Electron microscopic localization of calcium in vascular smooth muscle

Debbas, Gamil; Hoffman, Loren H.; Landon, Erwin J.; Hurwitz, Leon

doi:10.1002/ar.1091820405

Cited by 61 publications

(17 citation statements)

References 54 publications

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“…Ultrastructural localization of calcium, using analogous methods as that used in the present study, displayed four major distribution sites in smooth muscle cells: the microvesicies lining the plasma membrane, the mitochondria, the sarcoplasmic reticulum and the nucleus (3,5,6,10). Our results essentially show a similar dis tribution in smooth muscle cells of the rat caudal artery under control conditions.…”

Section: Discussionsupporting

confidence: 82%

Effects of Flunarizine on the Distribution of Calcium in Vascular Smooth Muscle

Borgers¹,

Ghoos²,

Thoné³

et al. 1980

J Vasc Res

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Exposure of depolarized caudal artery preparations of the rat to various calcium concentrations evoked sustained contractions of the smooth muscle in a dose-dependent way. Flunarizine was shown to suppress this sustained muscle contraction. Experiments were undertaken to determine the subcellular site where flunarizine interferes with the calcium-induced contractile process. The subcellular distribution of calcium was assessed by electron microscopy, using a combined oxalate-pyroantimonate method. In depolarized strips precipitated calcium was mainly distributed over the contractile elements and the microvesicles lining the cell membrane. When flunarizine was added to the preparation, the precipitate was predominantly confined to the extracellular space, whereas only spotty precipitates were seen in mitochondria and sarcoplasmic reticulum. The myofibrils were almost free of deposits. Without previous depolarization, the smooth muscle cells demonstrated a moderate amount of precipitate over the mitochondria, nuclei, sarcoplasmic vesicles, plasmalemmal microvesicles and myofibrils. In these conditions neither the amount nor the intracellular distribution of the precipitate was influenced by the addition of flunarizine. These observations suggest that flunarizine interferes with the entry of calcium at the plasma membrane level, but only in conditions where the influx of the ion is stimulated.

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Section: Discussionsupporting

confidence: 82%

Effects of Flunarizine on the Distribution of Calcium in Vascular Smooth Muscle

Borgers¹,

Ghoos²,

Thoné³

et al. 1980

J Vasc Res

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“…A number of studies have described the ability of intracellular organelles such as sarcoplasmic reticulum (SR) and mitochondria to accumulate Ca (Carsten, 1969;Somlyo & Somyo, 1971 ;Somlyo et al, 1974;Batra, 1975;Debbas et al, 1975). This ability is thought to illustrate their role in the reduction of cytoplasmic [Ca 2 § ] (Cacyt) during relaxation.…”

Section: Discussionmentioning

confidence: 99%

Agonist induced release of intracellular Ca2+ in the rabbit aorta

Deth

1976

J. Membrain Biol.

211

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Summary. The effects of hormonal agonists (norepinephrine, angiotensin, and histamine) on 45Ca efflux from the rabbit aorta were studied using a Ca-EGTA buffered efflux medium. Each caused a transient stimulation of efflux rate which probably reflected the release of an intracellular 45Ca store. The size of the stimulation of efflux correlated with the size of the initial rapid phase of contraction. The norepinephrine-sensitive intracellular Ca fraction was estimated to be greater than 21 gmoles/Kg wet tissue weight. This fraction is separate from intracellular Ca which is accumulated during relaxation. Evidence is presented for the lack of cyclic nucleotide involvement in the release of Ca a+, and possible alternative modes of coupling are discussed.The calcium movements which are responsible for norepinephrine (NE) induced contraction of vascular smooth muscle remain uncertain. Earlier studies by Bohr (1963) described the different sensitivity of the early phasic and latter tonic portions of the contractile response to changes in extracellular Ca. The initial rapid increase in tension was augmented in Ca-free solutions, and reduced in higher than normal Ca (10 raM), while the latter slow increase in tension was reduced in Ca-free solutions and increased in the presence of higher Ca. Hinke, Wilson and Burnham (1964), and later Hudgins (1969) andvan Breemen (1969), noted that the NE response was more resistant to Ca removal than was high K induced contraction, and that NE responsiveness returned at lower Ca levels than high K contractions. Since Briggs (1962) had reported that both NE and high K increased Ca influx, Hinke was led to conclude that NE initially utilizes a more tightly bound Ca fraction, probably located on the outside of the plasma membrane. A number of recent studies have concluded that NE activation involves a combination of cellular and extracellular Ca

