Deficient dopamine metabolism in the celiac ganglion of spontaneously hypertensive rats.

It has been established by others that dopamine (DA), in the small intensely fluorescent (SIF) cells of a sympathetic ganglion, is released on to sympathetic neurons as a result of preganglionic cholinergic stimulation. DA is known to suppress transmission in sympathetic ganglia. The concentration of 3,4-dihydroiyphenylacetic acid (DOPAC) within the ganglion is a relative measure of DA release and metabolism. We assayed DA, norepinephrine (NE), and DOPAC in the celiac ganglia of spontaneously hypertensive rats (SHR), during the development of hypertension, and in control Wistar-Kyoto rats (WKR). Blood pressure begins to rise in SHR after 4 to 6 weeks of age and becomes stable after about 10 weeks. In WKR, DOPAC concentrations are highest in the ganglion at 4 weeks and decline by about 45% at 6 weeks to levels at which they remain for 20 weeks. In contrast, DOPAC concentrations in SHR are lowest in the ganglion at 4 weeks, increase in parallel to blood pressure, and at 20 weeks are comparable to the concentration in WKR. Sectioning the greater splanchnic nerves does not induce major changes in the content of NE and DA in the celiac ganglion but strikingly reduces DOPAC concentrations in both SHR and WKR, supporting the notion that the conversion of DA to DOPAC is modulated by preganglionic cholinergic neuronal activity. Sectioning the nerves in SHR delays the development of hypertension but does not significantly alter blood pressure in WKR. Our studies suggest the hypothesis that young SHR are not able to modulate the sensitivity of sympathetic neurons to incoming cholinergic activity to the celiac ganglion because of a deficiency of SIF cell DA metabolism, and the consequences of this may play a critical role in the development of hypertension. Circ Res 44: 467-471, 1979