Roles of renal dopamine and kallikrein-kinin systems in antihypertensive mechanisms of exercise in rats

We have previously shown that both renal dopamine (DA) and kallikrein-kinin systems are activated by exercise in mild hypertensives. We aimed to confi rm the effects of exercise on the renal DA system and the stimulatory effec ts of DA on the renal kallikrein-kinin system in rats. In experiment 1, 12 male Dahl salt-sensitive (DS) rats given a 4% salt diet were divided into t wo groups. Rats in the exercise group were forced to run at 8 m/min, 60 min /day, 5 days/week for 4 weeks. Daily urinary volume, urinary excretion of s odium, free DA, and kallikrein activity were measured weekly. Renal aromati c-L-amino acid decarboxylase (AADC) activities were assayed at the end of t he experiment. In experiment 2, 15 male Sprague-Dawley (SD) rats were rando mly divided into 3 groups, a DA-5 (5 mu g of DA/kg/min), a DA-10 (10 mu g o f DA/kg/min), and a control group. DA or vehicle was administered subcutane ously with an osmotic pump for 2 weeks. Daily urinary volume, urinary excre tion of sodium, aldosterone, DA, and kallikrein activity were measured week ly. Plasma renin activity, aldosterone concentration, and renal kallikrein mRNA levels were determined at the end of the experiment. In experiment 1, urinary excretion of free DA and renal AADC activities in the exercise grou p were significantly higher than those in the non-exercise group at week 4. In experiment 2, renal kallikrein mRNA levels and urinary volume were sign ificantly increased in the DA-10 group compared to the control group, altho ugh there were no differences in urinary kallikrein activities. Plasma aldo sterone concentration was significantly decreased in the DA-10 group compar ed to that in the control group despite a lack of differences in plasma ren in activities. In conclusion, exercise increased the urinary excretion of f ree DA, probably through increased renal AADC activity in DS rats. DA ampli fied renal kallikrein mRNA levels and decreased plasma aldosterone levels, probably through its suppression of aldosterone in the adrenal glands. Acti vation of the kallikrein kinin system might be counteracted by post-transcr iptional modification of aldosterone. These results suggest that exercise e nhances renal dopamine production by activating renal AADC activity, which in turn stimulates the renal kallikrein-kinin system.