The accumulation of both Inositol-(1, 4, 5)-trisphosphate (IP₃) and Inositol-(1, 3, 4, 5)-tetrakisphosphate (IP₄) after hormonal stimulation has a physiological role, possibly in altering Ca²⁺ levels in cardiac tissue. However, the accumulation of inositol polyphosphate under pathophysiological conditions has not been studied. In our experiments the metabolism of phatidylinositol and IP₃ m cardiac myocytes as investigated. It was shown that basal levels of cytosolic phosphatidylinositol specific phospholipase C (PI-PLC), phosphatidylinositol-(4, 5)-bisphosphate specific phospholipase C (PIP₂-PLC) activities markedly increased in stroke-prone spontaneously hypertensive rats (SHRSP) with age compared with age matched Wistar Kyoto rats (WKY). IP₃ kinase and IP₃ phosphatase activities also increased in SHRSP hearts with age. Their activities increased in WKY, but to a lesser antent than in SHRSPs. These data suggest that a PI turnover pathway such as the phosphatidylinositol 4, 5-bisphosphate-IP₃-Ca²⁺ pathway or the diacylglyceride-protein kinase C pathway may have an important role in the development of hypertrophy in SHRSP heart.