scholarly journals Characteristic of the vasorlaxant action of the talatisamine alkaloid and its derivatives

2021 ◽  
Vol 4 (2) ◽  
pp. 01-05
Author(s):  
Mirzayeva Yu.T.
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Channel Blocker ◽  
Aortic Ring ◽  
Diterpenoid Alkaloids ◽  
Relaxant Effect ◽  
Ring Contraction ◽  
Voltage Dependent ◽  
Ca2 Channels ◽  
Isolated Rat

The aim of our research is to study the effect relaxant action of diterpenoid alkaloids talatisamine, 14-O-benzoylthalatisamine and 14-O-acetylthalatisamine was studied using isolated rat aortic rings. Alkaloids significantly and dose-dependently inhibited contraction of the aortic rings caused by high KCl content. At the same time, under these conditions, alkaloids significantly reduced Ca2+-induced contraction of the aortic rings. The relaxing effects of alkaloids are significantly suppressed by verapamil, a potent potentiometer-dependent Ca2+ channel blocker. The alkaloids also significantly reduced norepinephrine-induced aortic ring contraction in normal as well as Ca2+ free Krebs solutions. The data obtained indicate that talatisamine, 14-benzoylthalatisamine and 14-O-acetylthalatisamine exhibit a pronounced relaxant effect in almost the same way in the case of contraction induced by a high content of KCl and norepinephrine. The mechanism of the relaxant action of alkaloids is probably complex and may include suppression of Ca2+influx through voltage-dependent and receptor-driven Ca2+ channels, as well as inhibition of Ca2+transport in the sarcoplasmic reticulum.

scholarly journals Characteristic of the vasorlaxant action of the talatisamine alkaloid and its derivatives

2021 ◽  
Vol 4 (2) ◽  
pp. 01-05
Author(s):  
Mirzayeva Yu.T
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Channel Blocker ◽  
Aortic Ring ◽  
Diterpenoid Alkaloids ◽  
Relaxant Effect ◽  
Ring Contraction ◽  
Voltage Dependent ◽  
Ca2 Channels ◽  
Isolated Rat

The aim of our research is to study the effect relaxant action of diterpenoid alkaloids talatisamine, 14-O-benzoylthalatisamine and 14-O-acetylthalatisamine was studied using isolated rat aortic rings. Alkaloids significantly and dose-dependently inhibited contraction of the aortic rings caused by high KCl content. At the same time, under these conditions, alkaloids significantly reduced Ca2+-induced contraction of the aortic rings. The relaxing effects of alkaloids are significantly suppressed by verapamil, a potent potentiometer-dependent Ca2+ channel blocker. The alkaloids also significantly reduced norepinephrine-induced aortic ring contraction in normal as well as Ca2+ free Krebs solutions. The data obtained indicate that talatisamine, 14-benzoylthalatisamine and 14-O-acetylthalatisamine exhibit a pronounced relaxant effect in almost the same way in the case of contraction induced by a high content of KCl and norepinephrine. The mechanism of the relaxant action of alkaloids is probably complex and may include suppression of Ca2+influx through voltage-dependent and receptor-driven Ca2+ channels, as well as inhibition of Ca2+transport in the sarcoplasmic reticulum.

Na+-Ca2+ exchange contributes to increase of cytosolic Ca2+ concentration during depolarization in heart muscle

1986 ◽  
Vol 250 (4) ◽  
pp. C651-C656 ◽  
Author(s):  
S. S. Sheu ◽  
V. K. Sharma ◽  
A. Uglesity
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Channel Blocker ◽  
Ventricular Myocytes ◽  
Transport Systems ◽  
High K ◽  
K Concentration ◽  
Cardiac Excitation ◽  
Ca2 Channels ◽  
Isolated Rat

The possible role of Na+-Ca2+ exchange in contributing to depolarization-induced increase in cytosolic Ca2+ concentration ([Ca2+]i) of isolated rat ventricular myocytes was investigated. Measured with the Ca2+-sensitive indicator quin 2, [Ca2+]i increased from 177 +/- 12 (mean +/- SE, n = 11) to 468 +/- 41 nM when cells were depolarized with solutions containing 50 mM KCl [high extracellular K+ concentration ([K+]o)]. Approximately 73% of this high-[K+]o-induced increase in [Ca2+]i was abolished by the Ca2+ channel blocker verapamil (5 microM). For cells pretreated with 10 mM caffeine to deplete the Ca2+ stored in sarcoplasmic reticulum, 50 mM KCl still produced an increase in [Ca2+]i, even in the presence of 5 microM verapamil. However, if extracellular Na+ was replaced by Li+ or tris(hydroxymethyl)aminomethane, this increase was completely abolished. The results suggest that, in addition to voltage-sensitive Ca2+ channels, voltage-sensitive Na+-Ca2+ exchange can also contribute to the increase in [Ca2+]i on depolarization. Therefore both Ca2+ transport systems may play important roles in regulating cardiac excitation and contraction.

