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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Others have reported that the dorsomedial hypothalamus (DMH) mediates certain cardiovascular responses to behavioral stress. We sought to determine whether this variability is strain dependent and whether different stressors are similarly dependent on the DMH. We compared responses to cocaine (5 mg/kg, iv) with startle responses to 1 cm deep ice cold water (CWS) in Brown‐Norway (BN) and Dahl salt sensitive (DSS) rats. BN and DSS rats were instrumented for recording arterial pressure and for measuring blood flow changes in the abdominal aorta (hindquarters or Hq) and the superior mesenteric (Ms) artery using Doppler flowmetry. We calculated changes in vascular resistance (R) in animals. BN rats had greater increases in MsR (visceral) and HqR (skeletal muscle) to cocaine than DSS. In contrast, DSS rats had greater increases in MsR in response to CWS than BN rats. Microinjection of muscimol (80 pmol in 100 nl) in the DMH attenuated the increase in MsR in BN but not DSS rats in response to cocaine but not to CWS. DMH stimulation with kainate (10 pmol in 100 nl) elicited greater Ms vasoconstriction in BN compared to DSS rats. We conclude that there are unique strain‐dependent pathways mediating regional vascular resistance for specific stressors. The BN is more dependent on DMH in mediating cocaine‐induced visceral vasoconstriction. Supported by USPHS DA017371 and HL091440.

Cocaine elicits hemodynamic responses that are dependent on activation of central sympathoexcitatory pathways. We reported that greater vascular responses to cocaine are associated with greater increases in sympathetic nerve activity (SNA). We also reported that i.v. or intracerebroventricular propranolol enhances the cocaine induced increase in systemic vascular resistance (SVR). We hypothesized that this increase in SVR was due to a greater increase in SNA. Male Sprague Dawley rats were instrumented for measurement of cardiac output, heart rate, arterial pressure and renal SNA. After a minimum of 3 days for recovery, conscious animals were subjected to cocaine. Ganglionic blockade (trimethaphan, 10 mg/kg i.v.) was used to determine background activity. Cocaine (5 mg/kg i.v.) increased arterial pressure, SVR and renal SNA. Rats, pretreated with propranolol (1 mg/kg i.v.) 10 min. before administration of cocaine, had a greater cocaine‐induced increase in SVR that was associated with a greater increase in renal SNA. Therefore, there was a positive correlation between SVR and renal SNA. We conclude that propranolol increases SVR likely due to an increased central sympathoexcitation. Supported by USPHS NIH R01 DA0017371, DA05180 and training grant 5T32 GM008306.