A M Devlin1, B J Leckie. 1. Medical Research Council Blood Pressure Unit, Western Infirmary, Glasgow, UK.
Abstract
OBJECTIVE: Renin secretion in response to long-term exposure to isoprenaline, dibutyryl cyclic adenosine monophosphate (dbcAMP), forskolin and atrial natriuretic peptide (ANP) was measured in cultured human nephroblastoma cells. METHODS: Human nephroblastoma cells in culture were treated long-term (1-12 days) with isoprenaline, dbcAMP or forskolin, alone or in combination with ANP; renin release and cell growth were studied. RESULTS: The increase in renin output caused by isoprenaline and dbcAMP could be accounted for by stimulation of cell growth. The effect of isoprenaline was blocked by propranolol. Forskolin stimulated renin secretion per cell. ANP increased extracellular cyclic guanosine monophosphate and suppressed basal renin output. Suppression of basal renin output was due to a reduced secretion rate per cell, without a change in cell growth. ANP suppressed isoprenaline-induced and dbcAMP-induced renin output by blocking increased cell growth, and forskolin-induced renin output by blocking renin secretion. CONCLUSIONS: These results suggest that beta-receptor agonists and ANP interact within the kidney to control renin secretion, by helping to determine the number of renin-secreting cells.
OBJECTIVE:Renin secretion in response to long-term exposure to isoprenaline, dibutyryl cyclic adenosine monophosphate (dbcAMP), forskolin and atrial natriuretic peptide (ANP) was measured in cultured humannephroblastoma cells. METHODS:Humannephroblastoma cells in culture were treated long-term (1-12 days) with isoprenaline, dbcAMP or forskolin, alone or in combination with ANP; renin release and cell growth were studied. RESULTS: The increase in renin output caused by isoprenaline and dbcAMP could be accounted for by stimulation of cell growth. The effect of isoprenaline was blocked by propranolol. Forskolin stimulated renin secretion per cell. ANP increased extracellular cyclic guanosine monophosphate and suppressed basal renin output. Suppression of basal renin output was due to a reduced secretion rate per cell, without a change in cell growth. ANP suppressed isoprenaline-induced and dbcAMP-induced renin output by blocking increased cell growth, and forskolin-induced renin output by blocking renin secretion. CONCLUSIONS: These results suggest that beta-receptor agonists and ANP interact within the kidney to control renin secretion, by helping to determine the number of renin-secreting cells.