Secretion control for active and inactive renin: effects of calcium and potassium on rabbit kidney cortex slices.

Ginesi, L M; Munday, K. A.; Noble, A. R.

doi:10.1113/jphysiol.1983.sp014951

“…Mechanisms that are highly sensitive to potassium, and operate through membrane depolarization and calcium entry, have previously been reported (e.g., Ginesi et al, 1983). Measurement of intracellular potassium showed that fusioncompetent myoblasts contain 100-140 mM potassium, which gives a potassium equilibrium potential of -80 to -89 mV.…”

Section: A Role For Membrane For Depolarizationmentioning

confidence: 87%

The control of chick myoblast fusion by ion channels operated by prostaglandins and acetylcholine.

Entwistle

¹

,

Zalin

²

,

Bevan

³

et al. 1988

The Journal of Cell Biology

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Abstract. Chick myoblast fusion in culture was investigated using prostanoid synthesis inhibitors to delay spontaneous fusion. During this delay myoblast fusion could be induced by prostaglandin El (PGE0, by raising extracellular potassium and by addition of carbachol. Carbachol-induced fusion, but not PGEinduced fusion, was prevented by the acetylcholine receptor blocker ct-bungarotoxin. Fusion induced by any of these agents was prevented by the Ca channel blockers lanthanum and D600. The threshold for potassium-induced fusion was 7-8 raM; maximal fusion occurred at 16-20 mM. Low extracellular potassium inhibited spontaneous fusion. Intracellular potassium in fusion competent myoblasts was 101 m-moles/l cell. Calcium flux measurements demonstrated that high potassium increased calcium permeability in fusion-competent myoblasts. A 30-s exposure to high potassium or PGE~ was sufficient to initiate myoblast fusion.Anion-exchange inhibitors (SITS and DIDS) delayed spontaneous myoblast fusion and blocked fusion induced by PGE~ but not carbachol. Blocking the acetylcholine receptor shifted the dose-response relation for PGE-induced fusion to higher concentrations. PGEr induced fusion required chloride ions; carbacholinduced fusion required sodium ions. Provided calcium channels were available, potassium always induced fusion. We conclude that myoblasts possess at least three, independent pathways, each of which can initiate myoblast fusion and that the PGE-activated pathway and the acetylcholine receptor-activated pathway act synergistically. We suggest that fusion competent myoblasts have a high resting membrane potential and that fusion is controlled by depolarization initiated directly (potassium), by an increase in permeability to chloride ions (PGE), or by activation of the acetylcholine receptor (carbachol); depolarization triggers a rise in calcium permeability. The consequent increase in intracellular calcium initiates myoblast fusion.T tiE early development of skeletal muscle follows a predictable sequence of events both in vivo and in vitro. Initially the myoblasts divide and align along their long axes. This is followed by an increase in the duration of the myoblast cell cycle in preparation for cytodifferentiation and fusion into myotubes. Myoblast fusion is temporally closely linked to the appearance of muscle specific proteins such as actin, myosin, creatine phosphokinase, and the acetylcholine receptor (for review see Wakelam, 1985), although this link is not obligatory (Adamo et al., 1976). Contractile proteins and action potential generation, and therefore electrically driven contractile activity, also appear shortly after fusion. These early events can take place in the absence of innervation, although the subsequent differentiation of the myofibre is closely dependent on innervating motoneurones.A. Entwistle's current address is The Ludwig

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“…Zero [Ca2+] induced changes in active and inactive renin release: effect of ouabain In a previous paper the relationship between active and inactive renin secretion and [Ca2+] was examined using a range of Ca2+ concentrations (Ginesi et al 1983).…”

Section: Resultsmentioning

confidence: 99%

“…These include Ca channel blocking drugs such as verapamil (Park et al 1981), D600 (Churchill, 1981) and diltiazem (Churchill, McDonald & Churchill, 1981), calmodulin inhibitors such as trifluoperazine (Churchill & Churchill, 1983;Fray, Lush, Share & Valentine, 1983) and W-7 (Kawamura & Inagami, 1983), TMB-8, an antagonist to the release of Ca2+ from intracellular sites (Fray & Lush, 1984;Baxter, Lazzaro, Duggin, Horvath & Tiller, 1985) and blockers L. M. GJNESI AND A. R. NOBLE of the Na-K-ATPase such as ouabain (Lyons & Churchill, 1975), vanadate (Churchill & Churchill, 1980b) and quinacrine . The effect of ATPase inhibitors on renin secretion is dependent on the presence of extracellular Ca2+ (Churchill & Churchill, 1980a (Ginesi et al 1983). The Ca channel blockers verapamil and flunarizine increased inactive renin secretion (Ginesi & Noble, 1984).…”

