Differentiation of mechanisms for mobilization of calcium in smooth muscle

1987 ◽  
Vol 65 (4) ◽  
pp. 724-728 ◽  
Author(s):  
George B. Weiss ◽  
Hideaki Karaki ◽  
Kazuyasu Murakami
Keyword(s):  
Smooth Muscle ◽  
Rate Coefficient ◽  
Smooth Muscles ◽  
Rabbit Aorta ◽  
Vascular Smooth Muscles ◽  
Aortic Smooth Muscle ◽  
Renal Vessels ◽  
Experimental Approaches ◽  
Cellular Ca ◽  
Muscle Specificity

Techniques to dissociate different sites or stores important for Ca2+ entry or release in smooth muscle include washouts of 45Ca in cold La3+-substituted solutions, Scatchard-coordinate plots of Ca2+ uptake, substitution of Sr2+ for Ca2+, and both desaturation and rate coefficient plots. Rabbit aortic smooth muscle is particularly useful because Ca2+ mobilization components can be clearly separated. Other vascular preparations investigated (e.g., renal vessels, coronary arteries) appear to have similar components, but their relative importance varies. Respiratory smooth muscle also has similar Ca2+ mobilization components, but they are less readily dissociated by techniques employed in vascular smooth muscles. In guinea pig trachea, cold La3+ washouts do not retain cellular Ca2+ as well as in other preparations; use of other experimental approaches including the Ca2+ channel entry stimulator, CGP 28392, can demonstrate different Ca2+ uptake mechanisms for K+-stimulated and agonist-induced Ca2+ uptake. In rabbit aorta, CGP 28392 potentiates tension increases elicited with lower concentrations of added K+ but has no effect on norepinephrine-induced contraction. A general model illustrating different Ca2+ entry mechanisms present in three types of smooth muscle provides examples drawn from a spectrum of possible variations in smooth muscle specificity for Ca2+ mobilization.

Plasticity of KIR channels in human smooth muscle cells from internal thoracic artery

2003 ◽  
Vol 284 (6) ◽  
pp. H2325-H2334 ◽  
Author(s):  
Tom Karkanis ◽  
Shaohua Li ◽  
J. Geoffrey Pickering ◽  
Stephen M. Sims
Keyword(s):  
Smooth Muscle ◽  
Current Density ◽  
Internal Thoracic Artery ◽  
Smooth Muscles ◽  
Vascular Smooth Muscles ◽  
Rt Pcr ◽  
Regulation Of Proliferation ◽  
Negative Membrane Potential ◽  
Inwardly Rectifying ◽  
Contractile Cells

Inwardly rectifying K+ (KIR) currents are present in some, but not all, vascular smooth muscles. We used patch-clamp methods to examine plasticity of this current by comparing contractile and proliferative phenotypes of a clonal human vascular smooth muscle cell line. Hyperpolarization of cells under voltage clamp elicited a large inward current that was selective for K+ and blocked by Ba2+. Current density was greater in proliferative compared with contractile cells (−4.5 ± 0.9 and −1.4 ± 0.3 pA/pF, respectively; P < 0.001). RT-PCR of mRNA from proliferative cells identified transcripts for Kir2.1 and Kir2.2 but not Kir2.3 potassium channels. Western blot analysis demonstrated greater expression of Kir2.1 protein in proliferative cells, consistent with the higher current density. Proliferative cells displayed a more negative membrane potential than contractile cells (−71 ± 2 and −35 ± 4 mV, respectively; P < 0.001). Ba2+ depolarized all cells, whereas small increases in extracellular K+ concentration elicited hyperpolarization only in contractile cells. Ba2+ inhibited [3H]thymidine incorporation, indicating a possible role for KIR channels in the regulation of proliferation. The phenotype-dependent plasticity of KIR channels may have relevance to vascular remodeling.

