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Angiotensin has an effect on the sympathetic nervous system which results in an enhanced response to agents and procedures that cause release of endogenous norepinephrine while having little or no effect on response to exogenous norepinephrine. The effect is peripheral, it does not appear to involve sensitization of norepinephrine receptors, it is dependent upon a functionally intact sympathetic nervous system, and it appears unrelated to the direct vasoconstrictor action of angiotensin. The response to tyramine is increased in both acute and chronic renal hypertension; this suggests that only very small amounts of angiotensin, difficult to detect by present assay methods, continue to have an effect on the sympathetic nervous system in chronic renal hypertension. By intensifying the effect of normal neurogenic vasomotor activity, this action of angiotensin, along with the upward shift of threshold and range of response of the carotid sinus buffer mechanism, might account to a major degree for the large neurogenic component of chronic renal hypertension.
McCubbin et al. (Wed,) studied this question.