Angiotensin II sensitivity of anterior hypothalamic area neurons is enhanced in both spontaneously hypertensive rats and Dahl salt-sensitive rats.

We have previously demonstrated that some neurons in the anterior hypothalamic area (AHA) are tonically activated by endogenous angiotensins. Furthermore, we have demonstrated that intracerebroventricular injection of hypertonic saline increases the firing rate of AHA angiotensin II-sensitive neurons via angiotensins and that the central sodium-induced activation of AHA neurons is enhanced in spontaneously hypertensive rats (SHR) and Dahl salt-sensitive (Dahl S) rats. In this study, we examined whether sensitivities of AHA angiotensin II-sensitive neurons to angiotensin II are enhanced in SHR and Dahl S rats as compared with their respective controls. Male 15- to 16-week-old SHR and age-matched Wistar Kyoto rats (WKY), and male 15- to 16-week-old Dahl S rats and Dahl R rats were anesthetized and artificially ventilated. Extracellular potentials were recorded from single neurons in the AHA. In SHR, pressure application of angiotensin II (3 x 10(-9) to 3 x 10(-8) M) onto AHA angiotensin II-sensitive neurons increased their firing rate in a concentration-dependent manner. In WKY, only the highest concentration of angiotensin II increased the firing rate, while the lower concentrations of angiotensin II did not affect it. In Dahl S rats, pressure application of angiotensin II (10(-8) and 3 x 10(-8) M) onto AHA neurons increased their firing rate, while angiotensin II (3 x 10(-9) M) did not affect it. In Dahl R rats, the highest concentration of angiotensin II increased the firing rate, while the lower concentrations of angiotensin II did not affect it. These findings indicate that the sensitivity of AHA neurons to angiotenisn II is enhanced in SHR and Dahl S rats as compared with their respective controls.