scholarly journals Calcium metabolism and cardiovascular function after spaceflight

2002 ◽  
Vol 92 (1) ◽  
pp. 3-12 ◽  
Author(s):  
Daniel C. Hatton ◽  
Qi Yue ◽  
Jacqueline Dierickx ◽  
Chantal Roullet ◽  
Keiichi Otsuka ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Metabolism ◽  
Calcium Concentration ◽  
Dietary Calcium ◽  
Ionized Calcium ◽  
Free Calcium ◽  
Mineral Density ◽  
Spontaneously Hypertensive ◽  
Low Calcium ◽  
High Calcium

To determine the influence of dietary calcium on spaceflight-induced alterations in calcium metabolism and blood pressure (BP), 9-wk-old spontaneously hypertensive rats, fed either high- (2%) or low-calcium (0.02%) diets, were flown on an 18-day shuttle flight. On landing, flight animals had increased ionized calcium ( P < 0.001), elevated parathyroid hormone levels ( P < 0.001), reduced calcitonin levels ( P < 0.05), unchanged 1,25(OH)2D3levels, and elevated skull ( P < 0.01) and reduced femur bone mineral density. Basal and thrombin-stimulated platelet free calcium (intracellular calcium concentration) were also reduced ( P < 0.05). There was a tendency for indirect systolic BP to be reduced in conscious flight animals ( P = 0.057). However, mean arterial pressure was elevated ( P < 0.001) after anesthesia. Dietary calcium altered all aspects of calcium metabolism ( P < 0.001), as well as BP ( P < 0.001), but the only interaction with flight was a relatively greater increase in ionized calcium in flight animals fed low- compared with high-calcium diets ( P < 0.05). The results indicate that 1) flight-induced disruptions of calcium metabolism are relatively impervious to dietary calcium in the short term, 2) increased ionized calcium did not normalize low-calcium-induced elevations of BP, and 3) parathyroid hormone was paradoxically increased in the high-calcium-fed flight animals after landing.

scholarly journals Secretion and degradation of parathormone as a function of intracellular maturation of hormone pools

1979 ◽  
Vol 83 (3) ◽  
pp. 521-528 ◽  
Author(s):  
JJ Morrissey ◽  
DV Cohn
Keyword(s):  
Cyclic Amp ◽  
Half Life ◽  
Calcium Concentration ◽  
Hormone Secretion ◽  
Ionized Calcium ◽  
Dibutyryl Cyclic Amp ◽  
Low Calcium ◽  
High Calcium ◽  
Parathormone Secretion

The biosynthesis, processing, and secretion of parthormone and the effect of calcium on these processes were measured in dispersed porcine parthyroid cells incubated with [(35)S]methionine. Proparathormone was detected at 10 min, the earliest time measured, and was rapidly and apparently quantitatively converted to parathormone. The half-life of the prohomormone pool was 15 min. Secretion of parathormone was detected by 20 min. In pulse-chase experiments there was a period between 20 and 40 min during which the wave of newly-synthesized parathormone was secreted. After 40 min during little additional radioactive hormone was secreted, but dibutyryl cyclic AMP, an agent that can mobilize stored parathormone, when added to the incubation mixtures enhanced radioactive parathormone secretion but only after 60 min, although it increased net hormone secretion as determined by radioimmunoassay to the same extent at all times studied. When the ionized calcium concentration of the medium was lowered, more radioactive hormone was secreted at all times but the effect was greatest on that hormone that was synthesized less than 60 min previously ; however, net hormone secretion in contrast to radioactive hormone was enhanced equally at all intervals. These data could mean that the refractoriness to secretion of parathormone 40-60 min of age was related to maturation of secretory container preparatory to storage. Low calcium (0.5 mM) stimulated hormone secretion up to fivefold compared to high calcium (3.0 mM) but did not affect synthesis of parathormone or proparathormne or conversion of the latter to hormone. During processing at least 70 percent of the intracellular parathormone was lost, presumably through proteolysis and this degradation was greater at high calcium. These data have been interpreted in light of the concept that two secretable pools of parathormone exist within the parathyroid.

scholarly journals Hysteresis of the parathyroid hormone response to hypocalcemia in hemodialysis patients with low turnover aluminum bone disease.

