The renin angiotensin system plays an important role in the control of blood pressure and of renal function. The major source of renin is the juxtaglomerular cells of the kidney. A wide variety of stimulatory and inhibitory influences control the release of renin into the circulation, however the intracellular events regulating renin release are poorly understood. Previous studies have implicated roles for both cyclic adenosine monophosphate (cAMP) and intracellular calcium ions (Ca⁺⁺). These studies were carried out using in vitro preparations which retained some structural integrity and in consequence experimental data was difficult to interpret. The experiments described in this thesis set out to investigate the regulation of renin release using a preparation which is relatively free from indirect influences. The superfused disaggregated rat renal cortical cell preparation is shown to be more sensitive and more reliable than other widely used preparations. The data suggest that catecholamine induced renin release is mediated by a β-adrenoceptor located on the JG cells. It appears that an α-adrenoceptor similarly located inhibits renin release. The roles of cAMP and Ca⁺⁺ in the control of renin release were investigated. Cyclic AMP release was stimulated by catecholamines and factors which elevate intracellular cAMP were found to stimulate renin release. This suggests that cAMP acts as a stimulatory second messenger in the control of renin release. There appears to be an inverse relationship between intracellular [Ca⁺⁺] and renin release, in contrast to most other secretory systems. Indirect reduction of intracellular [Ca⁺⁺], using Ca channel antagonists or by reducing extracellular [Ca⁺⁺], stimulated renin release but did not affect cAMP release. It is therefore concluded that the stimulatory effect of low [Ca⁺⁺] is not mediated by cAMP. The fundamental hypothesis is that catecholamines appear to stimulate renin release, an effect mediated by cAMP. Decreased intracellular [Ca⁺⁺] stimulates renin release, an effect which may either occur distal to changes in cAMP, or may be part of an independent pathway mediating renin release.