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Do calcium-channel blockers (verapamil, flunarizine) and ionophore A23187 alter the secretion of active and inactive renin in rabbit kidney cortex slices?
Do calcium-channel blockers (verapamil, flunarizine) and ionophore A23187 alter the secretion of active and inactive renin in rabbit kidney cortex slices?
The mechanisms regulating the secretion of active and inactive renin are distinct, and differential release may contribute to the overall control of the renin-angiotensin system.
Animal data on calcium-channel blocker effects on renin forms warrant no clinical change; leaves open distinct active/inactive renin regulation in humans.
Secretion control for active and inactive (acid-activatable) renin was investigated using a rabbit kidney cortex slice preparation. In complete Krebs-Ringer bicarbonate buffer (pH 7.4) the calcium-channel-blocking drugs verapamil (50 microM) and flunarizine (50 microM) had no effect on active renin release but increased inactive renin secretion. In Ca-free or Ca-depleted (+EGTA) buffers secretion of both active and inactive renin was increased. Neither verapamil nor flunarizine under these conditions had any additional effect on active renin secretion but inactive renin release was stimulated by verapamil and inhibited by flunarizine. Although having no effect in the presence of Ca++ ions, the ionophore A23187 (17 microM) selectively abolished the secretion of inactive renin in the absence of calcium. The mechanisms regulating the secretion of the two forms of renin are clearly not identical. Differential release of active and inactive renin by the kidney may contribute to the overall control of the renin-angiotensin system.
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Ginesi et al. (1984) studied this question.
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