Contribution of Forebrain Structures to the Development of Neurogenic Hypertension

Abstract

During the last three decades a considerable amount of experimental evidence has been obtained suggesting that an imbalance in the normal operation of the autonomic nervous system contributes to the development or maintenance of high blood pressure (Abboud, 1982; Brody et al., 1980; Ciriello, 1987; Reis, 1981). This suggestion is based primarily on the observation that a rise in sympathetic nerve activity, resulting from increased activity of central or peripheral components of the autonomic nervous system, is normally accompanied by an increase in vascular resistance, cardiac rate and output, renin release, and sodium retention; factors that have been shown to contribute to a chronic elevation in systemic arterial pressure (Abboud. 1982). Increases in sympathetic nervous system activity may result from several factors including decreased activity of inhibitory reflex pathways, increased activity of excitatory reflex pathways, or changes in the excitability of neurons in the central nervous system that are components of sympathoexcitatory or sympathoinhibitory pathways. Recently, it has been shown that the selective removal of the reflex inhibi-tory influences on central vasomotor neurons from aortic baroreceptor results in a persistent elevation in systemic arterial pressure (Ciriello et al., 1980; Fink et al., 1980, 1981; Ito and Scher, 1978, 1979; Kline et al., 1983; Krieger, 1964; Werber and Fink, 1981). This increased arterial pressure after selective deafferentation of aortic baroreceptors is associated with increased adrenergic activity to several peripheral organs, including the kidney (Fink et al., 1980; Kline et al., 1983; Patel et al., 1981; Werber et al., 1984). The sympathetic drive to the kidney has been shown to alter both renal blood vessels (Werber et al., 1984) and the release of renin (Ciriello et al., 1991; Zhang and Ciriello, 1990).