Changes in vascular responsiveness following chronic exposure to cold in the rat

1983 ◽  
Vol 55 (3) ◽  
pp. 823-829 ◽  
Author(s):  
B. A. Bryar ◽  
M. J. Fregly ◽  
F. P. Field
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscles ◽  
Aortic Tissue ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Aortic Smooth Muscle ◽  
Beta Adrenergic Agonists ◽  
Adrenergic Antagonist ◽  
Vascular Responsiveness ◽  
High Concentrations

The responsiveness of smooth muscle from rings of aortic tissue of cold-acclimated (CA, 6 degrees C, 5-15 wk) rats to both alpha- and beta-adrenergic agonists and KCl was tested and compared with that of warm-adapted (25 degrees C) controls. alpha-Adrenergic stimulation, induced by low doses (10(-8)-10(-7) M) of phenylephrine and norepinephrine in the presence and absence of the beta-adrenergic antagonist, propranolol, resulted in the development of less active tension by aortic smooth muscle from CA rats than from controls. Similar results were observed with the weakly alpha 1-adrenergic agonistic activities of tyramine, clonidine, and high concentrations of isoproterenol (10(-6)-10(-4) M). There was also a significant reduction in the tension developed by smooth muscles of the aortas from CA rats when depolarized with KCl in concentrations ranging from 8 to 20 mM. In contrast, aortic smooth muscle, contracted to 75% of maximum with KCl, showed an enhanced relaxation to the beta-adrenergic agonist, isoproterenol, in CA rats. These studies suggest that acclimation of rats to cold results in both a decrease in alpha-adrenergic responsiveness and an increase in beta-adrenergic responsiveness in vascular smooth muscle as well as a change in the biochemical events that couple activation of adrenergic receptors to changes in vasomotor tone.

Effects of kinins on isolated blood vessels. Role of endothelium

1982 ◽  
Vol 60 (12) ◽  
pp. 1580-1583 ◽  
Author(s):  
D. Regoli ◽  
J. Mizrahi ◽  
P. D'Orléans-Juste ◽  
S. Caranikas
Keyword(s):  
Arachidonic Acid ◽  
Carotid Artery ◽  
Common Carotid Artery ◽  
Smooth Muscles ◽  
Rabbit Aorta ◽  
Arachidonic Acid Metabolism ◽  
Arachidonic Acid Cascade ◽  
Vascular Smooth Muscles ◽  
Acid Metabolites

Bradykinin (BK) and des-Arg9-BK were used to determine whether the stimulatory and inhibitory actions of the kinins in various isolated vessels require the presence of endothelium and may be mediated by arachidonic acid metabolites. It was found that the presence of intact endothelium is required only for the relaxation of the dog common carotid artery in response to bradykinin. Stimulatory actions of both BK and des-Arg9-BK in arterial (rabbit aorta) and venous (rabbit jugular and mesenteric vein) smooth muscle do not require the presence of endothelium. Inhibition of the arachidonic acid cascade at various levels affects the relaxing action of acetylcholine (rabbit aorta and dog common carotid artery) while being inactive against both the relaxing (dog common carotid artery) and contractile actions (rabbit aorta, rabbit jugular and mesenteric veins) of bradykinin and des-Arg9-BK. Inhibitors of the arachidonic acid cascade also do not affect the inhibitory action of isopropylnoradrenaline on the rabbit aorta. The present results indicate that stimulant actions of kinins in isolated vascular smooth muscles do not require the presence of endothelium. Endothelium is required for the inhibitory actions of acetylcholine and bradykinin but not for that of isopropylnoradrenaline on the dog carotid artery. Moreover, the inhibition of arachidonic acid metabolism only affects the response of isolated vessels to acetylcholine. The present results suggest that several mechanisms may be involved in the inhibition of vascular tone by vasodilators.

The Haemodynamic Consequences of Adaptive Structural Changes of the Resistance Vessels in Hypertension

1971 ◽  
Vol 41 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Björn Folkow
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Muscle Activity ◽  
Flow Resistance ◽  
Smooth Muscles ◽  
Vascular Smooth Muscles ◽  
Resistance Increase ◽  
Vascular Bed ◽  
Resistance Vessels ◽  
Vascular Beds

