This study aimed to assess the relevance of specific potassium channels, su
ch as inwardly or outwardly rectifying and calcium-regulated potassium chan
nels, to the control of renin secretion. For this purpose we examined the e
ffects of the: K+ channel blockers 4-aminopyridine (1 mmol/l), barium (100
mu mol/l), tetraethylammonium (2 mmol/l) and apamin (200 nmol/l) on basal r
enin secretion, on renin secretion stimulated by isoproterenol (10 nmol/l)
and oil the inhibition of renin secretion by angiotensin II (100-300 pmol/l
) in the isolated rat kidney perfused at constant pressure. Whilst all four
K+ channel blockers increased renal vascular resistance, only 4-aminopyrid
ine and barium attenuated isoproterenol-stimulated renin secretion in an ad
ditive fashion and augmented the inhibitory effect of angiotensin II. These
effects of K+ channel blockers were not changed by the L-type calcium chan
nel blocker amlodipine (5 mu mol/l), indicating that their effects on renin
secretion are not due to voltage-operated calcium influx. Our data, moreov
er, suggest that potassium efflux from renal juxtaglomerular cells is not i
mportant for the inhibitory action of angiotensin II on renin secretion. As
a consequence it appears that the membrane potential of renal juxtaglomeru
lar cells per se is relevant to renin secretion such that membrane depolari
zation inhibits the exocytosis of renin whilst hyperpolarization favors ren
in secretion. By their activity, potassium channels can contribute to membr
ane hyperpolarization and thus facilitate renin secretion.