Paradoxical nifedipine facilitation of 45Ca uptake into rat hippocampal synaptosomes

2006 ◽  
Vol 544 (1-3) ◽  
pp. 39-48 ◽  
Author(s):  
Joana Costa ◽  
M. Graça Lobo ◽  
Paulo Correia-de-Sá
Keyword(s):  
45Ca Uptake

scholarly journals Neuronal calcium channel inhibitors. Synthesis of omega-conotoxin GVIA and effects on 45Ca uptake by synaptosomes.

1987 ◽  
Vol 262 (3) ◽  
pp. 1194-1198
Author(s):  
J Rivier ◽  
R Galyean ◽  
W R Gray ◽  
A Azimi-Zonooz ◽  
J M McIntosh ◽  
...  
Keyword(s):  
Calcium Channel ◽  
45Ca Uptake ◽  
Calcium Channel Inhibitors ◽  
Neuronal Calcium Channel

Different effects of R 56865 and calcium entry blockers on K+- and noradrenaline-induced contractions and 45Ca uptake in rat aorta

1988 ◽  
Vol 158 (3) ◽  
pp. 183-190 ◽  
Author(s):  
Peter Koch ◽  
Doris Wilhelm ◽  
Detlef Wermelskirchen ◽  
Ute Nebel ◽  
Bob Wilffert ◽  
...  
Keyword(s):  
Rat Aorta ◽  
Calcium Entry ◽  
Calcium Entry Blockers ◽  
45Ca Uptake ◽  
R 56865

Effects of morphine and (D-Ala, Met)-enkephalinamide on 45Ca-uptake to rat brain striatal slices

Neuropeptides ◽  
1984 ◽  
Vol 5 (1-3) ◽  
pp. 57-60
Author(s):  
K. Saito ◽  
N. Fujita ◽  
M. Nakahiro ◽  
R. Inoki
Keyword(s):  
Rat Brain ◽  
Striatal Slices ◽  
45Ca Uptake

scholarly journals The stimulus–secretion coupling 4-methyl-2-oxopentanoate-induced insulin release

1979 ◽  
Vol 184 (2) ◽  
pp. 303-311 ◽  
Author(s):  
J C Hutton ◽  
A Sener ◽  
W J Malaisse
Keyword(s):  
Insulin Release ◽  
Metabolic Flux ◽  
Energy Charge ◽  
Hyperbolic Function ◽  
Maximal Response ◽  
Coupling Mechanism ◽  
Adenylate Energy Charge ◽  
Atp Content ◽  
45Ca Uptake ◽  
Stimulus Secretion Coupling

1. Pancreatic islet insulin secretion and 45Ca uptake showed similar responses to variation in the extracellular concentration of 4-methyl-2-oxopentanoate with a threshold at 4 mM and a maximal response at a 25 mM concentration. 2. Islet respiration, acetoacetate production and rates of substrate utilization, oxidation and amination all changed as a simple hyperbolic function of 4-methyl-2-oxopentanoate concentration and exhibited a maximal response at 25 mM. 3. The responses of ATP content, [ATP]/[ADP] ratio, adenylate energy charge and [NADH]/[NAD+] ratio were also hyperbolic in nature but were maximally elevated at lower concentrations of the secretagogue. The islet [NADPH]/[NADP+] ratio, however, was tightly correlated with parameters of metabolic flux, 45Ca uptake and insulin release. 4. NH4+ and menadione, agents that promote a more oxidized state in islet NADP, did not affect islet ATP content or the rates of [U-14C]4-methyl-2-oxopentanoate oxidation or amination, but markedly inhibited islet 45Ca uptake and insulin release. 5. It is proposed that changes in the redox state of NADP and Ca transport may serve as mediators in the stimulus-secretion coupling mechanism of insulin release induced by 4-methyl-2-oxopentanoate.

Evidence for calcium inactivation during hormone release in the rat neurohypophysis

1976 ◽  
Vol 65 (3) ◽  
pp. 669-683
Author(s):  
J. J. Nordmann
Keyword(s):  
Hormone Secretion ◽  
Calcium Ionophore ◽  
High Rate ◽  
Hormone Release ◽  
45Ca Uptake ◽  
High K ◽  
K Concentration ◽  
The Relationship ◽  
Internal Calcium

1. A study has been made of the relationship between 45Ca uptake into and hormone release from isolated rat neurohypophyses incubated in vitro. 2. Hormone secretion is triggered by high-K (56 mM) but long exposure to the stimulus does not generate a maintained release of hormone. 3. When hormone release began to wane, addition of Ba of La increased hormone output which suggests that the decline in output did not result from depletion of the neurosecretory granules at the nerve terminals. 4. 45Ca uptake is enhanced in the presence of high-K concentration, but the initial high rate declines during long exposure to the potassium stimulus with a time constant similar to that of the decline in hormone release. 5. After a period of incubation in a K-rich, calcium-free medium, addition of calcium to the medium induced hormone release. The magnitude of this release was dependent on the time of exposure to excess potassium. 6. After inactivation of secretion, mobilization of internal calcium by means of a calcium ionophore increased hormone release.

