Both potassium and sodium in the diet affect blood pressure. Humans are able to get rid of extra potassium and to conserve sodium. Aldosterone is the main hormone that helps get rid of potassium. Renin is secreted to conserve sodium. In patients with hypertension, aldosterone is usually elevated. Renin is sometimes elevated and sometimes not elevated. Its level is used to determine “salt sensitive hypertension,” which means blood pressure rises more easily when more salt is eaten.
Adrenal Gland, Diet And Hypertension
Previous posts discuss how dietary potassium and sodium affect the kidney and lead to hypertension. Another key organ in hypertension is the adrenal gland. The adrenal gland is also affected by potassium and sodium in the diet. When potassium is high or sodium low in the blood stream, the adrenal gland secretes aldosterone. Aldosterone has the effect on the kidney to increase the excretion of potassium and to recycle sodium. Also stimulating aldosterone secretion is angiotensin II.
Angiotensin II is increased when the kidney needs to conserve sodium. When the blood sodium level is low or the kidney blood flow is low, the kidney secretes renin, which acts on a precursor to eventually produce angiotensin II. Renin levels are related to the “salt sensitivity” of hypertension. Some insight into how potassium channels are involved in “salt sensitive hypertension” is provided by a recent study (1).
TASK and TREK are potassium channels that have been found to be involved with aldosterone secretion in human adrenal glands. Two TASK channels were recently studied in mice and give some insight into salt sensitive hypertension. However, because TREK channels also affect aldosterone secretion in humans, the findings may not be completely applicable to humans. But the study shows how important the electrical field across cell membranes is, and how a disturbance of that field can lead to hypertension.
TASK1 and TASK3 are 2 highly active potassium channels in the cell membranes of zona glomerulosa cells in the adrenal gland. These channels are involved with maintaining the resting potential in the cell membrane of these cells. When either one of these channels is not working, the cell membrane is more strongly depolarized at its resting potential. This means that the electric field is weaker and the cell can be stimulated more easily to produce aldosterone.
The normal process for the secretion of aldosterone is that a small increase in the potassium level in the blood or an increase of angiotensin II will depolarize the cell membrane in the zona glomerulosa cells. This change in voltage (electric field) opens the voltage sensitive T type calcium channels. Calcium then rushes into the cytoplasm of the cell. (Here are links to videos of normal calcium response and abnormal TASK3 calcium response to angiotensin II.) The increase in the cytoplasm of calcium results in a signaling cascade that leads to an increase in aldosterone synthase, the enzyme that makes aldosterone. This results in an increase in the amount of aldosterone made by the cell, and then secreted into the blood stream.
The researchers bred mice that were missing TASK3 potassium channels. They fed them diets with differing amounts of sodium and potassium, and measured blood pressure, aldosterone, and renin. They also examined adrenal gland slices and measured the electric field (voltage) across the cell membranes of zona glomerulosa cells in the adrenal gland slices.
The result of the study indicated that the cell membranes without TASK3 potassium channels could depolarize further, but could not hyperpolarize (increase the electric field like normal channels do). The animals had normal aldosterone levels on a normal diet, but lower than normal renin/angiotensin II. On a high potassium diet, aldosterone increased (normal response). On a low sodium diet, aldosterone increased (normal), and renin/angiotensin II increased (normal).
The diets that led to abnormal responses were those that required the cell membrane to hyperpolarize. When put on a low potassium diet, aldosterone levels did not drop as much as normally (especially in females). And on a high sodium diet, aldosterone actually rose (normally it would drop) even though renin/angiotensin II were extremely low (only 1/3 normal level). The blood pressure rose by 10 mm Hg (hypertension) when on the high sodium diet. The aldosterone-renin ratio of the mice lacking the TASK3 channel was more than double the ratio of normal mice for both a normal diet and a high sodium diet. This is the same pattern as occurs in human salt sensitive hypertension.
What It Means
So the absence of TASK3 potassium channels in the zona glomerulosa of the adrenal gland appears to create salt sensitive hypertension in mice. A genetic defect in just one type of potassium channel (in the study, TASK3) may be the cause of salt sensitive hypertension. Similar genetic differences, although not as extreme as the complete absence of a potassium channel, may be responsible for salt sensitive hypertension in humans. If so, a high potassium, low sodium diet may avoid a rise in blood pressure, as it did in the study.
1. Task3 potassium channel gene invalidation causes low renin and salt-sensitive arterial hypertension. Penton D, Bandulik S, Schweda F, Haubs S, Tauber P, Reichold M, Cong LD, El Wakil A, Budde T, Lesage F, Lalli E, Zennaro MC, Warth R, Barhanin J. Endocrinology. 2012 Oct;153(10):4740-8. Epub 2012 Aug 9.