How is aldosterone released?
- Particularly it begins with the electrolyte-fluctuation-sensitive kidneys (1). They stimulate aldosterone production by secreting renin, a proteolytic enzyme (1). The secretion happens whenever there is decreased perfusion pressure that’s sensed by receptors in the kidneys’ juxtaglomerular apparatuses (“kidney brains” that tell the kidneys’ functional units, its nephrons, what to do) (1). The renin hydrolyzes angiosteninogen, a free-wheeling protein coming from the liver, to angiotensin I (1). Another enzyme, appropriately named angiotensin-converging enzyme (ACE), converts angiotensin I to angiotensin II. Angiotensin II interacts with adrenal cortical cell receptors and voila! aldosterone is released (1).
- Decreased atrial natriuretic peptide will stimulate release. This hormone from atrial cells ends up occurring if blood pressure elevates and, as opposed to aldosterone, causes excretion of sodium (1).
- Other possibilities for release are increased potassium concentration, increased ACTH, or decreased sodium (1).
Aldosterone and hypertension
High aldosterone levels are also a good indicator for transient ischemia attack and stroke (2-4). ACE inhibitors are a leading therapy (and subject to numerous new research papers) for intervening in the renin-angiotensin-aldosterone system along with angiotensin II type 1 receptor antagonists (2-4). The research on these are proving they are useful for those with hypertenstion and helping to prevent cardiac arrhythmias and sudden cardiac death (2-4).
Vitamin D appears to have association with aldosterone and hypertension. Just a few days ago a French study reported what many have suspected--that as the seasons change and the days become warmer, blood pressure begins to lower (5). And according to ScienceDaily, the study may be explained due to vitamin D deficiency (6).
The data is supported by the Framingham Heart Study and Nurses Health Study, which found vitamin D deficiency increased risk of hypertension, heart attack and stroke (6). A 1989 study that showed that long-term vitamin D supplementation lowered blood pressure in patients with essential hypertension (7).
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism, 5th ed. Belmont, CA: Thomson Wadsworth, 2009, p 553.
3. Makkar KM, Sanoski CA, Spinler SA. Role of Angiotensin-Converting Enzyme Inhibitors, Angiotensin II Receptor Blockers, and Aldosterone Antagonists in the Prevention of Atrial and Ventricular Arrhythmias. Pharmacotherapy 2009;29:31-48.3.
4. Qian C, Schoemaker RG, van Gilst WH, Roks AJ. The role of the renin-angiotensin-aldosterone system in cardiovascular progenitor cell function. Clin Sci (Lond) 2009;116:301-14.4. Vyssoulis GP, Karpanou EA, Tzamou VE et al. Aldosterone levels and stroke incidence in essential hypertensive patients. Int J Cardiol 2009.
5. Alperovitch A, Lacombe JM, Hanon O et al. Relationship between blood pressure and outdoor temperature in a large sample of elderly individuals: the Three-City study. Arch Intern Med 2009;169:75-80.
6. ScienceDaily. Blood Pressure Varies by the Season. 20 Jan 2009. Available at: http://www.sciencedaily.com/releases/2009/01/090116091523.htm
7. Lind L, Wengle B, Wide L, Ljunghall S. Reduction of blood pressure during long-term treatment with active vitamin D (alphacalcidol) is dependent on plasma renin activity and calcium status. A double-blind, placebo-controlled study. Am J Hypertens 1989;2:20-5.