Different contributions of L- and Q-type Ca2+ channels to Ca2+ signals and secretion in chromaffin cell subtypes

1997 ◽  
Vol 272 (2) ◽  
pp. C476-C484 ◽  
Author(s):  
R. B. Lomax ◽  
P. Michelena ◽  
L. Nunez ◽  
J. Garcia-Sancho ◽  
A. G. Garcia ◽  
...  
Keyword(s):  
Chromaffin Cells ◽  
Chromaffin Cell ◽  
Channel Blocker ◽  
Cell Types ◽  
Bay K 8644 ◽  
High K ◽  
Voltage Dependent ◽  
Bovine Chromaffin Cells ◽  
P Type ◽  
Ca2 Channels

In this study, we investigated the contribution of different subtypes of voltage-dependent Ca2+ channels to changes in cytosolic free Ca2+ ([Ca2+]i) and secretion in noradrenergic and adrenergic bovine chromaffin cells. In single immunocytochemically identified chromaffin cells, [Ca2+]i increased transiently during high K+ depolarization. Furnidipine and BAY K 8644, L-type Ca2+ channel blocker and activator, respectively, affected the [Ca2+]i rise more in noradrenergic than in adrenergic cells. In contrast, the Q-type Ca2+ channel blocker omega-conotoxin MVIIC inhibited the [Ca2+]i rise more in adrenergic cells. omega-Agatoxin IVA (30 nM), which blocks P-type Ca2+ channels, had little effect on the [Ca2+]i signal. The N-type Ca2+ channel blocker omega-conotoxin GVIA similarly inhibited the [Ca2+]i rise in both cell types. The effects of furnidipine, BAY K 8644, and omega-conotoxin MVIIC on K+-evoked norepinephrine and epinephrine release paralleled those effects on [Ca2+]i signals. However, omega-conotoxin GVIA and 30 nM omega-agatoxin IVA did not affect the secretion of either amine. The data suggest that, in the bovine adrenal medulla, the release of epinephrine and norepinephrine are preferentially controlled by Q- and L-type Ca2+ channels, respectively. P- and N-type Ca2+ channels do not seem to control the secretion of either catecholamine.

Interaction Between L-Type Ca2+ Channels and Sarcoplasmic Reticulum in the Regulation of Vascular Tone in Isolated Rat Small Arteries

2000 ◽  
Vol 36 (5) ◽  
pp. 548-554 ◽  
Author(s):  
Masaharu Takeuchi ◽  
Jun Watanabe ◽  
Satoru Horiguchi ◽  
Akihiko Karibe ◽  
Hiroshi Katoh ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Vascular Tone ◽  
Small Arteries ◽  
Regulation Of Vascular Tone ◽  
Ca2 Channels ◽  
Isolated Rat

scholarly journals Effects Of F-18 On KCL And Phenylephrine - Induced Contractions Of Rat Aorta

2021 ◽  
Vol 03 (06) ◽  
pp. 100-108
Author(s):  
Abdisalim Zaripov ◽  
◽  
Adilbay Esimbetov ◽  
Pulat Usmanov ◽  
Durdona Shokirova ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Mechanism Of Action ◽  
Isometric Contraction ◽  
Functional Activity ◽  
Rat Aorta ◽  
Relaxant Effect ◽  
Voltage Dependent ◽  
Ca2 Channels

The mechanism of action of the alkaloid 1-(2´-bromine-4´,5´-dimethoxyphenyl) - 6,7-dimethoxy-1,2,3,4-tetrahydroisoquinoline (F-18) on the functional activity of smooth muscle cells of the rat aorta was studied. Isometric contraction activity was recorded using a Grass FT – 03 (Grass Instrument, USA) mechanotron. The relaxant effect of the F-18 alkaloid was found to be associated with blockade of Ca2 + (IP3R) channels in the SR, along with voltage- dependent and receptor-operated Ca2+channels in the aorta smooth muscle cell plasmalemma.

