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The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Published

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The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein. / Mukerji, M. S.; Leathard, H. L.; Huddart, Henry.
In: Journal of Pharmacy and Pharmacology, Vol. 52, No. 7, 07.2000, p. 843-849.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Mukerji, MS, Leathard, HL & Huddart, H 2000, 'The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein.', Journal of Pharmacy and Pharmacology, vol. 52, no. 7, pp. 843-849. https://doi.org/10.1211/0022357001774525

APA

Mukerji, M. S., Leathard, H. L., & Huddart, H. (2000). The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein. Journal of Pharmacy and Pharmacology, 52(7), 843-849. https://doi.org/10.1211/0022357001774525

Vancouver

Mukerji MS, Leathard HL, Huddart H. The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein. Journal of Pharmacy and Pharmacology. 2000 Jul;52(7):843-849. doi: 10.1211/0022357001774525

Author

Mukerji, M. S. ; Leathard, H. L. ; Huddart, Henry. / The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein. In: Journal of Pharmacy and Pharmacology. 2000 ; Vol. 52, No. 7. pp. 843-849.

Bibtex

@article{2955c43f1dda4472ae9783d7600b53a9,
title = "The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein.",
abstract = "The mechanisms underlying the suppression of vasocontractility caused by progesterone were investigated by studying changes in the contractile force of rat isolated aorta and portal vein, induced by altering extracellular concentrations of noradrenaline (NA) potassium ions (K+) and calcium ions (Ca2+). In the aorta, progesterone (10 M) had a general suppressive effect on NA-, Ca2+- and K+-induced contractions. In contrast, in the portal vein a more selective suppression of contractions was observed. Both tonic and phasic components of contractions induced by cumulative addition of Ca2+ to tissues equilibrated in Ca2+-free saline were suppressed. The phasic but not tonic components of contractions induced by NA addition were suppressed. There was no significant effect on tonic contractions induced by elevated (40–120 mM) K+, but a concentration-dependent suppression of the phasic component of contractions was observed during depolarisation with smaller elevations of K+ concentrations (5–20 mM). These results suggest that on the portal vein the suppressive effect of progesterone is due to a potassium channel opening action, whilst on the aorta a different or additional mechanism of suppression exists.",
author = "Mukerji, {M. S.} and Leathard, {H. L.} and Henry Huddart",
year = "2000",
month = jul,
doi = "10.1211/0022357001774525",
language = "English",
volume = "52",
pages = "843--849",
journal = "Journal of Pharmacy and Pharmacology",
issn = "0022-3573",
publisher = "Pharmaceutical Press",
number = "7",

}

RIS

TY - JOUR

T1 - The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein.

AU - Mukerji, M. S.

AU - Leathard, H. L.

AU - Huddart, Henry

PY - 2000/7

Y1 - 2000/7

N2 - The mechanisms underlying the suppression of vasocontractility caused by progesterone were investigated by studying changes in the contractile force of rat isolated aorta and portal vein, induced by altering extracellular concentrations of noradrenaline (NA) potassium ions (K+) and calcium ions (Ca2+). In the aorta, progesterone (10 M) had a general suppressive effect on NA-, Ca2+- and K+-induced contractions. In contrast, in the portal vein a more selective suppression of contractions was observed. Both tonic and phasic components of contractions induced by cumulative addition of Ca2+ to tissues equilibrated in Ca2+-free saline were suppressed. The phasic but not tonic components of contractions induced by NA addition were suppressed. There was no significant effect on tonic contractions induced by elevated (40–120 mM) K+, but a concentration-dependent suppression of the phasic component of contractions was observed during depolarisation with smaller elevations of K+ concentrations (5–20 mM). These results suggest that on the portal vein the suppressive effect of progesterone is due to a potassium channel opening action, whilst on the aorta a different or additional mechanism of suppression exists.

AB - The mechanisms underlying the suppression of vasocontractility caused by progesterone were investigated by studying changes in the contractile force of rat isolated aorta and portal vein, induced by altering extracellular concentrations of noradrenaline (NA) potassium ions (K+) and calcium ions (Ca2+). In the aorta, progesterone (10 M) had a general suppressive effect on NA-, Ca2+- and K+-induced contractions. In contrast, in the portal vein a more selective suppression of contractions was observed. Both tonic and phasic components of contractions induced by cumulative addition of Ca2+ to tissues equilibrated in Ca2+-free saline were suppressed. The phasic but not tonic components of contractions induced by NA addition were suppressed. There was no significant effect on tonic contractions induced by elevated (40–120 mM) K+, but a concentration-dependent suppression of the phasic component of contractions was observed during depolarisation with smaller elevations of K+ concentrations (5–20 mM). These results suggest that on the portal vein the suppressive effect of progesterone is due to a potassium channel opening action, whilst on the aorta a different or additional mechanism of suppression exists.

U2 - 10.1211/0022357001774525

DO - 10.1211/0022357001774525

M3 - Journal article

VL - 52

SP - 843

EP - 849

JO - Journal of Pharmacy and Pharmacology

JF - Journal of Pharmacy and Pharmacology

SN - 0022-3573

IS - 7

ER -