Abstract
This chapter discusses the role of central catecholamine pathways in spontaneous and renal hypertension in rats. Studies have indicated the role of central catecholamine (CA) pathways in the development of spontaneous hypertension. It has been found that 6-hydroxypdopamine (6-OH-DA) given intracisternally to rats can prevent the development of hypertension in spontaneous hypertensive rats. Therefore, it has been postulated that central CA mechanisms may trigger the development of spontaneous hypertension. Studies on noradrenalin (NA) and adrenaline levels, and turnover in the dorsal midline area of the caudal medulla oblongata (DCMO) and in the whole hypothalamus in spontaneous hypertensive and renal hypertensive rats show that a marked reduction of adrenaline turnover is present in DCMO during development of spontaneous hypertension in 4-week old rats. This change persists in adult spontaneous hypertensive rats. These results strongly support the view that an adrenaline vasodepressor mechanism facilitates the central baroreceptor reflex pathway that is disturbed in young spontaneous hypertensive animals. Studies in renal hypertension with salt and volume retention and low plasma angiotensin-II demonstrates relatively high NA and adrenaline levels in the DCMO and hypothalamus.
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