Mechanism of hyperosmolality stimulation of ANP secretion: its dependency on calcium and sodium

1995 ◽  
Vol 268 (3) ◽  
pp. E476-E483 ◽  
Author(s):  
R. J. Schiebinger ◽  
C. M. Joseph ◽  
Y. Li ◽  
E. J. Cragoe
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Channel Blocker ◽  
Calcium Influx ◽  
Voltage Dependent Calcium Channel ◽  
Sodium Dependent ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Sodium Dependency ◽  
Sarcoplasmic Reticulum Calcium ◽  
Stimulation Of

The calcium dependency of hyperosmolality stimulation of atrial natriuretic peptide (ANP) secretion was determined using isolated superfused nonbeating rat left atrium. Increasing osmolality by 65, 85, and 100 mosmol/kgH2O by superfusion with sucrose produced a peak rise in ANP secretion of 1.8-, 2.0-, and 2.7-fold. To determine whether calcium influx played a role in osmolality (osm)-stimulated ANP secretion, atria were superfused with 2 mM lanthanum, a calcium antagonist. Lanthanum inhibited by 85% the response to a 100 mosmol/kgH2O increase in osm. The voltage-dependent calcium channel blocker isradipine had no effect on osm-stimulated ANP secretion, suggesting that calcium influx via voltage-dependent calcium channels was not playing a significant role. Likewise, depleting sarcoplasmic reticulum calcium with 1 microM ryanodine did not block the response to osm, suggesting that calcium influx was not adequate to induce consequential release of calcium from the sarcoplasmic reticulum. To determine whether calcium influx was via Na(+)-Ca2+ exchange, we determined the sodium dependency of osm-stimulated ANP secretion. Replacement of sodium with lithium or choline blocked the secretory response to 100 mosmol/kgH2O. We conclude that osm-stimulated ANP secretion is calcium and sodium dependent. Calcium influx via Na(+)-Ca2+ exchange is highly implicated as the mechanism of cellular calcium entry.

scholarly journals Extracellular ATP-induced acidification leads to cytosolic calcium transient rise in single rat cardiac myocytes

1991 ◽  
Vol 274 (1) ◽  
pp. 55-62 ◽  
Author(s):  
M Pucéat ◽  
O Clément ◽  
F Scamps ◽  
G Vassort
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Myocytes ◽  
Membrane Conductance ◽  
Calcium Transient ◽  
Cytosolic Calcium ◽  
Extracellular Atp ◽  
Experimental Conditions ◽  
Extracellular Medium ◽  
Voltage Dependent ◽  
Ca2 Channels

The origin of the increase in cytosolic free Ca2+ concentration ([Ca2+]i) induced by extracellular ATP was investigated in single isolated cardiac myocytes loaded with indo-1. The nucleotide added at a concentration of 10 microM triggers a few Ca2+ spikes, followed by a cluster of Ca2+ oscillations, increasing [Ca2+]i to around 200 nM from a basal value of 70 nM. Neither caffeine nor ryanodine affects the magnitude of the Ca2+ transient, but both shorten it by preventing the Ca2+ oscillations. This indicates that the latter must be related to the release of Ca2+ from the sarcoplasmic reticulum. Since ATP also induces cell depolarization (as shown by experiments using the potential sensitive dye bis-oxonol), the initial Ca2+ spikes were attributed to the opening of voltage-dependent Ca2+ channels. A small Ca2+ transient still remains under experimental conditions designed to prevent Ca2+ influx from external medium (low-Ca2+ high-Mg2+ medium containing La3+) and after depletion of the sarcoplasmic-reticulum Ca2+ load with caffeine. Under these conditions, when this Ca2+ transient was buffered by 1,2-bis-(O-aminophenoxy)ethane-NNN′N′-tetra-acetic acid, ATP was unable to trigger the initial Ca2+ spikes. These results indicate that ATP mobilizes Ca2+ ions from an intracellular pool other than the sarcoplasmic reticulum and that this Ca2+ release is responsible for the depolarization. The effects of ATP on [Ca2+]i share the same characteristics as the acidification simultaneously induced by the nucleotide (as shown by experiments using the pH-sensitive probe snarf-1). These ionic variations are highly specific to ATP and its hydrolysis-resistant analogues. They both require the presence of Mg2+ and Cl- ions in the extracellular medium, and they are prevented by pretreatment of the cells with 4,4′-di-isothiocyanostilbene or probenecid. These results suggest that: (1) the ATP-induced acidification leads to displacement of Ca2+ ions from or close to the internal face of sarcolemma; (2) the Ca2+ ions activate a non-specific membrane conductance responsible for the depolarization of the cells; (3) the depolarization leads to a Ca2+ influx, owing to the opening of the voltage-dependent Ca2+ channels; (4) this increase in Ca2+ triggers the release of Ca2+ from the sarcoplasmic reticulum, which is facilitated by the increase in inositol trisphosphate following P2-purinergic stimulation.

scholarly journals Agonist-induced phasic and tonic responses in smooth muscle are mediated by InsP3

