Pharmacology of the Adrenoceptors and Cholinoceptors of the Bc3hi Nonfusing Muscle Cell Line

Mauger, Jean‐Pierre; Moura, A M; Worcel, Manuel

doi:10.1111/j.1476-5381.1978.tb08637.x

Cited by 24 publications

(7 citation statements)

References 17 publications

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“…4A) is in all respects identical to the desaturation from the medial strips. This finding was confirmed with cultures of the BC3H1 cell line (Schubert, Harris, Devine & Heinemann, 1974;Mauger et al 1978), which has many features of smooth muscle cells (Table 3). In all cases, 22Na efflux from smooth muscle cells is characterized by an important compartment B and a smaller compartment C. As expected, the 22Na desaturation curves from primary cultures of fibroblasts (Fig.…”

Section: Resultssupporting

confidence: 71%

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Identification of different sodium compartments from smooth muscle cells, fibroblasts and endothelial cells, in arteries and tissue culture

Garay

Moura

Osborne-Pellegrin

et al. 1979

The Journal of Physiology

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SUMMARY1. The 22Na efflux curve from the rat tail artery, at 35 0C, can be analysed as the sum of three distinct components, from 0 to 90 min of washout. After an initial diffusional component the two late exponential components Be-kBt and Ce-ket have the following values: B = 3-03 + 0-15 m-mole/kg wet wt. and C = 0-56 + 0-04; kB = 0-145 + 0-005 min-and kc = 0-015 + 0-007.2. In order to identify the cellular origin of the different compartments we compared the 22Na efflux curve from the rat tail artery with the curves obtained from whole rabbit aortal strips, rabbit aortal medial or adventitial strips; and primary cultures from rabbit aorta medial smooth muscle cells, cultures of a non-fusing muscle cell line (BC3H1), libroblasts and endothelial cells. 4. The efflux from compartment B of smooth muscle cells is inhibited by ouabain and in the absence of extracellular K+. The efflux from compartment C is inhibited only by ouabain but not by the suppression of extracellular K+.5. We propose a distribution of Na+ in smooth muscle cells in two intracellular compartments: (1) Na+ freely dissolved in the sarcoplasm, exchanging with the kinetics of compartment B and (2) a second cellular compartment which could be contained in the sarcoplasmic reticulum exchanging with the kinetics of compartment C.* To whom correspondence and reprint requests should be sent. R. P. GARA Y AND OTHERS 6. On the basis of the previous model of Na+ distribution, considering our values, and without any correction, the estimated sarcoplasmic concentration of Na+ is 9-6 mm, compatible with the direct measurements obtained in skeletal and heart muscle. The Na+ concentration in the sarcoplasmic reticulum would be 4-10 times higher than in the cytoplasm. In order to increase the accuracy of our calculations it would be necessary to account for the interdiffusion and back diffusion of Na+ between compartments. It is not possible to attain this goal at the present time.

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Section: Resultssupporting

confidence: 71%

“…A desaturation curve was obtained by adding in reverse order the washout curve to the radioactivity remaining in the tissue. The effluxes from cell cultures were also measured by a continuous flow technique (Mauger, Moura & Worcel, 1978). After loading, the slide was placed in a glass chamber kept at 37 0C.…”

Section: Methodsmentioning

confidence: 99%

Identification of different sodium compartments from smooth muscle cells, fibroblasts and endothelial cells, in arteries and tissue culture

Garay

Moura

Osborne-Pellegrin

et al. 1979

The Journal of Physiology

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“…The superfusate was collected in 2 min fractions and radioactivity was determined by gamma counting. Using a computer programme, a desaturation plot was constructed by adding, in reverse order, the radioactivity in each fraction to that remaining in the cells at the end of the experiment (Mauger, Moura & Worcel, 1978), and from these data the first-order rate constant of efflux (R) for each fraction was calculated and expressed in units of minl…”

Section: Aortic Stripsmentioning

confidence: 99%

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Gordon

Martin

1983

British J Pharmacology

162

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1 Bradykinin, adenosine triphosphate (ATP) and acetylcholine each relaxed histamine-contracted strips of pig aorta in a dose-dependent manner. These relaxations were abolished when the endothelium was removed. 2 Relaxation induced by ATP was mimicked by adenosine diphosphate (ADP) but adenosine monophosphate (AMP) and adenosine were about 120 times less potent. 3 Relaxation induced by acetylcholine was antagonized by atropine in a competitive manner, and carbachol induced the same degree of relaxation as acetylcholine, but was about 10 times less potent. 4 The calcium ionophore, A23 187, also induced a dose-dependent relaxation of pig aortic strips provided the endothelium was present, suggesting that a rise in the level of ionized calcium within the endothelial cells is one means by which vascular smooth muscle relaxation can be triggered. 5 Bradykinin, ATP, ADP, AMP, adenosine and A23 187 each induced a dose-dependent increase in 86Rb efflux from preloaded pig aortic endothelial cells. The dose-response curves for stimulation of 86Rb efflux and for endothelium-dependent relaxation were similar for each individual compound. ADP was equipotent with ATP, but AMP and adenosine were about 120 times less potent. 6 Neither acetylcholine nor carbachol, in concentrations that induce endothelium-dependent relaxation, had any effect on 86Rb efflux from isolated aortic endothelial cells. 7 Lanthanum, which blocks calcium influx, abolished the increases in 86Rb efflux induced by bradykinin and ATP, and the calcium ionophore A23187 was the most effective stimulant of 86Rb efflux, suggesting that the potassium transport induced by these agents is calcium-activated. 8 It is concluded that endothelial responses to bradykinin and ATP can be assessed by monitoring 86Rb efflux, which probably reflects a calcium-activated efflux of potassium associated with the endothelium-dependent vascular relaxation induced by these agents. This pathway is apparently not involved in endothelial responses to acetylcholine.

