Evidence Suggesting that Lateral Parabrachial Nucleus Is Responsible for Enhanced Medullary Cholinergic Activity in Hypertension

Abstract

Cholinergic activities in the rostral ventrolateral medulla are enhanced in hypertensive animals, and enhanced cholinergic activity contributes to hypertension. Neurons in the lateral parabrachial nucleus and baroreceptors are suggested to be involved in mediation of acetylcholine release in the ostral ventrolateral medulla. To investigate the hypothesis that the lateral parabrachial nucleus is involved in the increased medullary cholinergic activity in hypertensive rats, we measured choline acetyltransferase activity in the rostral ventrolateral medulla, and examined effects of electrolytic lesioning of the lateral parabrachial nucleus in deoxycorticosterone acetate-salt hypertensive rats. We found that choline acetyltransferase activity in the medullary region was increased in deoxycorticosterone acetate-salt hypertensive rats. Unilateral lesioning of the lateral parabrachial nucleus abolished the increase in choline acetyltransferase activity in the lesioned side of the medullary region of hypertensive rats, whereas such activity in the medullary region of control rats was unaffected by lesioning. Bilateral lesioning of the lateral parabrachial nucleus inhibited the development of hypertension in hypertensive rats. In contrast, baroreceptor denervation did not inhibit the increase in choline acetyltransferase activity in the medullary region of hypertensive rats. These results are compatible with the hypothesis that the lateral parabrachial nucleus area is involved in mediation of increased medullary cholinergic activity and thus plays a role in the development of hypertension. (Hypertens Res 1998; 21: 201-207)