It is generally accepted that a rise in systemic flow resistance constitutes the essential background of the increased arterial blood pressure in well-established hypertension, though the early ‘labile’ phases of essential hypertension in particular may exhibit a pattern simulating a moderately intense defence reaction, with enhanced cardiac output and muscle blood flow as the most characteristic features, apart from the rise in blood pressure. With respect to the increased flow resistance in the well-established phase, it is accepted that the vessels respond readily, and apparently normally, to vasodilator substances, from which the correct conclusion has been drawn that the resistance increase cannot be ascribed to any sclerotic narrowing of the resistance vessels (Pickering, 1968). However, this observation has also generally led to the assumption that an increased smooth-muscle tone of the resistance vessels must be the explanation of the increased flow resistance and, despite the fact that there are numerous reports of medial hypertrophy in the precapillary resistance vessels for instance (Pickering, 1968), the possible haemodynamic consequences of such a type of structural vascular adaptation has hardly been considered at all. Instead the debate has mainly been concerned about whether the assumed increase of vascular tone is due to enhanced myogenic activity, to an increased neurogenic and/or hormonal exogenous stimulation of the vascular smooth muscles or whether these muscles might exhibit an enhanced sensitivity or ‘reactivity’ to such extrinsic stimuli. In other words, if summarized in a diagram relating the extent of active smooth-muscle shortening to the degree of resistance increase in an idealized resistance vessel (Fig. 1), an increased smooth muscle activity, whatever its background, would mean a shift from the normal resting equilibrium at point O to a point B along the curve N. However, one cannot safely deduce levels of vascular smooth-muscle activity between different individuals, or vascular beds, by simply assuming that they are proportional to the respective levels of current flow resistance. In each individual, or vascular bed, one must first relate the actual resistance level to that present when the vascular smooth muscles are completely inactive; i.e. when the resistance vessels are maximally dilated and exposed to the same amount of distending pressure. This latter resistance value provides the necessary ‘baseline’, or an equivalent of fully relaxed muscle length for a particular vascular bed, from which its current level of smooth muscle activity has to be judged in terms of the ratio between these two resistance values. This is simple and straightforward reasoning, but surprisingly enough studies along these lines were apparently not performed systematically until our group used this approach in analyses of the level of ‘basal tone’ in different vascular beds or individuals (Celander & Folkow, 1953; Löfving & Mellander, 1956; Folkow, 1956).

11,12,15-Trihydroxyeicosatrienoic acid mediates ACh-induced relaxations in rabbit aorta

2003 ◽  
Vol 285 (6) ◽  
pp. H2648-H2656 ◽  
Author(s):  
William B. Campbell ◽  
Nancy Spitzbarth ◽  
Kathryn M. Gauthier ◽  
Sandra L. Pfister
Keyword(s):  
Smooth Muscle ◽  
Rabbit Aorta ◽  
Nordihydroguaiaretic Acid ◽  
Gas Chromatography Mass Spectrometry ◽  
Muscle Membrane ◽  
Lipoxygenase Pathway ◽  
Lipoxygenase Inhibitors ◽  
Aortic Smooth Muscle ◽  
Threefold Increase ◽  
Smooth Muscle Membrane

Rabbit aortic endothelium metabolizes arachidonic acid (AA) by the 15-lipoxygenase pathway to vasodilatory eicosanoids, hydroxyepoxyeicosatrienoic acids (HEETAs), and trihydroxyeicosatrienoic acids (THETAs). The present study determined the chemical identity of the vasoactive THETA and investigated its role in ACh-induced relaxation in the rabbit aorta. AA caused endothelium-dependent, concentration-related relaxations of the rabbit aorta. Increasing the extracellular KCl concentration from 4.8 to 20 mM inhibited the relaxations to AA by ∼60%, thereby implicating K+-channel activation in the relaxations. In addition, AA caused an endothelium-dependent hyperpolarization of aortic smooth muscle from –39.6 ± 2.7 to –56.1 ± 3.4 mV. In rabbit aortic rings, [14C]AA was metabolized to prostaglandins, HEETAs, THETAs, and 15-hydroxyeicosatetraenoic acid. Additional purification of the THETAs by HPLC resolved the mixture into its 14C-labeled products. Gas chromatography/mass spectrometry identified the metabolites as isomers of 11,12,15-THETA and 11,14,15-THETA. The 11,12,15-THETA relaxed and hyperpolarized the rabbit aorta, whereas 11,14,15-THETA had no vasoactive effect. The relaxations to 11,12,15-THETA were blocked by 20 mM KCl. In aortic rings pretreated with inhibitors of nitric oxide and prostaglandin synthesis, ACh caused a concentration-related relaxation that was completely blocked by 20 mM KCl. Pretreatment with the phospholipase A2 inhibitors mepacrine and 7,7-dimethyl-5,8-eicosadienoic acid, the lipoxygenase inhibitors cinnamyl-3,4-dihydroxy-α-cyanocinnamate, nordihydroguaiaretic acid, and ebselen, or the hydroperoxide isomerase inhibitors miconazole and clotrimazole also blocked ACh-induced relaxations. ACh caused a threefold increase in THETA release. These studies indicate that AA is metabolized by endothelial cells to 11,12,15-THETA, which activates K+ channels to hyperpolarize the aortic smooth muscle membrane and induce relaxation. Additionally, this lipoxygenase pathway mediates the nonnitric oxide, nonprostaglandin relaxations to ACh in the rabbit aorta by acting as a source of an endothelium-derived hyperpolarizing factor.