1991 ◽  
Vol 2 (6) ◽  
pp. 1136-1143
Author(s):  
A J Felsenfeld ◽  
D Ross ◽  
M Rodriguez
Keyword(s):  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Bone Disease ◽  
Calcium Concentration ◽  
Hemodialysis Patients ◽  
Ionized Calcium ◽  
Total Serum ◽  
High Calcium ◽  
The Mean ◽  
Pth Level

During the study of parathyroid function in 19 hemodialysis patients with low turnover aluminum bone disease, it was observed that serum parathyroid hormone (PTH) levels were higher during the induction of hypocalcemia than during the recovery from hypocalcemia. This type of PTH response has been termed hysteresis. Hypocalcemia was induced during hemodialysis with a calcium-free dialysate. When the total serum calcium level decreased to 7 mg/dL, the dialysate calcium concentration was changed to 3.5 mEq/L and the dialysis session was completed. One week later, hypercalcemia was induced during hemodialysis with a high-calcium dialysate. The mean basal PTH level was 132 +/- 37 pg/mL (normal, 10 to 65 pg/mL; immunoradiometric (IRMA), Nichols Institute, San Juan Capistrano, CA) and increased to a maximal PTH level of 387 +/- 91 pg/mL during hypocalcemia. For the same ionized calcium concentration, the PTH level was higher during the induction of hypocalcemia than during the recovery from hypocalcemia. Conversely, for the same ionized calcium concentration, the PTH level was greater when hypercalcemia was induced from the nadir of hypocalcemia than when hypercalcemia was induced from basal serum calcium. The set point of calcium (defined as the serum calcium concentration required to reduce maximal PTH by 50%) was greater during the induction of hypocalcemia than during the recovery from hypocalcemia (4.44 +/- 0.10 versus 4.25 +/- 0.09 mg/dL; P = 0.03). The mean basal ionized calcium concentration and the mean ionized calcium concentration at the intersection of the two PTH-calcium curves were the same (4.61 +/- 0.13 versus 4.61 +/- 0.12 mg/dL).(ABSTRACT TRUNCATED AT 250 WORDS)

Dietary calcium modulates blood pressure through alpha 1-adrenergic receptors

1993 ◽  
Vol 264 (2) ◽  
pp. F234-F238 ◽  
Author(s):  
D. C. Hatton ◽  
K. E. Scrogin ◽  
D. Levine ◽  
D. Feller ◽  
D. A. McCarron
Keyword(s):  
Blood Pressure ◽  
Adrenergic Receptor ◽  
Pressor Response ◽  
Dietary Calcium ◽  
Spontaneously Hypertensive ◽  
Low Calcium ◽  
High Calcium ◽  
Basal Blood Pressure ◽  
Receptor Blockers ◽  
The Difference

To investigate the role of adrenergic receptor activity in dietary calcium-induced alterations in blood pressure, weanling spontaneously hypertensive rats (SHR) were placed on either high-calcium (2.0%) or low-calcium (0.1%) diets for 1-2 wk. Baseline blood pressure was higher and pressor responses to exogenous norepinephrine (NE) were greater in the SHR on low-calcium diets than high-calcium diets. There was no difference between diet groups in circulating NE or in the pressor response to angiotensin II. The difference in basal blood pressure was eliminated by the alpha 1-adrenergic receptor blockers phentolamine and prazosin but was not altered by alpha 2-, beta 1-, or beta 2-adrenergic receptor blockade (idazoxan, metoprolol, and butoxamine, respectively). Furthermore, hypotension produced by either calcitonin gene-related peptide, captopril, or nitroprusside failed to eliminate the diet-induced difference in blood pressure. The results suggest the possibility that diet-induced differences in alpha 1-adrenergic activity may be responsible, in part, for variations in blood pressure on different calcium diets.

