Effect of lanthanum and reduced temperature on 45Ca efflux from rabbit aorta

1978 ◽  
Vol 234 (5) ◽  
pp. C139-C145 ◽  
Author(s):  
R. C. Deth
Keyword(s):  
Smooth Muscle ◽  
Time Course ◽  
Rabbit Aorta ◽  
Transport Processes ◽  
Calcium Efflux ◽  
45Ca Uptake ◽  
High K ◽  
45Ca Efflux ◽  
Reduced Temperature ◽  
Stimulation Of

The ability of lanthanum (La3+) to block calcium efflux from smooth muscle cells of the rabbit aorta has been examined. La3+ promotes the very early phase of 45Ca efflux, which is extracellular in origin, and partially inhibits the latter, cellular portion. Stimulation of 45Ca efflux caused by the release of intracellular 45Ca with either 10(-4) M dinitrophenol or 10 mM caffeine was not reduced by pretreatment with 10 mM La for 40 min, whereas stimulation due to norepinephrine was abolished. It was concluded that during the use of the "La method" for measuring cellular 45Ca there is an underestimation due to unblocked 45Ca loss. This loss can be reduced by processing tissue at 2 degrees C, which inhibits transport processes. The time course of 45Ca uptake and the stimulation of uptake by high K+ are qualitatively but not quantitatively similar if tissues are washed at 37 and 2 degrees C. Tissues washed in La3+ at 2 degrees C for 60 min retain approximately double the cellular 45Ca of those washed at 37 degrees C. This methodology provides an improved correlation between estimates of cellular calcium derived from 45Ca uptake and 45Ca efflux experiments.

Mobilization of a common source of smooth muscle Ca2+ by norepinephrine and methylxanthines

1981 ◽  
Vol 240 (5) ◽  
pp. C239-C247 ◽  
Author(s):  
R. C. Deth ◽  
C. J. Lynch
Keyword(s):  
Rabbit Aorta ◽  
Common Source ◽  
Previous Exposure ◽  
Efflux Rate ◽  
Threefold Increase ◽  
High K ◽  
Cellular Source ◽  
45Ca Efflux ◽  
Camp Levels ◽  
Stimulation Of

The ability of norepinephrine (NE), caffeine (CAF), theophylline (THEO), dinitrophenol (DNP), and potassium (high K) to mobilize cellular Ca2+ in rabbit aorta was examined using 45Ca-efflux techniques. After 10 min of Ca2+ deprivation using either Ca-free EGTA or Ca-free lanthanum (La3+) buffers, NE, CAF, and DNP still caused an increase in 45Ca-efflux rate, indicating a cellular source of 45Ca, while high K did not. Contractile behavior after Ca removal paralleled 45Ca-efflux events. CAF (10 mM) inhibited NE contractile responses, and this inhibition was associated with the depletion of the NE-releasable Ca2+ store. Previous exposure to CAF during 45Ca efflux reduced subsequent stimulation of 45Ca efflux was not additive. THEO caused a stimulation of 45Ca efflux similar to CAF. CAF, THEO, and 3-isobutyl-l-methylxanthine caused a two- to threefold increase in cAMP levels in association with their stimulation of 45Ca efflux. These results suggest that NE and methylxanthines mobilize a common cellular Ca2+ source that is associated with contraction in the case of NE but relaxation in the case of methylxanthines.

Mechanism of activation of isolated rabbit aorta by PGH2 analogue U-44069

1981 ◽  
Vol 241 (5) ◽  
pp. C243-C249 ◽  
Author(s):  
R. Loutzenhiser ◽  
C. van Breemen
Keyword(s):  
Smooth Muscle ◽  
Contractile Response ◽  
Rabbit Aorta ◽  
Calcium Content ◽  
Prior Exposure ◽  
Maximal Tension ◽  
Isolated Rabbit Aorta ◽  
Free Media ◽  
45Ca Efflux ◽  
Stimulation Of

