Stimulus-secretion coupling of renin. Role of hemodynamic and other factors.

Fray, J. C. S.

doi:10.1161/01.res.47.4.485

Cited by 84 publications

(33 citation statements)

References 89 publications

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“…Recent experiments have demonstrated that the mechanism by which hyperalbuminaemia induces renin secretion may not involve the more conventional macula densa receptor, vascular baroreceptor, or neurogenic receptor (Fray & Karuza, 1980), but that it may in part involve the lowering of Ca at the juxtaglomerular cell. Though this suggestion is consistent with the recent discovery that Ca plays a central, yet unconventional, role in the renin secretion process (Fray, 1980), direct evidence for an action of albumin on the juxtaglomerular cells has never been obtained. We have sought to obtain such evidence in an attempt to gain further insight into the secretary process at the cellular level.…”

Section: Introductionsupporting

confidence: 75%

Mechanism by which albumin stimulates renin secretion in isolated kidneys and juxtaglomerular cells.

Fray¹,

Laurens²

1981

The Journal of Physiology

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SUMMARY1. Raising albumin concentration stimulates renin secretion in isolated perfused kidneys and isolated juxtaglomerular cells.2. In isolated perfused kidneys, raising albumin concentration from 20 to 120 g/l. increased renin secretion and perfusate flow when the perfusion medium contained 1-82 mM-total or ionized Ca. Removing the renal capsule abolished the increased flow but not renin secretion.3. In isolated juxtaglomerular cells, raising albumin concentration from 0 to 60 g/l. increased renin secretion threefold. This was enhanced slightly by removing Ca. Raising Ca, removing or raising K to 50 mm, or lowering Na to 25 mm inhibited renin secretion.4. Raising pH from 7-36 to 7-64 inhibited renin secretion whether albumin was present or not. Keeping both pH and ionized Ca constant abolished the stimulatory effect of raising albumin.5. We conclude that raising albumin concentration in plasma may stimulate renin secretion by several mechanisms, two of which are by lowering ionized Ca and lowering pH, and that both effects may be on the juxtaglomerular cells directly. We also conclude that raising pH per se has a powerful inhibitory effect on renin secretion.

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Section: Introductionsupporting

confidence: 75%

Mechanism by which albumin stimulates renin secretion in isolated kidneys and juxtaglomerular cells.

Fray¹,

Laurens²

1981

The Journal of Physiology

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“…9 Inhibitors of renin release such as All or high perfusion pressure act by depolarizing the juxtaglomerular cell membrane, resulting in an influx of extracellular calcium and an increase in intracellular calcium levels. These effectors are therefore dependent on the presence of extracellular calcium and can be blocked by D-600 or verapamil.…”

Section: Discussionmentioning

confidence: 99%

“…Fray and Park 7 demonstrated that the renin-stimulating effects of a variety of agents were attenuated by raising extracellular calcium levels and that the effects of inhibitory stimuli were enhanced by raising extracellular calcium. 8 From these results Fray 9 has generalized that agents that inhibit renin release increase intracellular calcium levels while stimulators of renin release lower calcium concentrations.…”

mentioning

confidence: 99%

The role of calcium in the control of renin release.

Naftilan¹,

Oparil²

1982

Hypertension

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SUMMARY The effects of removing external calcium and inhibiting entry of calcium into the cell by treatment with D-600 on renin release from renal cortical slices of male Sprague-Dawley rats were examined. Baseline renin release, angiotensin II (All)-induced inhibition, and isoproterenol-induced stimulation of renin release were studied. Removal of external calcium by chelation with 5 mM EGTA inhibited basal renin release while treatment with 1 mM EGTA stimulated basal renin release slightly. Incubation of slices with zero calcium medium containing 1 mM EGTA had no effect on isoproterenolinduced stimulation of renin release. In contrast, similar treatment reduced the inhibitory effect of AH from 58.7% of baseline to 85.3% (p < 0.001). Similarly, blockage of calcium entry into cells with D-600 had no effect on isoproterenol-induced stimulation of renin release but abolished All-induced inhibition. Replacement of sodium in the bathing medium with choline had no effect on baseline renin release or on All-induced inhibition of renin release, ruling out the possibility that D-600 altered renin release via an effect on sodium influx. Taken together, the data strongly suggest that All-induced inhibition of renin release is partially dependent on the presence of external calcium but that isoproterenol-induced stimulation of renin release is not. T HE role of calcium in the control of renin release is incompletely understood. In vivo experiments have yielded conflicting results in that calcium infusion has been shown to inhibit renin release in some studies'-2 and stimulate renin release in others.3 Using the isolated perfused rat kidney preparation, Peart and colleagues 4 5 found that removal of external calcium from the perfusate by chelation with EDTA stimulated renin release and blocked the inhibitory effect of angiogensin II (All) on renin release but did not alter isoproterenol-induced stimulation of renin release. They further observed that the calcium ionophore A23187 inhibited renin release. 6 In a similar perfused rat kidney preparation. Fray and Park 7 demonstrated that the renin-stimulating effects of a variety of agents were attenuated by raising extracellular calcium levels and that the effects of inhibitory stimuli were enhanced by raising extracellular calcium.8 From these results Fray 9 has generalized that agents that inhibit renin release increase intracellular calcium levels while stimulators of renin release lower calcium concentrations.Using the rat renal cortical slice preparation, we 10 -" have shown that All inhibits renin release from renal cortical slices in a dose-dependent manner via a direct

