B.

doi:10.1159/000158805

Cited by 7 publications

(7 citation statements)

References 20 publications

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“…In addition, we have shown that non-selective depolarization by KCl does not evoke any potentiation of endothelin-1-evoked contractions [19]. Receptorreceptor interactions remain a possibility, and such interactions have been postulated between angiotensin II and α-adrenoceptors [21]. This might explain the different interactions of angiotensin II and various spasmogens, as well as the inability of other agonists, such as U46619 [19] or histamine ( J. E. Nally, N. C. Thomson, M. J. O. Wakelam and J. C. McGrath, unpublished work), to mimic angiotensin II.…”

Section: Discussionmentioning

confidence: 86%

Hydrocortisone abolishes the angiotensin II-mediated potentiation of endothelin-1 in bovine bronchi

Brown

Nally

2001

Clinical Science

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Angiotensin II potentiates methacholine-evoked bronchoconstriction both in bovine airways in vitro and in asthmatic patients in vivo. Angiotensin II also potentiates endothelin-1-evoked contractions in vitro, but fails to alter such contractions in vivo. One possible confounding factor in patients is their use of inhaled corticosteroids. Accordingly the present study examined the effects of hydrocortisone (cortisol) on contractions evoked by methacholine and endothelin-1 in the presence and absence of angiotensin II. Contractions of rings of isolated bovine airways were measured isometrically in organ baths. Concentration-response curves were obtained for endothelin-1 or methacholine in the presence and absence of angiotensin II, hydrocortisone and a combination of angiotensin II and hydrocortisone. Hydrocortisone abolished the angiotensin II-mediated potentiation of endothelin-1-evoked, but not methacholine-evoked, contractions. Hydrocortisone alone evoked the enhancement of methacholine responses, similar to the effect produced by angiotensin II. While species differences may exist, our present results suggest that the use of corticosteroids can have a profound effect on the interaction between angiotensin II and endothelin-1. Accordingly, the presence of inhaled corticosteroids might explain the differences between the results obtained in vitro and in vivo.

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Section: Discussionmentioning

confidence: 86%

Hydrocortisone abolishes the angiotensin II-mediated potentiation of endothelin-1 in bovine bronchi

Brown

Nally

2001

Clinical Science

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“…Various authors have demonstrated that placental vessels are much less sensitive to 5-HT than umbilical arteries (Panigel 1962;Mak et al 1984;MacLean et al 1992); this implies that the main role for 5-HT lies in the umbilical vessels. Responses to 5-HT in the feto-placental circulation have been demonstrated by several authors (McGrath et al 1990;Breslin 1991). McGrath et al (1988) have reported that there is no significant difference in response to 5-HT between rubbed (in which the endothelium is removed) and unrubbed preparations of the umbilical artery and vein from late pregnancy.…”

Section: Discussionmentioning

confidence: 87%

Electron-microscopic immunolabelling of vasoactive substances in human umbilical endothelial cells and their actions in early and late pregnancy

Sexton

Loesch

Turmaine

et al. 1996

Cell and Tissue Research

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Human umbilical vessels are devoid of nerves and therefore endothelial cells may play an important role in the control of feto-placental blood flow. The pharmacological effects of 5-hydroxytryptamine, histamine and endothelin were examined in umbilical arteries and veins from legal terminations (gestational age 8-17 weeks, n=12) and normal term vaginal deliveries (gestational age 38-41, n=12). Immunocytochemistry of human unbilical vessels indicated that 5-hydroxytryptamine, histamine and endothelin were localised in subpopulations of endothelial cells of both artery and vein in late, but not early, pregnancy. 5-Hydroxytryptamine (10 nM-30 microM) caused sustained concentration-dependent contractions in all vessels from early and late pregnancy. Histamine (0.1 microM-30 mM) also caused sustained contractions in all vessels from late pregnancy but only 27% of arteries and 41% of veins from early pregnancy responded. Endothelin (10 pM-30 nM) caused slow long-lasting contractions in all vessels from early and late pregnancy. Atrial natriuretic peptide and neuropeptide Y did not alter vascular tone. The endothelium may thus play an autocrine/paracrine role, by synthesizing and releasing the above reactive substances in late pregnancy to influence feto-placental blood flow.

