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Cellular and Molecular Mechanisms in Hypertension pp 55–69Cite as

Altered Phospholipase Activities Related to α1-Adrenergic Receptor Supersensitivity of Aortas from Aldosterone-Salt Hypertensive Rats

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 308))

Abstract

Vascular smooth muscle from several hypertensive models exhibits supersensitivity to catecholamines, which precedes the development of overt hypertension in rats given mineralocorticoid-salt treatment (1–5). In previous studies we did not find significant changes in αl-receptor characteristics (receptor type, dissociation constant or maximal receptor binding) in aorta from aldosterone-salt hypertensive rats (AHR) (6,7). Since we observed a 2–15 fold leftward shift in the NE EC50 (concentration of norepinephrine required for 50% response) for functional responses in AHR, we concluded that increased efficacy of post receptor events occurs in AHR (7,8).

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Author notes

  1. Jacquelyn M. Smith

    Present address: Department of Physiology, Chicago College of Osteopathic Medicine, Downers Grove, IL, 60515, USA

Authors and Affiliations

  1. Departments of Physiology and Pharmacology, University of Missouri, Columbia, MO, 65212, USA

    Allan W. Jones, Shivendra D. Shukla, Brinda B. Geisbuhler, Susan B. Jones & Jacquelyn M. Smith

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  1. Allan W. Jones
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  2. Shivendra D. Shukla
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  3. Brinda B. Geisbuhler
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  4. Susan B. Jones
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  5. Jacquelyn M. Smith
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Editors and Affiliations

  1. Bockus Research Institute, The Graduate Hospital and Department of Physiology, The University of Pennsylvania, 19104, Philadelphia, PA, USA

    Robert H. Cox

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© 1991 Plenum Press, New York

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Jones, A.W., Shukla, S.D., Geisbuhler, B.B., Jones, S.B., Smith, J.M. (1991). Altered Phospholipase Activities Related to α1-Adrenergic Receptor Supersensitivity of Aortas from Aldosterone-Salt Hypertensive Rats. In: Cox, R.H. (eds) Cellular and Molecular Mechanisms in Hypertension. Advances in Experimental Medicine and Biology, vol 308. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-6015-5_5

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  • DOI: https://doi.org/10.1007/978-1-4684-6015-5_5

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-6017-9

  • Online ISBN: 978-1-4684-6015-5

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