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  2. Aldosterone - Wikipedia

    en.wikipedia.org/wiki/Aldosterone

    Anxiety increases aldosterone, [36] which must have evolved because of the time delay involved in migration of aldosterone into the cell nucleus. [38] Thus, there is an advantage to an animal's anticipating a future need from interaction with a predator, since too high a serum content of potassium has very adverse effects on nervous transmission.

  3. Glucocorticoid remediable aldosteronism - Wikipedia

    en.wikipedia.org/wiki/Glucocorticoid_remediable...

    Aldosterone is increased by blood loss, pregnancy, and possibly by other circumstances such as physical exertion, endotoxin shock, and burns. Aldosterone feedback : [ citation needed ] Feedback by aldosterone concentration itself is of a non-morphological character (that is, other than changes in cell number or structure) and is relatively poor ...

  4. Hypoaldosteronism - Wikipedia

    en.wikipedia.org/wiki/Hypoaldosteronism

    Hypoaldosteronism causes low sodium (hyponatremia), high potassium (hyperkalemia), and metabolic acidosis, a condition in which the body produces excess acid.These conditions are responsible for the symptoms of hypoaldosteronism, which include muscle weakness, nausea, palpitations, irregular heartbeat, and abnormal blood pressure.

  5. Bone resorption - Wikipedia

    en.wikipedia.org/wiki/Bone_resorption

    Dentistry sees resorption as dissolution or breakdown of a tooth structure. This could be inflammation and dentine or cement loss. Bone tissue is a dynamic system with active metabolism. [24] Bone tissue remodelling or bone remodeling is a successive chain of old bone matrix removal and its replacement with a new one. [25]

  6. Homeostasis - Wikipedia

    en.wikipedia.org/wiki/Homeostasis

    This causes the release of aldosterone into the blood. Aldosterone acts primarily on the distal convoluted tubules and collecting ducts of the kidneys, stimulating the excretion of potassium ions into the urine. [65] It does so, however, by activating the basolateral Na + /K + pumps of the tubular epithelial cells. These sodium/potassium ...

  7. Renin–angiotensin system - Wikipedia

    en.wikipedia.org/wiki/Renin–angiotensin_system

    In the adrenal cortex, angiotensin II acts to cause the release of aldosterone. Aldosterone acts on the tubules (e.g., the distal convoluted tubules and the cortical collecting ducts) in the kidneys, causing them to reabsorb more sodium and water from the urine. This increases blood volume and, therefore, increases blood pressure.

  8. Mineralocorticoid - Wikipedia

    en.wikipedia.org/wiki/Mineralocorticoid

    Hyperaldosteronism (the syndrome caused by elevated aldosterone) is commonly caused by either idiopathic adrenal hyperplasia or by an adrenal adenoma. The two main resulting problems: Hypertension and edema due to excessive Na+ and water retention. Accelerated excretion of potassium ions (K+). With extreme K+ loss there is muscle weakness and ...

  9. Mineralocorticoid receptor - Wikipedia

    en.wikipedia.org/wiki/Mineralocorticoid_receptor

    The mineralocorticoid receptor (or MR, MLR, MCR), also known as the aldosterone receptor or nuclear receptor subfamily 3, group C, member 2, (NR3C2) is a protein that in humans is encoded by the NR3C2 gene that is located on chromosome 4q31.1-31.2. [5] MR is a receptor with equal affinity for mineralocorticoids and glucocorticoids.