1. Presynaptic regulation. The regulation of noradrenaline release by a wide variety of substances acting on presynaptic receptors suggests that local factors may play a greater role in the control of blood pressure than was previously believed and that a number of new approaches to the drug treatment of hypertension could be developed. It also raises the possibility that there might be differences in the presynaptic receptor populations of hypertensive and normotensive subjects or animals.
2. Central nerve pathways. There is a need for more precise delineation of central nerve tracts subserving a cardiovascular function and for greater use of morphological techniques to confirm the reliability of biochemical and physiological experiments in the central nervous system. Two appropriate techniques are described.
3. Models of experimental hypertension. (a) Neurogenic hypertension: interference with baroreceptor afferents can cause a permanent elevation of arterial pressure mediated by increased activity of peripheral sympathetic nerves and of descending noradrenergic nerves terminating in the spinal cord. Catecholamine nerve connections of the nucleus tractus solitarius serve mainly to modulate rather than to mediate baroreceptor reflexes. (b) DOCA—salt hypertension: increased peripheral sympathetic activity is important in both the initiation and the maintenance of this form of hypertension. The decrease in brain-stem noradrenaline turnover found in this model could play a determinant role in the development of the high blood pressure. (c) Renal hypertension: both central and peripheral nervous mechanisms contribute to the development and the early phase of ‘one-kidney’ hypertension in animals. Their role in the maintenance of this form of hypertension is still controversial. (d) Spontaneously hypertensive rats: peripheral and central mechanisms do not appear to have a major role in the maintenance of this form of hypertension. However, it seems possible that centrally evoked increases in peripheral sympathetic activity could be important in the initiation of the high blood pressure. (e) Central catecholamines and blood pressure control; central catecholaminergic nerves do not make up a single homogeneous system. For example, the activity of descending noradrenergic nerves in the spinal cord contributes to an elevation of arterial pressure, whereas the activity of catecholaminergic nerves in the dorsomedial medulla appears to have a depressor effect.
4. Human essential hypertension. (a) There is no good evidence that the nervous system plays the major primary role in the development or maintenance of essential human hypertension. (b) Effective treatment of raised blood pressure through nervous mechanisms requires an understanding of the factors that normally control the pressure and does not necessarily depend on reversing specific nervous processes responsible for producing the increase in pressure.
