Rate‐dependency of calcitonin secretion in response to increased plasma Ca<sup>2+</sup>

Wang, W.; Lewin, Ewa; Ølgaard, Klaus

doi:10.1046/j.1365-2362.2002.01052.x

Cited by 10 publications

(9 citation statements)

References 23 publications

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“…Similarly, this demonstration does not seek to explain the lack of peak hormone in subsequent stimulations that have been observed, for example, by Schwarz’s group (Schwarz et al, 1998). Similar findings have been reported with respect to calcitonin as well (Wang et al, 2002). …”

Section: Introductionsupporting

confidence: 91%

The apparent hysteresis in hormone-agonist relationships

Pruett

Hester

Coleman

2012

Journal of Theoretical Biology

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It has been noted in multiple studies that the calcium–PTH axis, among others, is subject to an apparent hysteresis. We sought to explain a major component of the observed phenomenon by constructing a simple mathematical model of a hormone and secretagogue system with concentration dependent secretion and containing two delays. We constructed profiles of the hormone–agonist axis in this model via four types of protocols, three of which emulating experiments from the literature, and observed a delay- and load-dependent hysteresis that is an expected mathematical artifact of the system described. In particular, the delay associated with correction allows for over-secretion of the hormone influencing the corrective mechanism; thus rate dependence is an artifact of the corrective mechanism, not a sensitivity of the gland to the magnitude of change. From these observations, the detected hysteresis is due to delays inherent in the systems being studied, not in the secretory mechanism.

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Section: Introductionsupporting

confidence: 91%

The apparent hysteresis in hormone-agonist relationships

Pruett

Hester

Coleman

2012

Journal of Theoretical Biology

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“…83 Our laboratory has previously demonstrated a rapid minute-to-minute regulation of p-Ca 2+ , where the set point for Ca 2+ on the bone surface was defined by the level of calciotropic hormones, activity of CaR, and the presence of kidneys. [84][85][86][87][88] The minute-to-minute regulation of P is not well understood. A rise in p-P resulted not only in an immediate dose-dependent drop in p-Ca 2+ but also in prolonged recovery in BNX rats.…”

Section: Discussionmentioning

confidence: 99%

Key role of the kidney in the regulation of fibroblast growth factor 23

Mace

Gravesen

Hofman-Bang

et al. 2015

Kidney International

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High circulating levels of fibroblast growth factor 23 (FGF23) have been demonstrated in kidney failure, but mechanisms of this are not well understood. Here we examined the impact of the kidney on the early regulation of intact FGF23 in acute uremia as induced by bilateral or unilateral nephrectomy (BNX and UNX, respectively) in the rat. BNX induced a significant increase in plasma intact FGF23 levels from 112 to 267 pg/ml within 15 min, which remained stable thereafter. UNX generated intact FGF23 levels between that seen in BNX and sham-operated rats. The intact to C-terminal FGF23 ratio was significantly increased in BNX rats. The rapid rise in FGF23 after BNX was independent of parathyroid hormone or FGF receptor signaling. No evidence of early stimulation of FGF23 gene expression in the bone was found. Furthermore, acute severe hyperphosphatemia or hypercalcemia had no impact on intact FGF23 levels in normal and BNX rats. The half-life of exogenous recombinant human FGF23 was significantly prolonged from 4.4 to 11.8 min in BNX rats. Measurements of plasma FGF23 in the renal artery and renal vein demonstrated a significant renal extraction. Thus the kidney is important in FGF23 homeostasis by regulation of its plasma level and metabolism.

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“…This labile pool functions as a short-term buffer, taking up or releasing calcium to correct for changes in ECF [ 22 ]. Knowledge concerning this process, as summarized in details by Parfitt, has with some exceptions [ 2 , 9 , 10 , 12 , 22 - 25 ], disappeared from the current texts [ 22 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

A potential kidney - bone axis involved in the rapid minute-to-minute regulation of plasma Ca2+

et al. 2015

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BackgroundUnderstanding the regulation of mineral homeostasis and function of the skeleton as buffer for Calcium and Phosphate has regained new interest with introduction of the syndrome “Chronic Kidney Disease-Mineral and Bone Disorder”(CKD-MBD). The very rapid minute-to-minute regulation of plasma-Ca2+ (p-Ca2+) takes place via an exchange mechanism of Ca2+ between plasma and bone. A labile Ca storage pool exists on bone surfaces storing excess or supplying Ca when blood Ca is lowered. Aim was to examine minute-to-minute regulation of p-Ca2+ in the very early phase of acute uremia, as induced by total bilateral nephrectomy and to study the effect of absence of kidneys on the rapid recovery of p-Ca2+ from a brief induction of acute hypocalcemia.MethodsThe rapid regulation of p-Ca2+ was examined in sham-operated rats, acute nephrectomized rats(NX), acute thyroparathyrectomized(TPTX) rats and NX-TPTX rats.ResultsThe results clearly showed that p-Ca2+ falls rapidly and significantly very early after acute NX, from 1.23 ± 0.02 to 1.06 ± 0.04 mM (p < 0.001). Further hypocalcemia was induced by a 30 min iv infusion of EGTA. Control groups had saline. After discontinuing EGTA a rapid increase in p-Ca2+ took place, but with a lower level in NX rats (p < 0.05). NX-TPTX model excluded potential effect of accumulation of Calcitonin and C-terminal PTH, both having potential hypocalcemic actions. Acute TPTX resulted in hypercalcemia, 1.44 ± 0.02 mM and less in NX-TPTX rats,1.41 ± 0.02 mM (p < 0.05). Recovery of p-Ca2+ from hypocalcemia resulted in lower levels in NX-TPTX than in TPTX rats, 1.20 ± 0.02 vs.1.30 ± 0.02 (p < 0.05) demonstrating that absence of kidneys significantly affected the rapid regulation of p-Ca2+ independent of PTH, C-PTH and CT.ConclusionsP-Ca2+ on a minute-to-minute basis is influenced by presence of kidneys. Hypocalcemia developed rapidly in acute uremia. Levels of p-Ca2+, obtained during recovery from hypocalcemia resulted in lower levels in acutely nephrectomized rats. This indicates that kidneys are of significant importance for the ‘set-point’ of p-Ca2+ on bone surface, independently of PTH and calcitonin. Our results point toward existence of an as yet unknown factor/mechanism, which mediates the axis between kidney and bone, and which is involved in the very rapid regulation of p-Ca2+.

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Rate‐dependency of calcitonin secretion in response to increased plasma Ca²⁺

Cited by 10 publications

References 23 publications

The apparent hysteresis in hormone-agonist relationships

The apparent hysteresis in hormone-agonist relationships

Key role of the kidney in the regulation of fibroblast growth factor 23

A potential kidney - bone axis involved in the rapid minute-to-minute regulation of plasma Ca2+

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Rate‐dependency of calcitonin secretion in response to increased plasma Ca2+

Cited by 10 publications

References 23 publications

The apparent hysteresis in hormone-agonist relationships

The apparent hysteresis in hormone-agonist relationships

Key role of the kidney in the regulation of fibroblast growth factor 23

A potential kidney - bone axis involved in the rapid minute-to-minute regulation of plasma Ca2+

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Rate‐dependency of calcitonin secretion in response to increased plasma Ca²⁺