Decreased intracellular Mg++ concentrations seem to be involved in the pathogenesis of primary hypertension. Of special interest is the smooth muscle cell with its electrolyte metabolism in primary hypertension, but also heart muscle cells and their Mg++ concentrations are of growing interest. Therefore in aortic smooth muscle cells and striated heart muscle cells (left ventricle) from 10 spontaneously hypertensive rats (SHR) of the Munster strain and 10 normotensive Wistar-Kyoto rats (WKY), the intracellular Mg++ content was measured. Electron-probe X-ray microanalysis technique was used to determine intracellular Mg++ concentrations in aortic cryosections 3 mum thick and striated heart muscle cells 4 aem thick (Camscan CS 24 apparatus). Vascular smooth muscle Mg++ content was 0.90 +/- 0.15 g/kg dry weight in SHR versus 1.15 +/- 0.10 g/kg dry weight in WKY (p<0.05). In striated heart muscle cell Mg++ concentrations, there was no significant difference in SHR and WKY (81.3 +/- 6.7 versus 79.0 +/- 8.3 mmol/kg dry weight). In conclusion the present study has revealed that genetic hypertension in the spontaneously hypertensive rat is accompanied by decreased intracellular Mg++ concentrations in vascular smooth muscle cells. These results are similar to those obtained in human blood cells. This Mg++ decrease may be due to transmembrane defects or disturbed Mg++ transport systems, e.g. Mg++/Na+ antiport or Mg++/Ca++ exchange. In striated heart muscle cells Mg++ content was not significantly different in SHR and WKY. As descriebed earlier, free, Mg++ content in hypertensive heart muscle cells is decreased, total heart muscle Mg++ content as shown here being not significantly different, a transport defect in hypertensive heart muscle cells has to be assumed. In conclusion Mg++ handling is different in vascular smooth muscle and striated heart muscle cells in WKY and SHR (p< 0.01).