Ca2+ transport pathways in brush-border membrane vesicles of crustacean antennal glands

1993 ◽  
Vol 264 (6) ◽  
pp. R1206-R1213 ◽  
Author(s):  
G. A. Ahearn ◽  
P. Franco
Keyword(s):  
Membrane Potential ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Brush Border Membrane Vesicles ◽  
Carrier System ◽  
Transport Pathways ◽  
45Ca Uptake ◽  
Negative Membrane Potential ◽  
Antennal Glands

Calcium uptake by brush-border membrane vesicles of Atlantic lobster (Homarus americanus) kidneys (antennal glands) in independent experiments was stimulated by outwardly directed Na or H gradients. In the absence of external amiloride, 45Ca uptake was strongly stimulated by an outwardly directed Na gradient, and this stimulation was enhanced by the addition of an inside-negative membrane potential. External amiloride (2 mM) reduced 45Ca uptake sixfold and lowered sensitivity to membrane potential. 45Ca influx kinetics (2.5-s uptake) in the presence of an outwardly directed H gradient and inside-negative membrane potential were composed of three components: 1) an amiloride-sensitive carrier system, 2) an amiloride-insensitive carrier system, and 3) a verapamil- and membrane potential-sensitive process that may represent diffusional transfer through a calcium channel. It was concluded that 45Ca entry by the amiloride-sensitive process occurred by a previously described electrogenic 2 Na-1 H antiport mechanism [Ahearn, G., and L. Clay. Am. J. Physiol. 257 (Regulatory Integrative Comp. Physiol. 26): R484-R493, 1989; Am. J. Physiol. 259 (Renal Fluid Electrolyte Physiol. 28): F758-F767, 1990; Ahearn, G., P. Franco, and L. Clay. J. Membr. Biol. 116: 215-226, 1990]. 45Ca influx by the amiloride-insensitive mechanism occurred by an apparent electroneutral 1 Ca-2 Na exchange. Transport stoichiometry of the latter mechanism was tentatively established by experiments determining intravesicular Na binding properties and by its apparent lack of response to a membrane potential. At physiological Na, Ca, and H concentrations in the antennal gland lumen and epithelial cytosol, these three calcium transport pathways individually may make significant contributions to net calcium reabsorption to the blood.

Reversal of renal and smooth muscle actions of the thromboxane mimetic U-44069 by diltiazem

1986 ◽  
Vol 250 (4) ◽  
pp. F619-F626 ◽  
Author(s):  
R. Loutzenhiser ◽  
M. Epstein ◽  
C. Horton ◽  
P. Sonke
Keyword(s):  
Smooth Muscle ◽  
Rat Kidney ◽  
Tension Development ◽  
45Ca Uptake ◽  
Aortic Smooth Muscle ◽  
Control Value ◽  
Potent Vasoconstrictor ◽  
Isolated Rat

U-44069 is a stable prostaglandin (PG) H2 analogue and a potent vasoconstrictor. Its in vivo and in vitro actions mimic those of thromboxane A2. We have studied the effects of the calcium antagonist diltiazem upon the vasoconstriction induced by U-44069 using isolated rat aortic smooth muscle and isolated perfused rat kidney (IPRK). The administration of 10(-6)M U-44069 elicited maximally effective contractions in isolated aortic rings and increased 45Ca uptake from a control value of 285 +/- 6 mumol/kg to 344 +/- 8 mumol/kg. Diltiazem reduced U-44069-induced tension development and 45Ca uptake of isolated aortic smooth muscle 73 +/- 2 and 91 +/- 3%, respectively. The dose dependency of each of these effects of diltiazem was similar (EC50 = 369 nM and 334 nM for tension and 45Ca flux, respectively). When administered to the IPRK, 10(-6) M U-44069 caused a 82 +/- 3% decrease in glomerular filtration rate (GFR) and a 80 +/- 4% decrease in filtration fraction but reduced renal perfusate flow (RPF) only 13 +/- 8% (P less than 0.005). Diltiazem completely reversed the actions of U-44069 on the IPRK (EC50 = 288 nM and 323 nM for GFR and RPF, respectively). Diltiazem thus inhibited U-44069-induced tension development and 45Ca uptake by vascular smooth muscle and increased GFR within identical dose ranges. The contractile response of isolated rat glomeruli was also assessed. U-44069 reduced the volume of isolated glomeruli, but this action was neither prevented nor reversed by diltiazem. These results are consistent with the hypothesis that diltiazem increased GFR by inhibiting U-44069-induced Ca influx at preglomerular vessels.

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