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“…In the tail artery of Fischer 344 rats, the ␣ 2 -AR antagonists idazoxan and rauwolscine shifted the NE concentration-response curves to the right, while the ␣ 2 -AR agonists UK-14304 and BHT-920 shifted the ␣ 1 -AR agonist methoxamine dose-response curves to the left (41). Other studies have suggested that the effects of postjunctional ␣ 2 -AR may be muted and are only observed when another type of agonist is present (18,26).…”

Section: Discussionmentioning

confidence: 93%

Pre- and postjunctional α₂-adrenergic receptors in fetal and adult ovine cerebral arteries

Bishai

Penninga

Nijland

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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In ovine cerebral arteries, adrenergic-mediated vasoconstrictor responses differ significantly with developmental age. We tested the hypothesis that, in part, these differences are a consequence of altered alpha(2)-adrenergic receptor (alpha(2)-AR) density and/or affinity. In fetal (approximately 140 days) and adult sheep, we measured alpha(2)-AR density and affinity with the antagonist [(3)H]idazoxan in main branch cerebral arteries and other vessels. We also quantified contractile responses in middle cerebral artery (MCA) to norepinephrine (NE) or phenylephrine in the presence of the alpha(2)-AR antagonists yohimbine and idazoxan and contractile responses to the alpha(2)-AR agonists clonidine and UK-14304. In fetal and adult cerebral artery homogenates, alpha(2)-AR density was 201 +/- 18 and 52 +/- 6 fmol/mg protein, respectively (P < 0.01); however, antagonist affinity values did not differ. In fetal, but not adult, MCA, 10(-7) M yohimbine significantly decreased the pD(2) for NE-induced tension in the presence of 3 x 10(-5) M cocaine, 10(-5) M deoxycorticosterone, and 10(-6) M tetrodotoxin. In fetal, but not adult, MCA, UK-14304 induced a significant decrease in pD(2) for the phenylephrine dose-response relation. In addition, stimulation-evoked fractional NE release was significantly greater in fetal than in adult cerebral arteries. In the presence of 10(-6) M idazoxan to block alpha(2)-AR-mediated inhibition of prejunctional NE release, the fractional NE release was significantly increased in both age groups. We conclude that in fetal and adult ovine cerebral arteries, alpha(2)-AR appear to be chiefly prejunctional. Nonetheless, the fetal cerebral arteries appear to have a significant component of postjunctional alpha(2)-AR.

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Physiological Modulation of α-Adrenoceptor and 5HT Receptor Expression in Blood Vessels

Cited by 7 publications

References 20 publications

Hydrocortisone abolishes the angiotensin II-mediated potentiation of endothelin-1 in bovine bronchi

Hydrocortisone abolishes the angiotensin II-mediated potentiation of endothelin-1 in bovine bronchi

Electron-microscopic immunolabelling of vasoactive substances in human umbilical endothelial cells and their actions in early and late pregnancy

Pre- and postjunctional α₂-adrenergic receptors in fetal and adult ovine cerebral arteries

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Physiological Modulation of α-Adrenoceptor and 5HT Receptor Expression in Blood Vessels

Cited by 7 publications

References 20 publications

Hydrocortisone abolishes the angiotensin II-mediated potentiation of endothelin-1 in bovine bronchi

Hydrocortisone abolishes the angiotensin II-mediated potentiation of endothelin-1 in bovine bronchi

Electron-microscopic immunolabelling of vasoactive substances in human umbilical endothelial cells and their actions in early and late pregnancy

Pre- and postjunctional α2-adrenergic receptors in fetal and adult ovine cerebral arteries

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Pre- and postjunctional α₂-adrenergic receptors in fetal and adult ovine cerebral arteries