A Temperature Sensitive Link in the Adrenergic Control of Renin Release.

Abstract

The release of renin from dog cortical kidney slice preparations incubated in a physiological salt solution, can be modulated by alpha and beta adrenergic drugs. When given to slices maintained at 37(DEGREES)C, the beta agonist isoproterenol (ISP) stimulated renin release from the slices. When the slices were maintained at 20(DEGREES)C, ISP had no effect on renin release. The alpha agonist phenylephrine inhibited renin release from the slices incubated at 20(DEGREES)C in a dose dependent manner, while its effect on slices incubated at 37(DEGREES)C was less pronounced. The change in response of the slices from beta dominant at 37(DEGREES)C to alpha dominant at 20(DEGREES)C appeared to be a receptor phenomenon. When the cortical slices were incubated with the irreversible alpha antagonist phenoxybenzamine (POB) at 20(DEGREES)C for one hour, they were unable to respond to ISP when returned to 37(DEGREES)C. However, POB had no effect on the response of slices to ISP when the POB was given at 37(DEGREES)C. Specific radiolig and binding of tritiated dihydroalprenolol to the renal beta adrenergic receptors in the presence or absence of POB was also measured in renal membrane preparations. Specific binding of membranes exposed to POB at 2-4(DEGREES)C for one hour decreased 67% from control. Membranes exposed to POB at 37(DEGREES)C for 5 minutes showed a decrease in binding of only 38%. These data are consistent with the hypothesis that with a decrease in temperature the renal beta receptors demonstrate properties normally associated with alpha receptors, namely the potential to be blocked by POB. This may be due to an interconversion of the renal alpha and beta adrenoceptors.