Active and inactive renin release from rabbit kidney cortex slices: effect of sodium concentration and of furosemide.

Munday, K. A.; Noble, A. R.; Richards, Hugh K.

doi:10.1113/jphysiol.1982.sp014274

Cited by 16 publications

(16 citation statements)

References 27 publications

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“…1 shows that in low [Na+] buffers active renin secretion was increased whereas inactive renin was reduced. This confirms data from previous studies Munday et al 1982). The changes in both forms of renin were abolished by adding 100 #uM-ouabain.…”

Section: Discussionsupporting

confidence: 92%

Secretion control for active and inactive renin: effect of ouabain on release from rabbit kidney cortex slices.

Ginesi¹,

Noble²

1986

The Journal of Physiology

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SUMMARY1. Release of active and inactive renin by rabbit kidney cortex slices was investigated. Inactive renin was estimated as the increase in renin activity after acidification (pH 2 8) of slice supernatant solutions.2. For kidney slices incubated in complete Krebs bicarbonate buffer, the Na-K-ATPase inhibitor ouabain (100 lm) reduced the secretion of both active (-19-2 %) and inactive (-78-9 %) forms of renin.3. In low Na buffers ([Na+] = 23 mM) active renin release was increased and inactive renin was suppressed. Both of these changes were abolished by addition of ouabain (100 /tM). The reduction in inactive renin secretion produced by ouabain in complete Krebs buffer did not occur in low [Na+] buffers.4. In zero Ca2+ buffers containing EGTA (5 mM), secretion of both active and inactive renin was increased but these changes were abolished by addition of ouabain (100 /tm).5. Incubating kidney slices in low Na+, zero Ca2+ media revealed differences between the secretion control mechanisms for the two forms of renin. The separate stimulatory effects of low Na+ and low Ca2+ were not additive for the release of active renin and inclusion of ouabain resulted in similar secretion rates to those under control conditions. For inactive renin secretion, in the absence of Ca2+ release mechanisms still respond to reduction in Na+ with decreased secretion. Conversely, in low Na+ buffers, removal of Ca2+ still promotes inactive renin secretion. These changes were abolished by the addition of ouabain (100 SUM).6. Slices did not change in weight during incubation in media which did not contain ouabain. Addition of this inhibitor to control buffers and low Na buffers did result in an increase in weight. This correlated with the presence of Ca2+ in the buffer and did not appear to be related to [Na+].7. These studies again show that the mechanisms regulating the secretion of active and inactive renin are not identical and support the hypothesis that Na+ have differing roles to play in the regulation of these two forms of renin.

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Section: Discussionsupporting

confidence: 92%

Secretion control for active and inactive renin: effect of ouabain on release from rabbit kidney cortex slices.

Ginesi¹,

Noble²

1986

The Journal of Physiology

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“…Lithium ions stimulate the release of active renin by rabbit kidney cortex slices and this effect is clearly not secondary to altered renal function. Furthermore, our previous studies with rabbit kidney cortex slices (Munday et al, 1982) have shown that this preparation responds to a decrease in [Na+] with increased release of active renin. Inhibition of proximal tubular sodium reabsorption by lithium ions would lead to increased [Na+] at the macula densa, the site at the start of the distal tubule which is presumed to act as a sodium load or concentration detector in the control of renin release.…”

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confidence: 91%

Direct effect of lithium on active and inactive renin secretion

Ginesi

Munday

Noble

1983

British J Pharmacology

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Rabbit kidney cortex slices were used to investigate the effect of lithium chloride (0 to 20 mm) on renin release. Secretion of active renin was increased in the presence of lithium but inactive (acid‐activatable) renin secretion was unchanged. Increased plasma renin activity in patients receiving lithium therapy may be the result of direct effects of lithium on renin secretion mechanisms rather than being secondary to altered renal sodium handling.

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“…In a previous study, using pentobarbitone-anaesthetized rabbits, we found that furosemide diuresis was associated with an increase in plasma active renin with a concurrent decrease in the inactive form (Richards, Lush, Noble & Munday, 1981). Rabbit kidney cortex slices also respond to a reduction in buffer [Na+] with increased active and decreased inactive renin release (Munday, Noble & Richards, 1982). We have therefore proposed that the relative amounts of active and inactive renin in plasma are determined intrarenally by a sodium-sensitive mechanism.…”

Section: Introductionmentioning

confidence: 99%

Furosemide fails to alter plasma active or inactive renin in conscious sheep but does so in anaesthetized animals.

Lush¹,

Munday²,

Noble³

1983

The Journal of Physiology

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SUMMARY1. Regulation of plasma levels of active and inactive renin was investigated using sheep with indwelling artery, vein and bladder catheters. Control and experimental studies were carried out in the same animals on different days. Volume depletion during any single experiment was limited to a maximum of 50 ml.2. Despite large changes in sodium and water excretion, the diuretic furosemide at two dose levels, 1 and 10 mg/kg, failed to alter plasma levels of either active or inactive renin in conscious sheep.3. Induction of pentobarbitone anaesthesia in the sheep did not, per se, alter either plasma active or inactive renin. Furosemide (10 mg/kg) in anaesthetized animals produced a similar diuresis and natriuresis response to conscious sheep, but plasma active renin increased by 270 % and inactive renin decreased to zero.4. In conscious sheep given an infusion of papaverine, furosemide also produced an increase in plasma active renin and a concurrent decrease in the inactive form.5. In both anaesthetized animals and in conscious sheep infused with papaverine, furosemide-induced intrarenal vasodilation, as evidenced by changes in clearance of p-aminohippuric acid, was much reduced in comparison to the conscious animals. This may be significant in relation to the control of renin secretion.6. It appears that the macula densa sodium receptor, which is considered to regulate renin release, will only function after it has been primed by other intra-or extrarenal factors. This is discussed, particularly in relation to the possible role played by the prostaglandin system.

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Active and inactive renin release from rabbit kidney cortex slices: effect of sodium concentration and of furosemide.

Cited by 16 publications

References 27 publications

Secretion control for active and inactive renin: effect of ouabain on release from rabbit kidney cortex slices.

Secretion control for active and inactive renin: effect of ouabain on release from rabbit kidney cortex slices.

Direct effect of lithium on active and inactive renin secretion

Furosemide fails to alter plasma active or inactive renin in conscious sheep but does so in anaesthetized animals.

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