The effects of a stable analogue of PGH2 on 45Ca fluxes and tension were studied in the isolated rabbit aorta. U-44069 produced maximal tension responses at a concentration of 10(-7) M. The analogue increased smooth muscle Ca2+ content and increased the unidirectional 45Ca influx. U-44069 also induced contractions of reduced magnitude in the absence of external Ca2+ and caused a transient stimulation of 45Ca efflux, suggesting that the analogue releases intracellularly bound Ca2+. Both the contractile response in CA2+-free media and the stimulation of 45Ca efflux were greatly attenuated by prior exposure to norepinephrine. The analogue-induced contractions in Ca2+-free media were also prevented by prior exposure to histamine but not angiotensin II. D-600 completely blocked the U-44069-induced gain in calcium content (IC50 = 10(-6) M) but inhibited the contractile response by only 40%. It was concluded that the PGH2 analogue activates rabbit aorta by activating a CA2+ influx pathway and releasing a fraction of the intracellular Ca2+ pool that is sensitive to norepinephrine and other agonists.

scholarly journals Properties of chloride-stimulated 45Ca flux in skinned muscle fibers.

1978 ◽  
Vol 71 (4) ◽  
pp. 411-430 ◽  
Author(s):  
E W Stephenson
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Time Course ◽  
Isometric Force ◽  
Frog Muscle ◽  
Published Data ◽  
Skinned Muscle ◽  
Skinned Muscle Fibers ◽  
45Ca Efflux ◽  
45Ca Release ◽  
Stimulation Of

Isometric force and 45Ca loss from fiber to bath were measured simultaneously in skinned fibers from frog muscle at 19 degrees C. In unstimulated fibers, 45Ca efflux from the sarcoplasmic reticulum (SR) was very slow, with little or no dependence on EGTA (0.1-5 mM) or Mg++ (20 micrometer-1.3 mM). Stimulation by high [Cl] at 0.11 mM Mg++ caused rapid force transients (duration approximately 10 s) and 45Ca release. This response was followed for 55 s, with 5 mM EGTA added to chelate myofilament space (MFS) Ca either (a) after relaxation, (b) near the peak of the force spike, or (c) before or with the stimulus. When EGTA was present during Cl application, stimulation of 45Ca release was undetectable. Analysis of the time-course of tracer loss during the three protocols showed that when EGTA was absent, 16% of the fiber tracer was released from the SR within approximately 3 s, and 70% of the tracer still in the MFS near the peak of the force spike was subsequently reaccumulated. The results suggest that (a) the Cl response is highly Ca-dependent; (b) stimulation increases 45Ca efflux from the SR at least 100-200-fold; and (c) the rate of reaccumulation is much slower than the influx predicted from published data on resting fibers, raising the possibility that depolarization inhibits active Ca transport by the SR.

Microtubule disruption stimulates system A transport in cultured vascular smooth muscle cells

1995 ◽  
Vol 268 (6) ◽  
pp. C1512-C1519 ◽  
Author(s):  
J. G. Chen ◽  
A. B. Strawbridge ◽  
S. A. Kempson
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Time Course ◽  
Serum Starvation ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
System A ◽  
Microtubule Disruption ◽  
Stimulation Of

This study has focused on the possible influence of microtubules for the regulation of Na(+)-dependent system A neutral amino acid transport in A10 cells, a cultured cell line derived from rat aortic vascular smooth muscle. When microtubules were disrupted by incubating cells for 5 h in serum-free medium containing colchicine, nocodazole, or vinblastine, there was a twofold increase in system A transport (Vmax change). The dose for the disruption of microtubules by colchicine was similar to the dose required for the stimulation of system A. The time course showed that system A stimulation did not occur until widespread disruption of microtubules was established. The stimulation was specific for system A; there were no changes in glucose transport and Na(+)-dependent transport of phosphate and glutamate. Serum refeeding of quiescent cells from 2 days of serum starvation led to stimulation of system A, glucose, and phosphate transport. However, only system A was activated when colchicine was added to the serum-free medium. Addition of colchicine during serum refeeding had no additive effect for the stimulation of system A. The stimulation by both colchicine and serum was blocked by cycloheximide and actinomycin D. These findings suggest that microtubule disruption may activate system A gene expression.