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“…The role of the macula densa in controlling renin release is still not clear; moreover renal vasodilators usually increase sodium excretion and stimulate renin release (Peart, 1978). Parathormone increases PRA (Smith et al, 1979;Peart et al, 1986), hypocalcaemia and calcitonin have no effect (Llach et al, 1974;Smith et al, 1979), but a direct increase in juxtaglomerular cytosolic calcium would inhibit renin release (Peart, 1978;Fray, 1980). CCK8 is believed to stimulate pancreatic enzyme secretion by a change in acinar cell calcium flux resulting in elevation of intracellular calcium (Christophe & Waelbroeck, 1981;Petersen, 1982).…”

Section: Main Effects In Rabbit and Manmentioning

confidence: 99%

Renal effects of gastrin C‐terminal tetrapeptide (as pentagastrin) and cholecystokinin octapeptide in conscious rabbit and man

Calam

Gordon

Peart

et al. 1987

British J Pharmacology

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1 Pentagastrin and cholecystokinin octapeptide (CCK8) were infused i.v. at three different doses in two sets of 4 conscious rabbits following a repeated measurements design (130, 1,300 and 13,000 pmol kg-' min-' pentagastrin; 5, 50 and 450 pmol kg-' min-' CCK8). In man, two different doses of pentagastrin (13 and 65 pmol kg-' min-') were infused in two groups of 6 subjects, and CCK8 (2 pmol kg-' min-') in a third group. According to published human postprandial levels, plasma CCK8-like immunoreactivity concentrations were supraphysiological at all doses infused. 2 In the rabbit, pentagastrin produced a dose-related fall in urine flow and free water clearance, but no significant change in systemic and renal haemodynamics, electrolyte excretion and measured plasma constituents; however, in human subjects, pentagastrin increased renal sodium excretion and reduced potassium excretion but did not change glomerular filtration rate. 3 In the rabbit, CCK8 produced a dose-related fall in plasma renin activity, plasma calcium concentration and mean arterial blood pressure; dose-dependent increases in effective renal plasma flow, glomerular filtration rate and renal sodium excretion. In man, changes in sodium and potassium excretion similar to pentagastrin were observed; there were no significant changes in plasma renin activity, plasma calcium concentration, blood pressure, effective renal plasma flow or glomerular filtration rate. 4 The pharmacological renal effects of pentagastrin in conscious water-loaded rabbits resemble vasopressin. In contrast, CCK8's most striking effect was vasodilatation and was unusual in inhibiting rather than stimulating renin release. In man the net changes in urine composition found during infusion of these peptides are similar to those produced by the potassium-sparing diuretics, amiloride and triamterene. However the generally weak renal effects observed, even at pharmacological doses, indicate that these peptides are unlikely to influence renal function under normal physiological conditions.

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Stimulus-secretion coupling of renin. Role of hemodynamic and other factors.

Cited by 84 publications

References 89 publications

Mechanism by which albumin stimulates renin secretion in isolated kidneys and juxtaglomerular cells.

Mechanism by which albumin stimulates renin secretion in isolated kidneys and juxtaglomerular cells.

The role of calcium in the control of renin release.

Renal effects of gastrin C‐terminal tetrapeptide (as pentagastrin) and cholecystokinin octapeptide in conscious rabbit and man

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