Rectifying effect of exercise on hypertension in spontaneously hypertensive rats via a calcium-dependent dopamine synthesizing system in the brain.
The effect of exercise on blood pressure in spontaneously hypertensive rats (SHR) was investigated assuming a mechanism involving calcium-dependent dopamine synthesis in the brain. Male SHR (13 weeks of age) were forced to run for 1 h at a speed of 10 m/min using a programmed motor-driven wheel cage. Systolic blood pressure was reduced after running, and this effect of exercise was decreased by prior intracerebroventricular administration of EDTA (1 nmol/rat), alpha-methyltyrosine (inhibitor of tyrosine hydroxylase, 1 mg/rat), sulpiride (D2 receptor antagonist, 50 microg/rat) or eticlopride (D2 receptor antagonist, 100 microg/rat), but was not changed by administration of SCH 23390 (D1 receptor antagonist, 30 microg/rat). Also, the calcium levels in the serum and brain were increased by exercise. Combining these results with our previous reports, it is suggested that exercise leads to an increase in the serum calcium level and subsequently an increase in the brain calcium level. This, in turn, leads to increased brain dopamine synthesis through a calmodulin-dependent system, with the increased dopamine levels inhibiting sympathetic nerve activity via the dopamine D2 receptor in the brain and causing a reduction in blood pressure.