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Systemic Diseases and the Skin
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Jana Kazandjieva, Razvigor Darlenski, Nikolai Tsankov
Overview: The adrenal gland, although small in size, provides a major power to human metabolism. Aldosterone regulates the body sodium content affecting the blood pressure. Cortisol contributes to the regulation of glucose and protein metabolism. Adrenal diseases are generally rare, but diseases like Addison’s disease and Cushing’s syndrome that affect the normal levels of these hormones can lead to potentially life-threatening consequences.
Tubular Function
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Aldosterone is produced in the adrenal cortex, and it stimulates both sodium reabsorption and potassium secretion by the principal cells of cortical collecting ducts. The renin–angiotensin system is an important regulator of aldosterone secretion.
The Endocrine System and Its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Hyperactivity of the adrenal cortex, or hyperadrenalism, produces Cushing's disease and adrenogenital syndrome. Both are related to a cortical tumor. Adrenal insufficiency, the inverse of hyperadrenalism, can be divided into two categories: hypoadrenalism associated with a primary inability of the adrenal to produce sufficient hormone and hypoadrenalism associated with a secondary failure of ACTH. Primary adrenocortical deficiency, also called Addison's disease or chronic glucocorticoid deficiency, results from progressive adrenocortical destruction. Anemia, weakness, fatigue, increased potassium, and decreased sodium levels in the blood are common symptoms. Secondary adrenocortical insufficiency is caused by a pituitary deficiency in ACTH production. Hypoaldosteronisim results from an isolated aldosterone deficiency.
The roles of hydrogen sulfide in renal physiology and disease states
Published in Renal Failure, 2022
Jianan Feng, Xiangxue Lu, Han Li, Shixiang Wang
Ang II can contract whole arterioles. In addition, it can promote secretion of aldosterone in the adrenal cortex. Aldosterone acts on the renal tubules and increases blood volume. Furthermore, Ang II induces OS by binding angiotensin receptor 1 to mediate excessive ROS accumulation, leading to endothelial damage. In the kidneys, Ang II exacerbates target organ inflammation by increasing superoxide formation and chemokine release [141,142]. In addition to H2S inhibiting renin release, another possible mechanism is that exogenous H2S inhibits the binding of Ang II to the Ang II type I receptor, reduces Ang II–mediated signaling and inhibits pathological progression in mice. In mice with Ang II–induced hypertension, H2S can also inhibit ROS production in blood vessels and remove ROS, improving antioxidant capacity [143].
Optimal cardiovascular medical therapy: current guidelines and new developments
Published in Baylor University Medical Center Proceedings, 2022
Shirley Cotty Reed, Nikita Dhir, R. Jay Widmer
When implementing use of aldosterone antagonists, caution is advised for patients with renal dysfunction or hyperkalemia. The RALES, EMPHASIS-HF, and EPHESUS trials excluded patients with serum creatinine >2.5 mg/dL (or estimated glomerular filtration rate <30 mL/min/1.73 m2 in EMPHASIS-HF) and serum potassium >5.0 mEq/L. In the RALES trial, incidence of serious hyperkalemia was not significantly different in patients treated with spironolactone compared to placebo. In the EPHESUS and EMPHASIS-HF trials, a higher incidence of potassium >5.5 mEq/L was reported in the eplerenone treatment groups compared to placebo; however, doses were titrated to 50 mg in the trials.26,27 With both trials, one notable finding was that the earlier these agents were implemented in the therapeutic regimen, the greater the improvement. Thus, aldosterone antagonists should be used early and often in patients with reduced ejection fraction—especially after large anterior MI—assuming there are no perturbations in renal function or potassium levels. Compared to spironolactone, eplerenone also appears to have a reduced proclivity toward causing gynecomastia, which can be a troubling side effect in men.
A patent review of aldosterone synthase inhibitors (2014-present)
Published in Expert Opinion on Therapeutic Patents, 2022
As a key component of the renin-angiotensin-aldosterone system (RAAS), mineralocorticoid aldosterone has been well recognized for its principal role in regulating fluid and electrolyte balance [1]. It promotes renal sodium (Na+) and water reabsorption, and induces potassium (K+) and hydrogen (H+) excretion in epithelial cells of the distal nephron [2]. Not surprisingly, dysregulation of aldosterone, either excess or deficiency, has been linked to the clinical conditions of various cardiovascular and metabolic diseases. ‘Hyperaldosteronism’ (excess aldosterone) contributes to arterial hypertension (AH), congestive heart failure, and chronic kidney disease (CKD) [3,4]. Meanwhile, aldosterone deficiency or ‘hypoaldosteronism’ results in hyponatremia, hyperkalemia, and acidosis [5,6].