PRODUCTION OF SUSTAINED HYPERTENSION BY LESIONS IN THE NUCLEUS TRACTUS SOLITARII OF THE AMERICAN FOXHOUND

The purpose of this study was to develop a model of sustained neurogenic hypertension in the dog. Thirteen female American foxhounds (mean arterial pressure 105 ± 12 mm Hg) with Indwelling arterial and venous cannulas were maintained on a constant 82 mEq/day sodium intake. After a control period of at least 10 days, under pentothal anesthesia and direct visualization, the animals had placement of bilateral electrical lesions of the nucleus tractus solitarii (NTS) at the level of the obex. After recovery from anesthesia, the dogs could be divided into two groups on the basis of blood pressure response. Group I (n = 6) developed sustained hypertension with an increase of mean arterial pressure of 25-35% above control values (p < 0.01) for 10 days after placement of the lesions. Group II (n = 7) had a transient increase of blood pressure on postoperative Day 1 but became nonnotensive for the subsequent 9 days of observation. The bemodynamic features of the dogs in Group I were increased total peripheral resistance, decreased cardiac output and slightly decreased heart rate; these changes were reversed to control by pbetolamine. Plasma renin activity, aldosterone concentration and blood pressure response to SQ20,881 were unchanged by NTS lesions. Group I dogs had sodium retention on postoperative Day 1, but no change in renal plasma flow or glomerular filtration rate was observed during the chronic hypertensive phase. One Group I dog remained hypertensive for 8 weeks. All dogs in Group I were hypertensive and all in Group II were nonnotensive at sacrifice. Histologic sections from Group I dogs showed complete cellular destruction of the nucleus and the tractus solitarius bilaterally at the obex. In Group II, unilateral or incomplete cellular destruction of the NTS at the obex, or bilateral NTS lesions caudal to the obex were present. Bilateral NTS lesions at the obex in the American foxhound result in sustained arterial hypertension characterized by increased peripheral sympathetic nervous system activity and lack of dependence on the renin-angiotensin-aJdosterone system. © 1979 American Heart Association, Inc.