Brain amines and models of experimental hypertension.

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Abstract
Central catecholaminergic nerves play an important role in the regulation of arterial blood pressure. Although they appear to have little importance in the maintenance of resting arterial blood pressure in normal unstressed animals, they play a major role in the reflex control of blood pressure through the arterial baroreceptor reflexes. The activity of bulbospinal noradrenergic nerves appears to facilitate the increase in arterial blood pressure in neurogenic hypertension and possibly in DOCA[deoxycortocosterone acetate]-salt hypertension. The activity of brainstem catecholaminergic nerves appears to inhibit the activity of bulbospinal noradrenergic and serotonergic nerves and has a depressor effect on arterial blood pressure. Disinhibition of bulbospinal noradrenergic and serotonergic fibers by deafferentation of arterial baroreceptors (neurogenic hypertension) or by decreased activity of inhibitory catecholaminergic nerves in the brainstem (DOCA-salt and renal hypertension) could play a significant role in the pathogenesis of experimental hypertension. The participation of central catecholaminergic nerves in genetic hypertension (the spontaneously hypertensive rat) has not yet been established. Central serotonergic nerves also appear to play a significant role in the regulation of arterial blood pressure in normal animals and in some models of experimental hypertension. Central serotonergic nerves do not appear to contribute to experimental renal hypertension, but they may play a role in elevating the pressure in the spontaneously hypertensive rat. The central connections of the autonomic nervous system utilize a variety of neurotransmitters in much the same way as do the peripheral components. Each of these central neurotransmitters could apparently be facilitatory or inhibitory in different pathways and each could synapse with a variety of functionally distinct receptors.