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“…The evaluation of ^Rb efflux was performed with an experimental protocol adapted from Mauger and co-workers. 17 The following drugs were used: RU 26988 [11/8, 17/3-dihydroxy-17a-(l-propynyl) androesta-1,4,6 trien-3-one], a specific glucocorticoid receptor agonist,"-l2 was administered at a dose of 20 mg/kg/day by stomach tube. RU 38486 [ 17/3-hydroxy-1l/3-(4-dimethylaminophenyl)-17a-(prop-l-ynyl)-estra-4,9-dien-3-one] is a steroid with mainly antiprogesterone properties; in addition, it exerts antiglucocorticoid activity.…”

Section: Methodsmentioning

confidence: 99%

Effects of antiglucocorticoids on glucocorticoid hypertension in the rat.

Grünfeld¹,

Eloy²,

Moura³

et al. 1985

Hypertension

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SUMMARY The early phase of hypertension induced in rats by a glucocorticoid agonist RU 26988 was studied. Systolic blood pressure increased by 35 mm Hg. Water and sodium urinary excretion increased transiently, and plasma volume decreased. Total and ouabain-sensitive sodium efflux, as well as rubidium efflux, were enhanced by glucocorticoid administration. Low salt intake did not prevent hypertension. Pretreatment with RU 38486, a steroid with antiglucocorticoid properties, largely prevented the rise in blood pressure ( + 10 mm Hg) and suppressed transient natriuresis and the decrease in plasma volume. Changes in total and ouabain-sensitive sodium efflux were completely prevented, whereas changes in rubidium efflux were only partly reversed. Similarly, administration of progesterone, a steroid with antiglucocorticoid effects, prevented glucocorticoid hypertension (+11 mm Hg) and vascular ionic changes. In contrast administration of RU 28318, an antimineralocorticoid agent, was without effect on glucocorticoid hypertension (+ 38 mm Hg). Progesterone or RU 38486 administered after glucocorticoid also decreased blood pressure. Present data indicate that glucocorticoid hypertension may be prevented or reversed in its early phase by steroid drugs with antiglucocorticoid properties. These drugs also appeared to prevent the sodium and rubidium flux abnormalities induced by glucocorticoid. We suggest that activation of the vascular glucocorticoid receptors may be involved in the pathophysiology of glucocorticoid hypertension. (Hypertension 7: 292-299, 1985 We therefore initiated a study of the in vivo effects of RU 26988 in the rat. RU 26988 is a specific glucocorticoid receptor agonist that exhibits high affinity for glucocorticoid receptor sites and does not compete with aldosterone for the mineralocorticoid receptor."12 We attempted to antagonize glucocorticoidinduced hypertension by administration of an antimineralocorticoid (RU 28318) and steroid derivatives known to bind competitively at the glucocorticoid receptor-progesterone and RU 38486. The latter steroid has mainly antiprogesterone properties; in vitro studies have also shown antiglucocorticoid activity. 13-I4 Lastly, we investigated the ionic changes induced by glucocorticoid and antiglucocorticoids on the rat tail artery after in vivo administration of the steroid drugs.

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Pharmacology of the Adrenoceptors and Cholinoceptors of the Bc3hi Nonfusing Muscle Cell Line

Cited by 24 publications

References 17 publications

Identification of different sodium compartments from smooth muscle cells, fibroblasts and endothelial cells, in arteries and tissue culture

Identification of different sodium compartments from smooth muscle cells, fibroblasts and endothelial cells, in arteries and tissue culture

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Effects of antiglucocorticoids on glucocorticoid hypertension in the rat.

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Pharmacology of the Adrenoceptors and Cholinoceptors of the Bc3hi Nonfusing Muscle Cell Line

Cited by 24 publications

References 17 publications

Identification of different sodium compartments from smooth muscle cells, fibroblasts and endothelial cells, in arteries and tissue culture

Identification of different sodium compartments from smooth muscle cells, fibroblasts and endothelial cells, in arteries and tissue culture

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of 86Rb efflux from isolated endothelial cells

Effects of antiglucocorticoids on glucocorticoid hypertension in the rat.

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Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells