Extracellular space and the ionic distribution in the isolated arterial wall

Villamil, M. F.; Rettori, Valéria; Barajas, Luciano; Kleeman, Charles R.

doi:10.1152/ajplegacy.1968.214.5.1104

Cited by 36 publications

(15 citation statements)

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“…The amounts of apparently bound Cl-found in mature rats in the present study are comparable with those reported for dog carotid artery by Villamil, Rettori, Barajas & Kleeman (1968), although Siegel et al (1976) failed to detect binding in this vessel.…”

Section: Discussionsupporting

confidence: 89%

“…Several workers (e.g. Hagemeijer, Rorive & Schoffeniels, 1965;Friedman, Gustafson, Hamilton & Friedman, 1968;Villamil, Rettori, Barajas & Kleeman, 1968;Villamil, Ponce, Amorena & Muller, 1979) have drawn attention to the fact that arterial tissue is very sensitive to rough handling. In the present study particular care was taken (a) never to stretch the aorta beyond its length in situ, (b) to cut away rather than tear away the connective tissue, (c) to remove all tissue which had been held by forceps during excision.…”

Section: Introductionmentioning

confidence: 99%

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The Influence of Age on Fluid and Sodium Chloride Distribution in Rat Aortic Wall

Law

1984

Exp Physiol

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SUMMARYFluid, Na+ and Cl-content and distribution have been examined in incubated segments of thoracic and abdominal aorta from male Wistar rats aged 1, 3 and 18 months. Na+ and Clwere determined under conditions of total metabolic blockade (cyanide+iodoacetate). The total aortic mural fluid content, relative to solute-free dry weight, fell from I to 3 months, due mainly to relative contraction of the extracellular (e.c.) (inulin) space. It increased from 3 to 18 months due mainly to an increased intracellular (i.c.) (non-inulin) space. Total mural free and bound Na+ content, as well as i.c. Na+ content and concentration, fell from 1 to 3 months and increased from 3 to 18 months. No bound Na+ was detectable in segments which had been incubated in the presence of chondroitinase ABC. I.c. Cl-content and concentration fell from 1 to 3 months, but thereafter did not alter significantly. Bound Cl-in the aortic wall of 3-month-old rats was markedly reduced by incubation in the presence of a non-specific protease preceded by treatment with glycerol. The results are discussed in relation to previously established age-related characteristics of aortic and arterial walls.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

The Influence of Age on Fluid and Sodium Chloride Distribution in Rat Aortic Wall

Law

1984

Exp Physiol

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“…One could do a simple calculation to assess whether this calcium capacity is adequate to lower the cytoplasmic free calcium below 10" 7 M which prevents actomyosin adenosinetriphosphatase (ATPase) activity and tension development (8) Choosing 45 /uM as the calcium concentration at activation and 0.7 ml/g as the tissue water content (29,30) in this relationship, the calculation shows that the vesicular material has a more than adequate capacity to lower the cytoplasmic calcium concentration to zero. This calculation is a gross oversimplification of the true picture, since it ignores the lessening of the vesicular calcium uptake as a result of the decreasing cytoplasmic free calcium level and any buffering influence of other calcium binding sites such as the mitochondria or the calcium-sensitive element of the contractile apparatus.…”

Section: Discussionmentioning

confidence: 99%

Calcium-accumulating properties of subcellular fractions of bovine vascular smooth muscle.

Ford¹,

Heß²

1975

Circulation Research

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This study examined the calcium transport properties of two subcellular fractions of bovine aorta obtained by differential centrifugation. The vesicular fraction had a high-affinity (K m = 1.05 x 10~6M) calcium transport mechanism which could be potentiated by using the calcium-precipitating anion, oxalate. The mitochondriaenriched fraction's calcium transport system had a lower affinity for calcium than did that of the vesicular fraction. The calcium capacity of the vesicular fraction was determined by comparing the steady-state calcium uptake in the presence of oxalate in the whole homogenate with the same uptake by the vesicular fraction alone. A calcium capacity of about 100 /imoles Ca 2+ /kg aorta was obtained. It is concluded that the vesicular fraction has all of the properties of a major site of subcellular calcium regulation in vascular smooth muscle.• It is generally accepted that intracellular free calcium is the connection between stimulation and contraction in vascular smooth muscle (1, 2). However, the identification of the sources and sinks of the activator calcium remains an unsettled question. Numerous indirect experiments have shown that at least part of the activator calcium is intracellular in origin (1-4). Recent electron microscopic studies indicate that there are at least two different subcellular organelles potentially capable of serving as intracellular sinks for calcium: one is the mitochondria and the other is the sarcoplasmic reticulum (5-7). Both of these structures are capable of sequestering the divalent ion strontium in contracting muscle, and the mitochondria can also sequester barium. To determine if these or any other subcellular structures are capable of playing major roles in the regulation of the intracellular calcium concentration of vascular smooth muscle, numerous questions must be answered. Are these structures capable of accumulating calcium at the very low cytoplasmic level (10~5M) sufficient for maximal activation of the contractile process (8)? If they are capable of sequestering calcium at this low level, what is the relative competitive position of each structure? Can these structures, alone or in

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“…27 This study demonstrates that cerebral arteries possess two distinct calcium binding sites, a highaffinity site and a low-affinity site (Figure 4). Peripheral vessels also have two distinct calcium binding sites.…”

mentioning

confidence: 74%

Effects of prostaglandin F2 alpha and thromboxane A2 analogue on bovine cerebral arterial tone and calcium fluxes.

Wendling

Harakal

1991

Stroke

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We determined sources of activator calcium for prostanoid-induced cerebrovascular constriction by measuring isometric tension and calcium-45 ("Ca) fluxes in bovine middle cerebral arteries. Constriction induced by prostaglandin F^ or the stable thromboxane A 2 analogue SQ-26,655 was near-maximally inhibited in calcium-deficient solutions but only partially inhibited by calcium antagonists (10~! M verapamil or 33xlO~7 M nifedipine). Studies of ^Ca binding at different external Ca 2+ concentrations showed that cerebral arteries possess two calcium binding sites, a high-affinity site and a low-affinity site. Each prostanoid significantly increased low-affinity ^Ca uptake (external Ca 2+ concentration = 1.2 mmol/l) during 5 minutes of '"Ca loading; for prostaglandin F^ ^Ca uptake increased from 69 to 108 nmol/g and for SQ-26,655, from 78 to 141 nmol/g. The prostanoid-induced increases in low-affinity ^Ca uptake were completely abolished by pretreatment with verapamil or nifedipine. Prostaglandin F^, SQ-26,655, verapamil, and nifedipine had no effect on high-affinity ^Ca uptake (external Ca J+ concentration=45 /umol/l) or ^Ca efflux (after 60 minutes' preincubation in calcium-deficient media). Prostaglandin F^ and SQ-26,655 each appear to constrict cerebral arteries by two mechanisms: first, by promoting calcium uptake from low-affinity binding sites through receptor-operated channels sensitive to the calcium antagonists, and second, by releasing calcium from depletable internal stores. (Stroke 1991;22:66-72)

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Extracellular space and the ionic distribution in the isolated arterial wall

Cited by 36 publications

References 0 publications

The Influence of Age on Fluid and Sodium Chloride Distribution in Rat Aortic Wall

The Influence of Age on Fluid and Sodium Chloride Distribution in Rat Aortic Wall

Calcium-accumulating properties of subcellular fractions of bovine vascular smooth muscle.

Effects of prostaglandin F2 alpha and thromboxane A2 analogue on bovine cerebral arterial tone and calcium fluxes.

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