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“…Chemical analyses showed that some calcium was retained in tissues after fixation. The results suggest that there are different mechanisms for lesion delimitation and age-induced resistance.The subcellular localization of Ca has been the subject of many investigations of animal tissues (7)(8)(9)22). By several procedures, primarily those using fixation with PPA2 or ammonium oxalate, Ca has been reported to occur within mitochondria, Golgi vesicles, sarcoplasmic reticulum, as well as on glycogen particles, heterochromatin, and the nucleolus.…”

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confidence: 99%

Cytohistochemical Techniques for Calcium Localization and Their Application to Diseased Plants

Stockwell¹,

Hanchey²

1982

Plant Physiol.

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Lesion delimitation and resistance of old bean (Phaselous vulgaris L., cv. Red Kidney) plants to Rhizoctonia solani Kuhn have been suggested to result from increased calcium pectate formation in walls. Ultrastructural histochemistry was used to determine the site of calcium in tissues adjacent to lesions and in older bean hypocotyls. Hypocotyl lesion tissue and uninoculated control tissue were treated with ammonium oxalate or potassium pyroantimonate during fixation. Treatment with potassium pyroantimonate, but not with oxalate, resulted in granular deposits in cell walls of healthy and lesion tissue. Granules also occurred on the plasma membrane of cells adjacent to lesions and in organelles of damaged cells, but wall granule density was not increased. Cell walls from healthy 24-day-old plants had a greater granule density than those for 8-day-old plants. Wall granules were removed from thin sections with ethylene glycol bis(.8-aminoethyl ether)-N,NA,N'-tetraacetic acid. Energy dispersive analysis of x-rays also suggested that potassium pyroantimonate localized calcium. Chemical analyses showed that some calcium was retained in tissues after fixation. The results suggest that there are different mechanisms for lesion delimitation and age-induced resistance.The subcellular localization of Ca has been the subject of many investigations of animal tissues (7)(8)(9)22). By several procedures, primarily those using fixation with PPA2 or ammonium oxalate, Ca has been reported to occur within mitochondria, Golgi vesicles, sarcoplasmic reticulum, as well as on glycogen particles, heterochromatin, and the nucleolus. In some cases, the presumed localization of Ca was correlated with chemical and electron microprobe analysis of the sections.Fewer studies have concerned the ultrastructural localization of Ca in plant tissues (6, 15, 17,18,20,21). Antimonate precipitates containing Ca were found in the nucleus, mitochondria, dictyosomes, cell wall, phragmoplast, plasma membrane, and ER in cells of both Marsilea sporocarps and Hordeum leaves in a study by Wick and Hepler (21). Antimonate deposits have also been found within nuclei of Allium cepa root and anther cells (18) In a previous study of bean stem canker, cell walls within lesions were severely degraded, whereas walls at the periphery of mature lesions were intact (13). At the lesion margin, walls stained densely following either potassium permanganate or osmium tetroxide fixation. The purpose of the present study was to evaluate methods for Ca localization at the ultrastructural level, to determine whether these methods could be applied to studies of stem canker on beans, and to evaluate the nature of wall changes in older bean plants and in tissue surrounding lesions. MATERIALS AND METHODS

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Electron microscopic localization of calcium in vascular smooth muscle

Cited by 61 publications

References 54 publications

Effects of Flunarizine on the Distribution of Calcium in Vascular Smooth Muscle

Effects of Flunarizine on the Distribution of Calcium in Vascular Smooth Muscle

Agonist induced release of intracellular Ca2+ in the rabbit aorta

Cytohistochemical Techniques for Calcium Localization and Their Application to Diseased Plants

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