Platelet cytosolic free calcium concentration and parathyroid hormone: changing relationships with haemodialysis in end-stage renal disease

1992 ◽  
Vol 82 (6) ◽  
pp. 651-658 ◽  
Author(s):  
R. J. Fluck ◽  
A. C. McMahon ◽  
F. M. Alameddine ◽  
A. B. S. Dawnay ◽  
L. R. I. Baker ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Concentration ◽  
Cytosolic Calcium ◽  
Ionized Calcium ◽  
Free Calcium ◽  
Dialysis Session ◽  
Hormone Concentration ◽  
Serum Parathyroid Hormone ◽  
Cytosolic Calcium Concentration ◽  
End Stage

1. Twelve patients receiving haemodialysis for end-stage renal failure were studied at a single dialysis session. Platelet cytosolic calcium concentration, plasma ionized calcium concentration and serum parathyroid hormone concentration were measured before dialysis, mid-dialysis and 30 min after dialysis. 2. Plasma ionized calcium concentration increased towards dialysate calcium concentrations, falling insignificantly after cessation of dialysis. Serum parathyroid hormone concentration fell by 39% during dialysis, with incomplete recovery afterwards. There was no overall change in platelet cytosolic calcium concentration. 3. Patients were divided into two subgroups: low parathyroid hormone (serum parathyroid hormone concentration < 10 pmol/l) and high parathyroid hormone (serum parathyroid hormone concentration > 10 pmol/l). Before dialysis, values of platelet cytosolic calcium concentration or plasma ionized calcium concentration were not statistically different between the subgroups, but the platelet cytosolic calcium concentration was higher in the high-parathyroid hormone subgroup during and after dialysis. 4. Before haemodialysis there was a linear correlation between plasma ionized calcium concentration and platelet cytosolic calcium concentration, which disappeared during dialysis. In contrast, there was no relationship between serum parathyroid hormone concentration and platelet cytosolic calcium concentration before dialysis, but after dialysis a hyperbolic relationship was evident. 5. These results suggest that uraemic toxins may interfere with cytosolic calcium homoeostasis, allowing passive diffusion of extracellular calcium to influence the resting concentration, and that this effect is reversible by haemodialysis.

Effect of phorbol myristate acetate on secretion of parathyroid hormone

1988 ◽  
Vol 254 (1) ◽  
pp. E63-E70 ◽  
Author(s):  
J. J. Morrissey
Keyword(s):  
Protein Kinase C ◽  
Parathyroid Hormone ◽  
Protein Kinase ◽  
Membrane Fraction ◽  
Hormone Secretion ◽  
Myristate Acetate ◽  
Kinase C ◽  
Low Calcium ◽  
Protein Kinase C Activity ◽  
High Calcium

The influence of phorbol myristate acetate (PMA), an activator of protein kinase c, on the secretion of parathyroid hormone from collagenase-dispersed bovine parathyroid cells was tested. The cells were incubated at low (0.5 mM) or high (2.0 mM) concentrations of calcium in the medium, and the hormone secreted into the medium was measured by a radioimmunoassay that recognizes both intact and C-terminal fragments of hormone. At low calcium, the secretory rate averaged 32 +/- 3.8 ng.h-1.(10(5) cells)-1. The addition of 1.6 microM PMA did not affect secretion. At high calcium there was a significant suppression of secretion by 38% to 19.8 +/- 3 ng.h-1.(10(5) cells)-1. The addition of 1.6 microM PMA significantly stimulated hormone secretion to 35.8 +/- 8 ng.h-1.(10(5) cells)-1, a rate indistinguishable from low calcium. This stimulatory effect of PMA at high calcium was seen at PMA concentrations as low as 1.6 nM, did not occur with a biologically inactive 4 alpha-isomer of phorbol ester, and was independent of changes in cellular adenosine 3',5'-cyclic monophosphate levels. Examination of 32P-labeled phosphoproteins by two-dimensional gel electrophoresis revealed acidic proteins of approximately 20,000 and 100,000 Da that were phosphorylated at low and high calcium + 1.6 microM PMA but not at high calcium alone. The protein kinase c activity associated with the membrane fraction of parathyroid cells significantly decreased 40% when the cells were incubated at high vs. low calcium. The data suggest that calcium may regulate parathyroid hormone secretion through changes in protein kinase c activity of the membrane fraction of the cell and protein phosphorylation.