Section: Discussionmentioning

confidence: 99%

“…Because of the technical difficulty of obtaining a homogenous preparation of juxtaglomerular cells from the kidney, this concept has not yet been substantiated by direct measurements of intracellular [Ca2+]. It is based on studies in which the extracellular [Ca2+] bathing in vitro preparations was changed (Van Dongen & Peart, 1974;Fray, 1977;Park & Malvin, 1978;Baumbach & Sk0tt, 1981;Churchill, 1981;Park et al 1981;Ginesi et al 1983) and also on experiments with a number of pharmacological agents. These include Ca channel blocking drugs such as verapamil (Park et al 1981), D600 (Churchill, 1981) and diltiazem (Churchill, McDonald & Churchill, 1981), calmodulin inhibitors such as trifluoperazine (Churchill & Churchill, 1983;Fray, Lush, Share & Valentine, 1983) and W-7 (Kawamura & Inagami, 1983), TMB-8, an antagonist to the release of Ca2+ from intracellular sites (Fray & Lush, 1984;Baxter, Lazzaro, Duggin, Horvath & Tiller, 1985) and blockers L. M. GJNESI AND A. R. NOBLE of the Na-K-ATPase such as ouabain (Lyons & Churchill, 1975), vanadate (Churchill & Churchill, 1980b) and quinacrine .…”

Section: Discussionmentioning

confidence: 99%

“…Details of the methods used for measuring active and inactive renin and their evaluation have also been published elsewhere (Richards, Lush, Noble & Munday, 1981) and further discussion of the methodology for measuring inactive renin appears in another paper (Ginesi et al 1983). Inactive renin can only be measured after activation in vitro.…”

Section: Methodsmentioning

confidence: 99%

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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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Endocrine Control of Sodium Balance

Fray

¹

2000

Comprehensive Physiology

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The sections in this article are: Components of the Renin–Angiotensin System Prorenin/Renin Renin Gene Structure, Evolutionary Function, and Regulation Biosynthesis and Chemiosmotic Activation Tissue Distribution in Health and Disease Kidney Heart and Blood Vessels Adrenal Brain Eye, Liver, and Intestine Ovary, Uterus, Testis, and Sex Accessory and Subcutaneous Tissue Submandibular Gland Spontaneously Hypertensive Rat Renal Hypertensive Rat Growth Retardation Relative Renin Plasma Levels and Suggestive Meaning Angiotensinogen Biochemical Properties Tissue Expression and In Situ Regulation Factors Regulating Release Mechanism of Action and Physiological Effects Summary and Challenges Angiotensin I–Converting Enzyme Molecular Structure and Regulation Active Sites and Catalytic Properties Tissue Distribution Summary and Challenges Angiotensin Peptides Aldosterone Biosynthesis and Metabolism Secretion and Its Regulation Angiotensin II Potassium Corticotropin and Other Proopiomelanocortin Peptides Various Stimulators of Aldosterone Secretion Various Inhibitors of Aldosterone Secretion Cellular Actions Disorders of Aldosterone Secretion Systemic Regulation of Sodium Volume Homeostasis Regulation of Sodium Volume Homeostasis Integrative Regulation of Sodium Volume and Blood Pressure Homeostasis Integrative Regulation of Sodium and Potassium Homeostasis Integrative Regulation by Potassium and Hydrogen in Volume Homeostasis Polyendocrinopathy Type III: Systemic Dysregulation of Sodium Volume Homeostasis Primary and Pseudoprimary Aldosteronism Secondary Aldosteronism: Renin Tumors and Edematous States High‐Renin States and Low‐Renin Syndromes Summary and Challenges: Defining Functions and Processing Strategies of Renin–Angiotensin System Molecules

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Secretion control for active and inactive renin: effects of calcium and potassium on rabbit kidney cortex slices.

Cited by 17 publications

References 34 publications

The control of chick myoblast fusion by ion channels operated by prostaglandins and acetylcholine.

The control of chick myoblast fusion by ion channels operated by prostaglandins and acetylcholine.

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

Endocrine Control of Sodium Balance

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