Tell me who your friends are and I will tell you who you are: NaHCO3 isn't NaCl
Posted May 05 2011 4:54pm
When managing patients with metabolic acidosis, some nephrologists are afraid of prescribing NaHCO3 because of the potential adverse consequences of increasing ECF volume and worsening blood pressure. However, there is significant evidence that the kidneys handle NaCl in a different way than they handle NaHCO3.
As far back as 1929, there have been several reports showing that blood pressure increased in hypertensive individuals on a high NaCl diet, but not on high NaHCO3 diet (Berghoff RS et al. IMJ. 1929; 56: 395–397). In 1983, Kurtz et al published a seminal paper in Science . They performed studies in uninephrectomized rats treated with desoxycorticosterone (DOC), a model for sodium-dependent hypertension. They exposed these animals to a high NaCl diet, a high NaHCO3, or Na+-ascorbate diet. The rats exposed to a high NaCl diet developed more hypertension that rats exposed to non-chloride Na+ salts. This study strongly suggests that Na+ has to be administered as a Cl- salt to raise blood pressure.
The explanation for this might be found in the cross talk between Pendrin and the epithelial sodium channel (ENaC) . Pendrin is a Cl-/HCO3- exchanger located in the apical membrane of type B and non-A-non-B intercalated cells. ENaC is a major sodium transporter located in the apical membrane of principal cells. Pendrin and ENaC reside in two different cell types that do not communicate through gap junctions. Therefore, it is not readily apparent that Na+ reabsorption is linked molecularly to Cl- transport. Despite this, significant evidence indicates that Pendrin plays a major role in ECF volume regulation , possibly via its influence on ENaC. How does this occur? The mechanism has not been completely elucidated but because Pendrin mediates HCO3- secretion, an increase in luminal or basolateral HCO3- is at least partially responsible for ENaC activation and subsequent sodium retention.