A mathematical model of parathyroid hormone response to acute changes in plasma ionized calcium concentration in humans

2010 ◽  
Vol 226 (1) ◽  
pp. 46-57 ◽  
Author(s):  
Rajiv P. Shrestha ◽  
Christopher V. Hollot ◽  
Stuart R. Chipkin ◽  
Claus P. Schmitt ◽  
Yossi Chait
Keyword(s):  
Mathematical Model ◽  
Parathyroid Hormone ◽  
Calcium Concentration ◽  
Ionized Calcium ◽  
Hormone Response ◽  
Acute Changes

scholarly journals Magnesium modulates parathyroid hormone secretion and upregulates parathyroid receptor expression at moderately low calcium concentration

2013 ◽  
Vol 29 (2) ◽  
pp. 282-289 ◽  
Author(s):  
M. E. Rodriguez-Ortiz ◽  
A. Canalejo ◽  
C. Herencia ◽  
J. M. Martinez-Moreno ◽  
A. Peralta-Ramirez ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Concentration ◽  
Hormone Secretion ◽  
Receptor Expression ◽  
Low Calcium

Vasopressin increases cytosolic free calcium in LLC-PK1 cells through a V1-receptor

1987 ◽  
Vol 253 (2) ◽  
pp. F328-F332 ◽  
Author(s):  
M. A. Burnatowska-Hledin ◽  
W. S. Spielman
Keyword(s):  
Parathyroid Hormone ◽  
Arginine Vasopressin ◽  
Calcium Concentration ◽  
Mdck Cells ◽  
Free Calcium ◽  
Base Line ◽  
Cytosolic Free Calcium ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration ◽  
Dose Dependent

We examined the effects of arginine vasopressin (AVP), parathyroid hormone (PTH), and bradykinin (BK) on the cytosolic free calcium concentration ([Ca]i) in cultured LLC-PK1 and MDCK kidney cell lines by use of the fluorescent Ca chelator fura-2. In LLC-PK1 cells, the addition of AVP but not [1-desamino-8-D-arginine]vasopressin (dDAVP, V2 agonist), PTH, or BK (10(-6) M) caused a significant increase in [Ca]i. The AVP-induced increase in [Ca]i from 61 +/- 6 to 225 +/- 44 nM (n = 7, P less than 0.01) was rapid and transient, returning to base line in 2 to 3 min. The effect of AVP was dose dependent and was present at 1 (61% increase) but not 5 min after extracellular Ca was removed. The effect of 10(-6) M AVP could be blocked with the pressor (V1) antagonist, d(CH2)5Tyr(Me)AVP, but not dDAVP. In MDCK cells, BK, but not AVP and PTH, increased [Ca]i from 146 +/- 11 to 281 +/- 31 nM (n = 9, P less than 0.001). The removal of extracellular Ca (5 min), reduced but did not abolish this effect. These results indicate that [Ca]i mobilized by activation of V1-receptors may mediate AVP-regulated function in some transporting epithelia.

Influence of dietary calcium on sodium and calcium intake of spontaneously hypertensive rats

1992 ◽  
Vol 262 (3) ◽  
pp. R370-R381 ◽  
Author(s):  
M. G. Tordoff
Keyword(s):  
Calcium Intake ◽  
Spontaneously Hypertensive Rats ◽  
Salt Intake ◽  
Dietary Calcium ◽  
Hypertensive Rats ◽  
Deficient Diet ◽  
Spontaneously Hypertensive ◽  
High Salt Intake ◽  
High Calcium ◽  
Wistar Kyoto

Spontaneously hypertensive rats (SHRs) fed nutritionally complete diets voluntarily ingest more calcium and more NaCl solution than do their normotensive Wistar-Kyoto (WKY) controls. SHRs also have several anomalies in calcium metabolism. Given that calcium availability modulates NaCl intake of other rat strains, we examined whether sodium and calcium intake of the SHR was unusually responsive to manipulations of dietary calcium. In three experiments, groups of SHRs and WKYs ate diets differing in calcium content (0-1,000 mmol/kg) and drank solutions of sodium (50 and 300 mM NaCl or 50 mM sodium lactate) and/or calcium (50 and 110 mM calcium lactate or 50 mM CaCl2). Relative to WKYs, SHRs fed calcium-deficient diet (0 mmol Ca2+/kg) drank the same amount or less calcium solution, drank more NaCl, and increased NaCl intake more rapidly when the diet was first introduced. SHRs fed diets sufficient for normal growth (50-1,000 mmol Ca2+/kg) drank consistently more calcium and sodium solution than did WKYs. However, NaCl intake of SHRs was decreased by high-calcium diets, whereas NaCl intake of WKYs was not. Taken together, these results suggest that a mechanism dependent on the availability of calcium is at least partially responsible for the high salt intake of the SHR.

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