2002 ◽  
Vol 115 (10) ◽  
pp. 2207-2218 ◽  
Author(s):  
John G. McCarron ◽  
John W. Craig ◽  
Karen N. Bradley ◽  
Thomas C. Muir
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Channel Blocker ◽  
Single Cells ◽  
Smooth Muscle Contraction ◽  
Receptor Activation ◽  
Tonic Component ◽  
Voltage Dependent ◽  
Ca2 Channels ◽  
Insp3 Receptor

Many cellular functions are regulated by agonist-induced InsP3-evoked Ca2+ release from the internal store. In non-excitable cells, predominantly, the initial Ca2+release from the store by InsP3 is followed by a more sustained elevation in [Ca2+]i via store-operated Ca2+ channels as a consequence of depletion of the store. Here, in smooth muscle, we report that the initial transient increase in Ca2+, from the internal store, is followed by a sustained response also as a consequence of depletion of the store (by InsP3), but, influx occurs via voltage-dependent Ca2+ channels. Contractions were measured in pieces of whole distal colon and membrane currents and [Ca2+]i in single colonic myocytes. Carbachol evoked phasic and tonic contractions; only the latter were abolished in Ca2+-free solution. The tonic component was blocked by the voltage-dependent Ca2+ channel blocker nimodipine but not by the store-operated channel blocker SKF 96365. InsP3 receptor inhibition, with 2-APB, attenuated both the phasic and tonic components. InsP3 may regulate tonic contractions via sarcolemma Ca2+ entry. In single cells,depolarisation (to ∼-20 mV) elevated [Ca2+]i and activated spontaneous transient outward currents (STOCs). CCh suppressed STOCs, as did caffeine and InsP3. InsP3 receptor blockade by 2-APB or heparin prevented CCh suppression of STOCs; protein kinase inhibition by H-7 or PKC19-36did not. InsP3 suppressed STOCs by depleting a Ca2+ store accessed separately by the ryanodine receptor (RyR). Thus depletion of the store by RyR activators abolished the InsP3-evoked Ca2+ transient. RyR inhibition (by tetracaine) reduced only STOCs but not the InsP3transient. InsP3 contributes to both phasic and tonic contractions. In the former, muscarinic receptor-evoked InsP3 releases Ca2+ from an internal store accessed by both InsP3 and RyR. Depletion of this store by InsP3 alone suppresses STOCs, depolarises the sarcolemma and permits entry of Ca2+ to generate the tonic component. Therefore, by lowering the internal store Ca2+ content,InsP3 may generate a sustained smooth muscle contraction. These results provide a mechanism to account for phasic and tonic smooth muscle contraction following receptor activation.

Mechanisms of hemolysate-induced [Ca2+]i elevation in cerebral smooth muscle cells

1995 ◽  
Vol 269 (6) ◽  
pp. H1874-H1890 ◽  
Author(s):  
H. Zhang ◽  
B. Weir ◽  
L. S. Marton ◽  
R. L. Macdonald ◽  
V. Bindokas ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Channel Blocker ◽  
Cyclopiazonic Acid ◽  
Muscle Cells ◽  
Excitation Wavelength ◽  
Free Solution ◽  
Voltage Dependent ◽  
Cytochrome P 450 ◽  
Isolated Rat

The effects of hemolysate on free cytosolic [Ca2+] ([Ca2+]i) homeostasis were studied in freshly isolated rat basilar artery smooth muscle cells using fura 2 and dual excitation wavelength microfluorimetry. Hemolysate reversibly produced a transient [Ca2+]i peak followed by a slowly decaying plateau which was absent in Ca(2+)-free solution. This effect of hemolysate was attenuated by 1) the sarcoplasmic reticulum Ca2+ pump inhibitors thapsigargin and cyclopiazonic acid, 2) the Ca2+ release-blocking agents ryanodine and dantrolene, 3) the cytochrome P-450 inhibitor econazole, and 4) the inorganic Ca2+ channel blocker lanthanum but was not significantly attenuated by 1) the receptor-regulated Ca2+ channel blocker SKF-96365 or 2) the voltage-dependent Ca2+ channel blocker nimodipine. Fractionation of hemolysate using membranes with specific pore sizes (0.5, 1, and 12-14 kDa) indicated that a component(s) > 0.5 but < 1 kDa could produce a similar [Ca2+]i peak and plateau while fractions > 1 and > 12-14 kDa produced a small and slow [Ca2+]i rise without a significant peak. ATP, which was found in hemolysate, produced a [Ca2+]i response similar to that of hemolysate. P2-purinoceptor antagonists significantly attenuated the effect of ATP, hemolysate, and the fractions < 1 and < 12-14 kDa. We conclude that hemolysate elevates [Ca2+]i by both releasing Ca2+ from internal stores and triggering Ca2+ entry, possibly from a voltage-independent Ca2+ influx pathway, an effect apparently identical to that of ATP.

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