the nephrons. Experimentally, the membrane potential at which the channels show no net movement of ions at a given chloride concentration drops significantly with the mutation, indicating altered function in situ. This manifests as a chronic salt wasting disorder similar to Bartter syndrome, as sodium reabsorption is coupled with chloride reabsorption. The salt loss results in a decreased blood volume and consequently hyperreninemia leading (via the end product angiotensin II and aldosterone) to increased vascular tone, heart rate, water reabsorption, and blood pressure, collectively referred to as cardiorenal syndrome. Being heterozygous for this Arg83Gly variant increases the risk of heart failure by 27%, while homozygosity increases the risk by 54%. The additive stress on the heart from increased blood pressure and heart rate often only manifests as a pathology with an additional cardiovascular problem such as hypertension. Treatment for the SNP associated hyperreninemia involves drugs to block the Renin-Angiotensin-Aldosterone system to relieve the aforementioned stresses on the heart. See also Chloride channel BSND, barttin, accessory subunit beta for this channel References Further reading External links Ion channels