Introduction DURING the past few years, substantial advances have been made in our understanding of renin secretion. Chiefly responsible for the advances is the proposition by Peart (1) that Ca plays a central role in controlling renin secretion as it does in smooth muscle contraction and relaxation. This has led to the view, based mainly on indirect evidence, that cytosolic Ca is an intracellular signal which regulates renin secretion through the baroreceptor, macula densa, and neurohormonal pathways. The specific proposal is that factors which physiologically stimulate renin secretion do so by lowering cytosolic Ca, and those which inhibit secretion do so by raising Ca (2). Thus, for example, hemodynamic factors such as renal perfusion pressure and intrarenal tissue pressure, which control renin secretion through the baroreceptor pathway, regulate Ca flux in the juxtaglomerular (JG) cells (2). Increased NaCl load at the macula densa increases adenosine production at the macula densa, and this adenosine acts on the JG cells to raise cytosolic Ca and inhibit renin secretion (3–7). The neurohormonal pathway, by β-adrenergic mechanism, stimulates renin secretion through a cAMP cascade which leads to a reduced cytosolic Ca (3), and, by aadrenergic mechanism, inhibits secretion by increasing Ca inflow and thereby cytosolic Ca (8). Several reviews have appeared which point to Ca as the common signal most likely responsible for controlling renin secretion (2, 3, 8–10). Park and co-workers (11) have recently demonstrated an inverse relationship between renin secretion and cytosolic Ca, thereby providing the first direct evidence to support the proposition of Peart (1).