Ca2+ coupling in vascular smooth muscle: Mg2+ and buffer effects on contractility and membrane Ca2+ movements

1982 ◽  
Vol 60 (4) ◽  
pp. 459-482 ◽  
Author(s):  
B. M. Altura ◽  
B. T. Altura ◽  
A. Carella ◽  
P. D. M. V. Turlapaty
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Reactivity ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Vascular Smooth Muscles ◽  
Disease States ◽  
Naturally Occurring ◽  
Ca Uptake ◽  
Coupling Processes

An examination of the literature, over the past two decades, reveals that (1) in studies of different types of vascular smooth muscles, Mg2+ is often either left out of physiological salt solutions or reduced in concentration compared with that in blood; and (2) when excitation–contraction coupling processes have been examined in isolated vascular tissues and cells, a number of artificial (synthetic) amine and organic zwitterion buffers have often been substituted for the naturally occurring bicarbonate and phosphate anions found in the blood and in cells. The influence of extracellular magnesium ions ([Mg2+]o) on tone, contractility, reactivity, and divalent cation movements in vascular smooth muscles, and how they may relate to certain vascular disease states, is reviewed. Data are presented and reviewed which indicate that many of the most commonly used artificial buffers (e.g., Tris. HEPES, MOPS, Bicine, PIPES, imidazole) can exert adverse effects on contractility and reactivity of certain arterial and venous smooth muscles. The data reviewed herein suggest that [Mg2+]o and membrane Mg are important in the regulation of vascular tone, vascular reactivity, and in control of Ca uptake, content, and distribution in smooth muscle cells. [Formula: see text] and (or) PO42−anions may be important for normal maintenance of excitability and reactivity and in the control of Ca uptake, content, and distribution in smooth muscle cells.

scholarly journals Human smooth muscle VLA-1 integrin: purification, substrate specificity, localization in aorta, and expression during development.

1990 ◽  
Vol 111 (5) ◽  
pp. 2159-2170 ◽  
Author(s):  
V M Belkin ◽  
A M Belkin ◽  
V E Koteliansky
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Type I ◽  
Dependent Manner ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Sds Page ◽  
Aortic Media

A membrane glycoprotein complex was isolated and purified from human smooth muscle by detergent solubilization and affinity chromatography on collagen-Sepharose. The complex was identified as VLA-1 integrin and consisted of two subunits of 195 and 130 kD in SDS-PAGE. Liposomes containing the VLA-1 integrin adhered to surfaces coated with type I, II, III, and IV collagens, Clq subcomponent of the first component of the complement, and laminin. The liposomes specifically adhered to these proteins in a Ca2+, Mg2(+)-dependent manner, but did not bind to gelatin, fibronectin, and thrombospondin substrates. The expression of VLA-1 integrin in different human tissues and cell types, and during aorta smooth muscle development was studied by SDS-PAGE, and subsequent quantitative immunoblotting was performed with antibodies recognizing alpha 1 and beta 1 subunits of the VLA-1 integrin. A high level of VLA-1 integrin expression was an exceptional feature of smooth muscles. Fibroblasts, endothelial cells, keratinocytes, striated muscles, and platelets contained trace amounts of VLA-1 integrin. In the 10-wk-old human fetal aorta, VLA-1 integrin was found only in smooth muscle cells whereas mesenchymal cells, surrounding aortic smooth muscle cells, were VLA-1 integrin negative. By the 24th wk of gestation, the amount of VLA-1 integrin was significantly reduced in the aortic media (4.3-fold for alpha 1 subunit and 2.5-fold for beta 1 subunit) compared with that in the 10-wk-old aortic smooth muscle cells. After birth, the expression of VLA-1 integrin increased and in the 1.5-yr-old child aorta the VLA-1 integrin level was almost the same as in adult aortic media. Smooth muscle cells from intimal thickening of adult aorta express five times less alpha 1 subunit of VLA integrin that smooth muscle cells from adult aortic media. In primary culture of aortic smooth muscle cells, the content of the VLA-1 integrin was dramatically reduced and subcultured cells did not contain VLA-1 integrin at all.

