Increased number of aldosterone-sensitive NTS neurons in Dahl salt-sensitive rats.

Dahl salt-sensitive rats develop severe hypertension during a high-sodium diet, but the basis of their salt-sensitive phenotype is not completely understood. A subset of neurons in the nucleus tractus solitarius (NTS) are uniquely sensitive to the adrenal steroid hormone aldosterone, which is critically involved in sodium homeostasis, due to their expression of the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2). The number of HSD2 neurons in the NTS was counted in prehypertensive 7-week-old Dahl salt-sensitive rats and compared with two control strains: Dahl salt-resistant and Sprague-Dawley rats. Dahl salt-sensitive rats had more HSD2 neurons than age-matched Dahl salt-resistant and Sprague-Dawley rats (24% and 21%, respectively). Cell counts were also made in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats; the number of HSD2 neurons in both of these strains was similar to the values obtained for Sprague-Dawley rats. The increased number of HSD2-immunoreactive neurons counted in Dahl salt-sensitive rats suggests that they may have a greater number of aldosterone-sensitive NTS neurons. Alternatively, an increase in HSD2 expression in Dahl salt-sensitive rats could increase the overall immunoreactivity, permitting detection of more of these neurons. In either case, the roughly 20% increase in HSD2 neurons in the NTS of prehypertensive Dahl salt-sensitive rats is a novel factor associated with their salt-sensitive phenotype. These neurons may play a role in regulating sodium appetite, which is abnormally suppressed in Dahl salt-sensitive rats.