Historically, aldosterone was considered a hormone released from the adrenal cortex in response to low salt intakes. It was thought to exert its effects solely through mineralocorticoid receptors, thereby causing sodium retention and potassium loss. More recently, however, a much wider role for aldosterone has been recognized.
Research efforts have revealed a host of new pathophysiologic mechanisms associated with elevated aldosterone that could be expected to contribute to the progression of congestive heart failure and sudden cardiovascular death.
More importantly, the recent evidence is based upon research into the actual metabolic mechanisms rather than epidemiological or observational studies, which are generally open to a range of mechanistic interpretations and confounding errors. A growing body of evidence suggests that . The endothelium is the thin layer of cells that line the interior surface of all blood vessels. It serves as the interface between the circulating blood and the rest of the vessel wall. The condition of the endothelium plays a critical role in the regulation of vascular tone, platelet aggregation within the vessel, the adhesion of leukocytes and overall blood coagulation. When the endothelium is not right, as in endothelial dysfunction, it is predictive of future cardiovascular events.
Because low salt diets stimulate elevated aldosterone levels, this phenomenon may very well explain the repeated findings that more people on low salt diets succumb to cardiovascular disease than those on normal or high salt diets, which we reported on previously.
In the past, experimental studies have focused on the pathological effects of angiotensin II, rather than aldosterone, and demonstrated that angiotensin-converting enzyme inhibitors confer significant cardiovascular protection. However, more recently, research has revolutionized our view of aldosterone and its biological actions, and identified mineralocorticoids as important mediators of cardiovascular injury. Elevated aldosterone levels can cause cardiovascular injury without raising the blood pressure, and aldosterone blockers can exert significant protective effects without lowering the blood pressure.
Infants born with a low birth weights tend to have higher aldosterone levels when they are older. This corresponds to recent research, which we previously reported on demonstrating that low birth weight babies are also born with low sodium in their blood serum because their mothers were on low salt intakes.
The current evidence concludes that that a long-term increase in aldosterone production from early on in life is determined by an interaction of genetic and environmental factors, such as diets that are low in salt. This leads to cardiovascular damage in middle age and beyond. These results have been confirmed by at least two other studies, one from Israel and one from Japan, which further state that the current upper limit of 2300 mg sodium per day (6 g of salt), described in the Institute of Medicine Dietary Reference Intakes is insufficient to prevent the triggering of elevated aldosterone levels.
As more and more high quality evidence mounts on the malignant impact of elevated aldosterone levels upon cardiovascular function, it is hoped that the voice of the medical establishment and the new Dietary Guidelines on sodium will take this squarely into account.
