Rat Juxtaglomerular Cells are Endowed with DA-1 Dopamine Receptors Mediating Renin Release

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Abstract
Summary: Under control conditions a primary culture containing about 80–90% of granular juxtaglomerular (JG) cells prepared from rat kidneys continuously released renin into the culture medium at a rate of 17.9 ± 1.4 ng angiotensin I/h per mg of cell proteins per 30 min (n = 14). Dopamine (1.0 μM), the DA-I dopamine receptor agonist fenoldopam (0.5 μM), and isoproterenol (1.0 μM) increased renin secretion markedly (130–200%). Propranolol (0.1 μM) reduced the effects of isoproterenol significantly (809?), but not those of dopamine or fenoldopam. In contrast, SCH 23390 (0.01 μM), a DA-1 dopamine receptor antagonist, inhibited markedly only the renin release evoked by the latter two agonists, whereas S-sulpiride (10 μM), a DA-2 dopamine receptor antagonist, and phentolamine (10 μ.M), a nonselective α-adrenoceptor antagonist, did not modify the effects of either dopamine or fenoldopam. In rats, pithed to eliminate reflex-ogenic mechanisms regulating renin release, at the end of a 15 min i.v. infusion of fenoldopam (20 μg/kg per min) there was a significant increase in plasma renin activity. This effect was completely prevented by SCH 23390 (0.1 mg/kg i.v.) but not significantly changed by S-sulpiride (0.3 mg/kg i.v.) or phentolamine (3.0 mg/kg i.v.) plus propranolol (0.75 mg/kg i.v.). In conclusion, these results indicate that DA-1 dopamine receptors are present in rat kidney JG cells and that pharmacological stimulation of these receptors with dopamine or fenoldopam leads to renin secretion.