Calcium and excitation–contraction coupling in vascular smooth muscles

1982 ◽  
Vol 60 (4) ◽  
pp. 483-488 ◽  
Author(s):  
George B. Weiss
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Relative Size ◽  
Smooth Muscles ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
High K ◽  
Renal Vessels ◽  
Quantitative Separation ◽  
High Concentrations

The roles of Ca2+ in excitation–contraction coupling in vascular smooth muscle have been difficult to delineate, primarily because unambiguous association of specific Ca2+ components with morphologically defined cellular structures could not be attained. More recent use of washouts in La3+-substituted solutions at low temperature (to remove superficial Ca2+ and retain cellular Ca2+), Scatchard-coordinate plots (to identify incubation conditions appropriate for examining predominantly high or low affinity Ca2+ components), and high concentrations of Sr2+ (to remove high but not low affinity Ca2+) have facilitated qualitative and quantitative separation of different Ca2+ fractions. The release of high affinity Ca2+ elicited with norepinephrine and the increase in uptake of low affinity Ca2+ obtained with high K+ have been clearly demonstrated, and may directly measure or indirectly reflect changes in the level of intracellular free Ca2+. In other types of vascular smooth muscle (e.g., renal vessels, coronary arteries), similar Ca2+ components also appear to be present, but their relative size and functional importance for regulation of contractile responsiveness can differ.

Calcium and angiotensin tachyphylaxis in rat uterine smooth muscle

1975 ◽  
Vol 228 (5) ◽  
pp. 1423-1430 ◽  
Author(s):  
RJ Freer
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscles ◽  
Rabbit Aorta ◽  
Rat Uterus ◽  
Uterine Smooth Muscle ◽  
Normal Tissues ◽  
High Concentrations ◽  
The Relationship ◽  
Very High ◽  
Stimulation Of

Studies were carried out to investigate the relationship between extracellular Ca++ and the ability of a particular smooth muscle to develop tachyphylaxis to angiotensin II (AII). Stimulation of rat uterus by AII was found to be dependent on extracellular Ca++. Placing the tissue in 0 Ca++ completely blocked AII-induced contractions as did the presence of the "Ca++ antagonists" verapamil (10- minus 5M), SKF 525-A (10- MINUS 5M), tetracaine (10- minus 4M), Mn++ (8 times 10- minus 3M), or La-3+ (10- minus 3M). In addition, it is no longer possible to produce tachyphylaxis to AII in deplorazed rat uterus under conditions of pH and Ca++ concentration in which a normally polarized preparation would be unresponsive. Verapamil, on the other hand, was an even more effective antagonist of AII in depolarized preparations (ID50 of 10- minus 8M) than in normal tissues (ID50 of 2.0 times 10- minus 7M). Like the rat uterus, the smooth muscle of the guinea pig ileum also develops tachyphylaxis to AII, and the effect of this peptide was also blocked by 10- minus 5 M verapamil. Rabbit aorta, however, was found to be relatively resistant to both development of tachyphylaxis under conditions of low Ca++ and low pH and also to inhibition by even very high concentrations of verapamil (10- minus 4M). The results of these studies suggest that the Ca++ site involved in the tachyphylactic response to AII may be a physiologically important one in those smooth muscles in which movement of extracellular Ca++ contributes to the inward ion currents during excitation. Verapamil, however, appears to act at a common step in the excitation-contraction sequence in rat uterus. A working model of the interaction of AII with rat uterine smooth muscle is presented.

Sign in / Sign up

Export Citation Format

Share Document