Adrenal steroid synthesis inhibitors


This schedule is designed to ensure adequate therapy during acute episodes, while minimizing the risk of overdosage in chronic cases.
In cerebral edema, Dexamethasone Sodium Phosphate injection, USP is generally administered initially in a dosage of 10 mg intravenously followed by 4 mg every six hours intramuscularly until the symptoms of cerebral edema subside. Response is usually noted within 12 to 24 hours and dosage may be reduced after two to four days and gradually discontinued over a period of five to seven days. For palliative management of patients with recurrent or inoperable brain tumors, maintenance therapy with either Dexamethasone Sodium Phosphate injection, USP or dexamethasone tablets in a dosage of 2 mg two or three times daily may be effective.

  1. Encyclopædia Britannica articles are written in a neutral objective tone for a general audience.
  2. You may find it helpful to search within the site to see how similar or related subjects are covered.
  3. Any text you add should be original, not copied from other sources.
  4. At the bottom of the article, feel free to list any sources that support your changes, so that we can fully understand their context. (Internet URLs are the best.)

Like all steroid hormones, cortisol and aldosterone bind to their respective receptors, and the resulting hormone-receptor complexes bind to a hormone response element to modulate transcription of responsive genes. Although the physiologic effects of these two steroid hormones are distinctly different, their receptors are quite similar and, most interestingly, they bind to the same consensus response element in DNA! How then is it possible to get hormone-specific responses? Follow the path to the next topic to find out at least part of the answer.

The primary mineralocorticoid , aldosterone , is produced in the adrenocortical zona glomerulosa by the action of the enzyme aldosterone synthase (also known as CYP11B2 ). [5] [6] Aldosterone is largely responsible for the long-term regulation of blood pressure . [7] Aldosterone effects on the distal convoluted tubule and collecting duct of the kidney where it causes increased reabsorption of sodium and increased excretion of both potassium (by principal cells) and hydrogen ions (by intercalated cells of the collecting duct). [7] Sodium retention is also a response of the distal colon, and sweat glands to aldosterone receptor stimulation. Although sustained production of aldosterone requires persistent calcium entry through low-voltage activated Ca 2+ channels , isolated zona glomerulosa cells are considered nonexcitable, with recorded membrane voltages that are too hyperpolarized to permit Ca 2+ channels entry. [8] However, mouse zona glomerulosa cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity; this innate electrical excitability of zona glomerulosa cells provides a platform for the production of a recurrent Ca 2+ channels signal that can be controlled by angiotensin II and extracellular potassium , the 2 major regulators of aldosterone production. [8] Angiotensin II originates from plasmatic angiotensin I after the conversion of angiotensinogen by renin produced by the juxtaglomerular cells of the kidney . [9]

Adrenal steroid synthesis inhibitors

adrenal steroid synthesis inhibitors

The primary mineralocorticoid , aldosterone , is produced in the adrenocortical zona glomerulosa by the action of the enzyme aldosterone synthase (also known as CYP11B2 ). [5] [6] Aldosterone is largely responsible for the long-term regulation of blood pressure . [7] Aldosterone effects on the distal convoluted tubule and collecting duct of the kidney where it causes increased reabsorption of sodium and increased excretion of both potassium (by principal cells) and hydrogen ions (by intercalated cells of the collecting duct). [7] Sodium retention is also a response of the distal colon, and sweat glands to aldosterone receptor stimulation. Although sustained production of aldosterone requires persistent calcium entry through low-voltage activated Ca 2+ channels , isolated zona glomerulosa cells are considered nonexcitable, with recorded membrane voltages that are too hyperpolarized to permit Ca 2+ channels entry. [8] However, mouse zona glomerulosa cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity; this innate electrical excitability of zona glomerulosa cells provides a platform for the production of a recurrent Ca 2+ channels signal that can be controlled by angiotensin II and extracellular potassium , the 2 major regulators of aldosterone production. [8] Angiotensin II originates from plasmatic angiotensin I after the conversion of angiotensinogen by renin produced by the juxtaglomerular cells of the kidney . [9]

Media:

adrenal steroid synthesis inhibitorsadrenal steroid synthesis inhibitorsadrenal steroid synthesis inhibitorsadrenal steroid synthesis inhibitorsadrenal steroid synthesis inhibitors

http://buy-steroids.org