Myoplasmic Ca2+-force relationship studied with fura-2 during stimulation of rat aortic smooth muscle

1988 ◽  
Vol 254 (5) ◽  
pp. H840-H854 ◽  
Author(s):  
G. Bruschi ◽  
M. E. Bruschi ◽  
G. Regolisti ◽  
A. Borghetti
Keyword(s):  
Smooth Muscle ◽  
Adherent Cell ◽  
Aortic Smooth Muscle ◽  
Fura 2 ◽  
Parallel Increase ◽  
High K ◽  
Intracellular Ca ◽  
Cell Layers ◽  
Force Relationship ◽  
Stimulation Of

The intracellular Ca indicator fura-2 was used for simultaneous measurements of intracellular free Ca (Ca2+i) and force in arterial smooth muscle. Rat aortic medial rings were submitted to fluorometry in a geometrical arrangement resembling that of adherent cell layers. A rigid force-transducing system served to immobilize the tissue and record the developed force quasi-isometrically. Stimulation was performed with norepinephrine (NE), KCl depolarization (high K), and a nonfluorescent Ca ionophore (ionomycin) at varying extracellular Ca concentrations. The following facts were observed. NE, high K, and ionomycin increased tension along with fura-2-reported Ca2+i; under any circumstances tension was Ca2+i dependent and could be varied by manipulating Ca2+i. However, NE and high K determined a parallel increase in the effectiveness of Ca2+i in comparison with the simple ionophore, i.e., they increased the force-to-Ca2+i ratio. NE and high K produced half-maximal tension at fura-2 estimated Ca2+i of 0.10 and 0.13 microM, whereas ionomycin required 0.6 microM to achieve the same amount of force. It is inferred that Ca2+i is a determinant of vascular contraction, but some results suggest the existence of factors that sensitize the contractile machinery to Ca.

Studies on Locust Rectum: II. Identification of Specific Ion Transport Processes Regulated by Corpora Cardiaca and Cyclic-AMP

1980 ◽  
Vol 86 (1) ◽  
pp. 225-236
Author(s):  
J. H. SPRING ◽  
J. E. PHILLIPS
Keyword(s):  
Cyclic Amp ◽  
Ion Transport ◽  
Time Course ◽  
Transport Processes ◽  
Electrogenic Transport ◽  
Corpora Cardiaca ◽  
Before And After ◽  
Net Flux ◽  
Unidirectional Fluxes ◽  
Stimulation Of

Please send reprint requests to J. E. Phillips. 1. The unidirectional fluxes of 36Cl− and 22Na+ across short-circuited locust recta bathed in a simple NaCl saline were followed with time. Unidirectional fluxes and net flux of 22Na+ to the haemocoel side all remained constant for at least 4 h and were unaffected by either corpora cardiaca homogenate (CC) or cAMP. 2. Both CC and cAMP stimulated influx and net flux of 36Cl− to the haemocoel side. Over the whole time course of the experiment, i.e. both before and after stimulation, net Cl− flux approximately equalled the shortcircuit current (ISC). 3. Neither CC nor cAMP caused substantial stimulation of ISC or transepithelial electropotential difference (PD) if all Cl− in the bathing saline was replaced by either sulphate or nitrate or acetate. 4. Acetate saline sustains ISC, PD and transepithalial resistance (R) at higher levels than does simple Cl-saline. 5. Experiments with Cl-free, SO4-salines suggest that alternate electrogenic transport processes can be slowly turned on when Cl− is absent, provided a complex saline which contains several organic constituents, or simple acetate saline, is present.

