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Adrenergic Receptors: ɑ Subtype01:31

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Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
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Adrenergic Receptors: β Subtype01:26

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β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
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Endocrine Signaling01:45

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Endocrine cells produce hormones to communicate with remote target cells found in other organs. The hormone reaches these distant areas using the circulatory system. This exposes the whole organism to the hormone but only those cells expressing hormone receptors or target cells are affected. Thus, endocrine signaling induces slow responses from its target cells but these effects also last longer.
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Parasympathetic Signaling01:30

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Adiponectin Signaling Regulates Urinary Bladder Function by Blunting Smooth Muscle Purinergic Contractility.

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    Biorxiv : the Preprint Server for Biology
    |November 18, 2024
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    Adiponectin (ADPN) signaling impacts bladder function. ADPN deficiency in mice caused lower urinary tract symptoms (LUTS), suggesting a novel pathway for obesity-related bladder dysfunction.

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    Area of Science:

    • Endocrinology
    • Urology
    • Metabolic Syndrome Research

    Background:

    • Lower urinary tract symptoms (LUTS) affect over 50% of individuals over 40 and are linked to obesity and metabolic syndrome.
    • Adipose tissue releases adipokines, like adiponectin (ADPN), which regulate metabolism and inflammation, but their role in LUTS is unclear.

    Purpose of the Study:

    • To investigate the role of adiponectin (ADPN) in regulating bladder function and its potential involvement in LUTS associated with metabolic dysfunction.

    Main Methods:

    • Utilized a global ADPN knockout mouse model (Adpn-/-) to assess bladder function.
    • Examined voiding patterns, bladder smooth muscle (BSM) contractility, and molecular pathways.
    • Administered ADPN receptor agonist (AdipoRon) and AMPK modulators to evaluate their effects on BSM contraction.

    Main Results:

    • Adpn-/- mice displayed increased urination frequency, smaller void volumes, and diminished BSM contractility, notably lacking purinergic contraction.
    • Molecular analysis revealed significant alterations in metabolic and purinergic signaling pathways in Adpn-/- mice.
    • AdipoRon treatment abolished acute BSM contraction, and both AMPK activators and inhibitors also inhibited BSM purinergic contraction.

    Conclusions:

    • A novel ADPN signaling pathway is crucial for regulating BSM contractility.
    • Dysregulation of this ADPN pathway may represent a key mechanism underlying LUTS in obesity and metabolic syndrome.