The neurohormonal natural history of essential hypertension

towards primary or tertiary aldosteronism?

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    39 Citations (Scopus)

    Abstract

    Use of the aldosterone-to-renin ratio has controversially suggested that approximately 10% of hypertensives have primary aldosteronism, and most of these individuals are thought to have idiopathic hyperaldosteronism. The usual renin-angiotensin system control is intact in these individuals and is similar to that in low renin and essential hypertensives, differing only in the degree of sensitivity. There is recent evidence suggesting that hyperaldosteronism relates to aldosterone synthase genetic polymorphism, and also that increased angiotensin II stimulation of the adrenal glands appears to paradoxically upregulate the receptors increasing angiotensin II sensitivity. Taken together, the possibility arises that, in susceptible hypertensives, hyperaldosteronism could be acquired. Indeed, it is well known that renin-driven renovascular hypertension is associated with the development of hyperaldosteronism. Hypothetically, within the wider hypertensive population, these findings set the scene that angiotensin II adrenal sensitivity increases over time until the secretion of aldosterone becomes "autonomous" and hence "tertiary" aldosteronism in a significant proportion of hypertensives.
    Original languageEnglish
    Pages (from-to)11-15
    Number of pages5
    JournalJournal of Hypertension
    Volume20
    Issue number1
    Publication statusPublished - 2002

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    Hyperaldosteronism
    Natural History
    Renin
    Aldosterone
    Angiotensin II
    Cytochrome P-450 CYP11B2
    Renovascular Hypertension
    Angiotensin Receptors
    Genetic Polymorphisms
    Renin-Angiotensin System
    Adrenal Glands
    Essential Hypertension
    Up-Regulation
    Population

    Cite this

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    title = "The neurohormonal natural history of essential hypertension: towards primary or tertiary aldosteronism?",
    abstract = "Use of the aldosterone-to-renin ratio has controversially suggested that approximately 10{\%} of hypertensives have primary aldosteronism, and most of these individuals are thought to have idiopathic hyperaldosteronism. The usual renin-angiotensin system control is intact in these individuals and is similar to that in low renin and essential hypertensives, differing only in the degree of sensitivity. There is recent evidence suggesting that hyperaldosteronism relates to aldosterone synthase genetic polymorphism, and also that increased angiotensin II stimulation of the adrenal glands appears to paradoxically upregulate the receptors increasing angiotensin II sensitivity. Taken together, the possibility arises that, in susceptible hypertensives, hyperaldosteronism could be acquired. Indeed, it is well known that renin-driven renovascular hypertension is associated with the development of hyperaldosteronism. Hypothetically, within the wider hypertensive population, these findings set the scene that angiotensin II adrenal sensitivity increases over time until the secretion of aldosterone becomes {"}autonomous{"} and hence {"}tertiary{"} aldosteronism in a significant proportion of hypertensives.",
    author = "Lim, {Pitt O} and Struthers, {Allan D} and MacDonald, {Thomas M}",
    year = "2002",
    language = "English",
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    TY - JOUR

    T1 - The neurohormonal natural history of essential hypertension

    T2 - towards primary or tertiary aldosteronism?

    AU - Lim, Pitt O

    AU - Struthers, Allan D

    AU - MacDonald, Thomas M

    PY - 2002

    Y1 - 2002

    N2 - Use of the aldosterone-to-renin ratio has controversially suggested that approximately 10% of hypertensives have primary aldosteronism, and most of these individuals are thought to have idiopathic hyperaldosteronism. The usual renin-angiotensin system control is intact in these individuals and is similar to that in low renin and essential hypertensives, differing only in the degree of sensitivity. There is recent evidence suggesting that hyperaldosteronism relates to aldosterone synthase genetic polymorphism, and also that increased angiotensin II stimulation of the adrenal glands appears to paradoxically upregulate the receptors increasing angiotensin II sensitivity. Taken together, the possibility arises that, in susceptible hypertensives, hyperaldosteronism could be acquired. Indeed, it is well known that renin-driven renovascular hypertension is associated with the development of hyperaldosteronism. Hypothetically, within the wider hypertensive population, these findings set the scene that angiotensin II adrenal sensitivity increases over time until the secretion of aldosterone becomes "autonomous" and hence "tertiary" aldosteronism in a significant proportion of hypertensives.

    AB - Use of the aldosterone-to-renin ratio has controversially suggested that approximately 10% of hypertensives have primary aldosteronism, and most of these individuals are thought to have idiopathic hyperaldosteronism. The usual renin-angiotensin system control is intact in these individuals and is similar to that in low renin and essential hypertensives, differing only in the degree of sensitivity. There is recent evidence suggesting that hyperaldosteronism relates to aldosterone synthase genetic polymorphism, and also that increased angiotensin II stimulation of the adrenal glands appears to paradoxically upregulate the receptors increasing angiotensin II sensitivity. Taken together, the possibility arises that, in susceptible hypertensives, hyperaldosteronism could be acquired. Indeed, it is well known that renin-driven renovascular hypertension is associated with the development of hyperaldosteronism. Hypothetically, within the wider hypertensive population, these findings set the scene that angiotensin II adrenal sensitivity increases over time until the secretion of aldosterone becomes "autonomous" and hence "tertiary" aldosteronism in a significant proportion of hypertensives.

    M3 - Article

    VL - 20

    SP - 11

    EP - 15

    JO - Journal of Hypertension

    JF - Journal of Hypertension

    SN - 0263-6352

    IS - 1

    ER -