DECREASE OF CENTRAL DOPAMINE LEVEL IN THE ADULT SPONTANEOUSLY HYPERTENSIVE RATS RELATED TO THE CALCIUM-METABOLISM DISORDER

The metabolism of calcium and brain dopamine in spontaneously hypertensive rats (SHR) after the development of hypertension was investigated as a possible model for the hypertension mechanism. Serum calcium level in SHR was lower than that in the normotensive control, Wistar Kyoto rats (WKY, the parent strain of SHR). Conversely, bone calcification of SHR was higher than that in WKY. Possible mechanisms for the lower serum calcium level seen in SHR include a decrease in the availability of calcium from bone. The immunohistochemical dopamine levels in the neostriatum and nucleus accumbens in SHR were lower than those in WKY. In these regions, the dopamine level was increased by the intraventricular administration of CaCl2 through a central, calmodulin-dependent system. This study suggests, based upon previous pharmacological studies, that the decrease of the serum calcium level in SHR causes a decrease in central, calcium-calmodulin-dependent dopamine synthesis and a subsequent low level of dopamine in the brain that produces an increase in blood pressure through functions of cerebral dopaminergic neurons and peripheral sympathetic nerves. Our results suggest that this could be one of the mechanisms of hypertension in SHR.