Cortisol aldosterone

Primary adrenal insufficiency (Addison s disease) most often involves the destruction of all regions of the adrenal cortex. There are deficiencies of cortisol, aldosterone, and the various androgens. Medications that inhibit cortisol synthesis (e.g., ketoconazole) or accelerate cortisol metabolism (e.g., phenytoin, rifampin, phenobarbital) can also cause primary adrenal insufficiency. 

An example of the importance of enzymatic modification of hormones for the tissue specificity of hormone action is the effect of the mineral corticoid aldosterone in the presence of a large excess of the glucocorticoid cortisol. Aldosterone regulates the Na -export and K -retention in the kidney by binding on the aldosterone receptor. 

Inhibition of adrenocortical synthetic function. Etomidate inhibits the activity of ll-p-hydroxylase, an enzyme necessary for the synthesis of cortisol, aldosterone, 17-hydroxyprogesterone, and corticosterone. Even after a single dose, adrenal suppression persists for 5-8 hours. Although the clinical significance of short-term suppression of cortisol synthesis is unknown, maintenance infusions for anaesthesia cannot be recommended. 

Albumin is a major transport facilitator of hydrophobic compounds which would otherwise disrupt cellular membranes. These compounds include free fatty acids and bilirubin as well as hormones such as cortisol, aldosterone, and thyroxine when these materials have exceeded the capacity of proteins normally associated with them. Albumin also binds ions, including toxic heavy metals and metals such as copper and zinc which are essential for normal physiological functioning but may be toxic in quantities in excess of their binding capacity for their carrier proteins. Binding of protons is the basis for the buffering capacity of albumin. 

Corticotropin can promote the development of a more or less pronounced Cushingoid state. Corticotropin also increases the metabolic clearance rate of cortisol, aldosterone, and desoxycorticosterone (SEDA-1, 282). 

Small quantities of progesterone, testosterone, and estradiol are also produced by the adrenal gland. However, they play a minor role compared to the testicular and ovarian hormones. Progesterone, which is the precursor of cortisol, aldosterone, testosterone, and estradiol, is synthesized from 5-pregnenolone by 3-P-ol-dehydrogenase. Deficiency of this enzyme results in cortisol and aldosterone deficiencies. Such patients require replacement therapy with both glucocorticoids and mineralocorticoids. 

Ueda K, Okamura N, Hirai M, et al. Human P-glycoprotein transports cortisol, aldosterone, and dexamethasone, but not progesterone. J Biol Chem 1992 267... 

Strenuous exercise for 10 minutes increases plasma renin activity by 400%. Cortisol secretion is stimulated and the normal diurnal variation may be abolished. Urinary free cortisol excretion and the plasma concentrations of cortisol, aldosterone, growth hormone, somatotropin, and prolactin are also increased by exercise. Plasma insulin concentration is decreased by exercise. Strenuous exercise increases both the plasma and urinary concentrations of catecholamines. The changes in hormone concentrations are probably responsible for the increase in leukocyte count to about 25,000 cells/juL that has been observed following strenuous exercise. 

Figure 50-8 The regulatory feedback loop of the hypothalamic-pituitary-adrenal axis. CRH under the influence of neural factors and other modifiable factors that control its pulsatile and circadian secretion acts on the pituitary to produce hormone (ACTH). ACTH in turn stimulates the adrenal gland to form cortisol, aldosterone, dehydroepiandrosterone (DHEA), and androstenedione. Corticosteroids and gamma amino butyric acid (GABA) are inhibitory to CRH and ACTH release, and AVP stimulates ACTH release.

Uhr, M., Holshoer, F., and Muller, M.B. (2002) Penetration of endogenous steroid hormones corticosterone, cortisol, aldosterone and progesterone into fhe brain is enhanced in mice deficient for both mdrla and mdrlb P-glycoproteins. Journal of Neuroendocrinology, 14, 753-759. 

Addison s disease (primary adrenal insufficiency) is a defi- ciency in cortisol, aldosterone, and various androgens resulting from the loss of function of all regions of the adrenal cortex. 

Steroid hormones like testosterone, progesterone, cortisol, aldosterone, and estradiol are important endocrine chemical messengers that are involved in a vast number of physiological processes including metabolism, inflammation, electrolyte and fluid balance, and secondary sex differentiation (Foster, 2004 Ghayee and Auchus, 2007 Newton and Holden, 2007 Williams-Ashman and... 

The steroid hormones, derived from cholesterol, include the adrenal cortical hormones (e.g., cortisol, aldosterone, and the adrenal sex steroids dehy-droepiandrosterone [DHEA] and androstenedione) and the gonadal hormones (e.g., the ovarian and testicular sex steroids, such as testosterone and estrogen). 

These include the female sex hormones (oestrogens), the male sex hormones (androgens) and progesterone, as well as cortisol, aldosterone and corticosterone, which are produced in the adrenal cortex. The adrenal hormones have an important role in the control of glucose and fat metabolism. 

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