Related Experiment Video

Updated: Aug 11, 2026

Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy
11:27

Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy

Published on: April 29, 2014

Are mineralocorticoid receptors present in human renal adenocarcinoma?

M E Rafestin-Oblin, C Roth-Meyer, M Claire

    Clinical Science (London, England : 1979)
    |November 1, 1979
    PubMed

    Insights

    Mineralocorticoid receptors, crucial for aldosterone binding in normal kidney tissue, appear absent in renal adenocarcinoma. This suggests a potential link between tumor origin and receptor status.

    Area of Science:

    • Endocrinology
    • Oncology
    • Nephrology

    Background:

    • Normal human renal tissue exhibits high-affinity binding sites for aldosterone.
    • Renal adenocarcinoma is a significant clinical concern, and understanding its cellular characteristics is vital.

    Purpose of the Study:

    • To investigate the presence and binding characteristics of mineralocorticoid and glucocorticoid receptors in human renal adenocarcinoma.
    • To compare receptor binding in neoplastic tissue with that in normal renal cortex.

    Main Methods:

    • Radioligand binding assays using [3H]aldosterone and [3H]dexamethasone were performed on cytosol and nuclear fractions.
    • Tissue samples from 22 patients with renal adenocarcinoma and uninvolved external cortex were analyzed.

    Main Results:

    • Cytosol [3H]aldosterone binding was significantly lower (6-7 fold) in renal adenocarcinoma compared to normal tissue (P < 0.001).
    • [3H]Aldosterone binding was also reduced in both cytosol and nuclear fractions of adenocarcinoma.
    • While [3H]dexamethasone binding was slightly higher in neoplastic tissue, the difference was not statistically significant.

    Conclusions:

    • The significantly diminished binding of [3H]aldosterone suggests a lack of functional mineralocorticoid receptors in renal adenocarcinoma.
    • This finding supports the hypothesis that renal adenocarcinomas may originate from proximal tubule cells, which have fewer mineralocorticoid receptors.

    More Related Videos

    Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium08:46

    Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium

    Published on: September 1, 2015

    Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions06:32

    Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions

    Published on: June 13, 2025

    Related Concept Videos

    Hormonal Regulation01:33

    Hormonal Regulation

    The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
    Transducer Mechanism: Nuclear Receptors01:31

    Transducer Mechanism: Nuclear Receptors

    Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
    About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
    Adrenergic Receptors (Adrenoceptors): Classification01:27

    Adrenergic Receptors (Adrenoceptors): Classification

    Adrenergic receptors, or adrenoceptors, respond to the autonomic neurotransmitter noradrenaline and other endogenous catecholamine agonists. They are classified into two main families, α and β, based on their pharmacological response and are further subdivided depending on their location, elicited response, and affinity to specific agonists or antagonists.
    α-Adrenoceptors
    α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors, which are found on postsynaptic...
    Adrenergic Receptors: &#593; Subtype01:31

    Adrenergic Receptors: ɑ Subtype

    Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
    Adrenaline ≥ Noradrenaline >> Isoprenaline
    α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
    α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase C—inositol-1,4,5-trisphosphate...
    Adrenergic Receptors: &#946; Subtype01:26

    Adrenergic Receptors: β Subtype

    β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
    Isoprenaline > Adrenaline > Noradrenaline
    Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
    β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
    Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

    Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

    The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...