Neurogenic Component of Chronic Renal Hypertension

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Abstract
Infusion of angiotensin or renin in small quantities affects the sympathetic nervous system so that responses are increased to either drugs or reflexes that cause release of norepinephrine at nerve endings. Response to injected norepinephrine is relatively unchanged. This action of angiotensin is dependent upon an intact sympathetic nervous system. The direct vasoconstrictor action of angiotensin is not an essential part of the enhanced response. The phenomenon was shown to have relevance to acute and chronic experimental renal hypertension in dogs by the fact that in both the pressor response to tyramine was enhanced. We believe that the ability of angiotensin to intensify the effect of normal neurogenic vasomotor activity, along with an upward reset of the carotid sinus buffer mechanism, might account importantly for the neurogenic component of renal hypertension.

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