Involvement of Dopamine in Development of Hypertension in Spontaneously Hypertensive Rat: Effect of Carbidopa, Inhibitor of Peripheral DOPA Decarboxylase

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Abstract
The demonstration of acceleration of hypertension was investigated in spontaneously hypertensive rats (SHR) treated with carbidopa, inhibitor of peripheral dopa decarboxylase. Oral administration of carbidopa to young SHR for 4 weeks accelerated significantly (P<0.05) development of hypertension as compared to SHR treated with vehicle. Urinary excretion of dopamine (DA) (P<0.01) and renal content of DA (P<0.02) were significantly decreased by carbidopa treatment. Urinary excretion of sodium (P<0.05) was significantly decreased and renal content of norepinephrine (NE) (P<0.01) was significantly increased by carbidopa. Urinary excretion of NE and epinephrine (E) did not change during the experimental period. Negative correlation between systolic blood pressure and urinary excretion of sodium (P<0.05) or dopamine (P<0.01) and positive correlation between systolic blood pressure and renal content of NE (P<0.05) were significantly observed in both groups of SHR treated with carbidopa and with vehicle for 4 weeks.