Characterization of the vasorelaxation to methanandamide in rat gastric arteries

2006 ◽  
Vol 84 (11) ◽  
pp. 1121-1132 ◽  
Author(s):  
Joke Breyne ◽  
Johan Van de Voorde ◽  
Bert Vanheel
Keyword(s):  
Smooth Muscle ◽  
Cannabinoid Receptors ◽  
Cannabinoid Receptor ◽  
Relaxant Effect ◽  
High K ◽  
Calcitonin Gene ◽  
Perivascular Nerves ◽  
High Concentrations ◽  
Stimulation Of

In the present study, the relaxant effect of the cannabinoid methanandamide was explored in rat gastric arteries. Since in some vessels cannabinoids have been shown to release calcitonin gene-related peptide (CGRP) from perivascular nerves, the influence of methanandamide was compared with that of exogenous CGRP. Methanandamide and CGRP elicited concentration-dependent, endothelium-independent relaxations. Methanandamide-induced relaxations were unaffected by the CB1 receptor antagonist AM251, the CB2 receptor antagonists AM630 and SR144528, and combined pre-exposure to AM251 and SR144528. Pre-exposure to O-1918, an antagonist of a novel nonCB1/nonCB2 cannabinoid receptor, did not influence the relaxations to methanandamide. Capsaicin or capsazepine treatment slightly inhibited methanandamide-induced relaxations. Preincubation with 30 mmol/L extracellular K+ or 3 mmol/L TEA had no significant effect on the responses elicited by methanandamide, but reduced CGRP-induced relaxations. Relaxation to 10−5 mol/L methanandamide was significantly blunted by Bay K8644 and by preincubation with nifedipine. Furthermore, 10−5 mol/L methanandamide significantly inhibited CaCl2-induced contractions in norepinephrine-stimulated vessels previously depleted of intra- and extracellular Ca2+. Finally, preincubation with 10−5 mol/L methanandamide almost completely abolished high K+-induced contractions. These findings suggest that the vasorelaxant action of methanandamide in rat gastric arteries is not mediated by stimulation of known cannabinoid receptors and only partly related to stimulation of TRPV1 receptors on perivascular nerves. At high concentrations, methanandamide might induce relaxation by reducing calcium entry into the smooth muscle cells.

Synthetic atrial peptide inhibits intracellular calcium release in smooth muscle

1986 ◽  
Vol 250 (1) ◽  
pp. C171-C174 ◽  
Author(s):  
K. D. Meisheri ◽  
C. J. Taylor ◽  
H. Saneii
Keyword(s):  
Smooth Muscle ◽  
Calcium Release ◽  
Rabbit Aorta ◽  
Inhibitory Effect ◽  
Physiological Salt Solution ◽  
Phasic Contraction ◽  
Dependent Inhibition ◽  
Isolated Rabbit Aorta ◽  
Dose Dependent Inhibition ◽  
45Ca Efflux

The effects of a synthetic atrial peptide (atriopeptin II; AP II) on the agonist-induced intracellular Ca2+ release was examined in the isolated rabbit aorta. The agonist-induced phasic contraction in a Ca2+-free physiological salt solution containing 2 mM ethyleneglycol-bis(beta-aminoethyl-ether)-N,N'-tetraacetic acid (EGTA-PSS) was used as an indicator of the intracellular Ca2+ release. The addition of AP II (10(-9)-10(-7) M) for 15 min to the tissue during the EGTA-PSS exposure caused a dose-dependent inhibition of norepinephrine (NE; 10(-6) M)-induced phasic contraction. The half-maximal inhibiting concentration of AP II was 3 X 10(-9) M, with 10(-7) M AP II causing 91% inhibition. This was confirmed by studying the inhibitory effect of AP II (10(-7) M) on NE-stimulated 45Ca efflux. Furthermore, the internal Ca2+ release by histamine (10(-5) M) and caffeine (25 mM), both of which share this internal Ca2+ pool with NE, was also inhibited by AP II. Thus AP II appears to be a potent inhibitor of the intracellular Ca2+ release that is utilized by various agonists for the activation of vascular smooth muscle. This may be an important mechanism by which AP II produces relaxation of blood vessels.

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