This brief review describes the role of neural and non-neural mechanisms during different phases of deoxycorticosterone acetate (DOCA)-salt hypertension. There are contradictory data for and against a role of the sympathetic nervous system and neurohumoral agents, including endothelin and vasopressin. Elucidating the factors responsible for DOCA-salt hypertension will be helpful in understanding the causes of hypertension resulting from hypervolaemia, hyperaldosteronism and high salt intake.

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Prior studies have provided indirect evidence suggesting sympathetic nerve activity (SNA) contributes to the development of hypertension. We hypothesized that evoked and resting SNA would be elevated 2‐3 weeks after inducing DOCA‐NaCl hypertension. We instrumented male Sprague‐Dawley rats to measure arterial pressure, ECG and renal SNA before inducing hypertension. We recorded resting SNA before and after implanting DOCA and administering 1% NaCl drinking water. Responses to acute stress were also recorded prior to inducing and during development of hypertension (2‐3 weeks). Background activity was determined with ganglionic blockade (trimethaphan). We observed that DOCA‐salt treatment (n=8) elicited an increase in arterial pressure that started within 2‐3 days. During the early phase, renal SNA did not seem to be elevated as the decrease in SNA in response to trimethaphan was unchanged (‐41± 6% control vs. ‐38 ± 6% on day 12). We examined the acute response to cold water stress (1 cm deep for 1 min) and observed that initial evoked responses during cold stress were progressively smaller in DOCA‐salt hypertension over 12 days. Our data suggest that SNA does not play a role in the development of DOCA‐salt hypertension, although it will be necessary to verify this in other sympathetic nerves. Supported by USPHS NIH R01 DA0017371, HL 091440 and 5T32 GM008306.