Ca dependence of Na influx during treatment of rabbit aorta with NE and high K solutions

Aaronson, Philip I.; Jones, Allan W.

doi:10.1152/ajpcell.1988.254.1.c75

Cited by 10 publications

(9 citation statements)

References 32 publications

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“…45Ca2+ net uptake values are similar to previously reported values in the same vessels and in arteries [10], 22Na+ net uptake val ues in our experimental conditions are difficult to com pare to previously reported Na+ concentrations [20,[23][24][25][26], Nevertheless, attempts to estimate intracellular Na+ concentration in the RFV give values several-fold smaller than these previously reported concentrations. This dis crepancy might be due to the different technique used, as vein segments were mounted in a myograph during flux measurements, and/or to the type of vessel used, as no measurement of 22Na+ fluxes has been reported as yet in the RFV.…”

Section: Discussionsupporting

confidence: 66%

Intraluminal Flow Preferentially Increases Net Sodium Uptake in the Rabbit Facial Vein

Henrion

Bevan²

1995

J Vasc Res

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The infusion of physiological salt solution into the lumen of ring segments of the isolated rabbit facial vein induces an increase in vessel wall tone. Changes in ²²Na⁺ and ⁴⁵Ca²⁺ net uptake as well as ²²Na⁺ unidirectional efflux in response to flow in this vessel were compared to the response to histamine (1 µM) and to angiotensin II (0.1 µM). ²²Na⁺ net uptake per unit force developed in response to flow was 7.9-fold greater than that for histamine (1 µM) and twice that for angiotensin II (0.1 µM). In comparison, ⁴⁵Ca²⁺ net uptake per unit force in response to flow, histamine and K⁺ were similar. Flow-induced contraction and the related ⁴⁵Ca²⁺ and ²²Na⁺ net uptake were decreased by amiloride (30 µM) and methyl isobutyl amiloride (30 µM) without changes in ⁴⁵Ca²⁺ or ²²Na⁺ net uptake per unit force. Ouabain (10 µM) enhanced flow-induced contraction and the related ²²Na⁺ net uptake. Both ouabain (10 µM) and Bay K 8644 (1 µM) increased flow-induced contraction and the related ⁴⁵Ca²⁺ net uptake whereas they decreased the ⁴⁵Ca²⁺ net uptake per unit force. Flow, histamine and angiotensin II increased the unidirectional efflux of ²²Na⁺. This increase in ²²Na⁺ unidirectional efflux was attenuated by ouabain (10 µM). These experiments demonstrate that the increases in wall force due to flow, histamine and angiotensin II are associated with increases in ²²Na⁺ net uptake and unidirectional efflux. Flow preferentially promotes the entry of Na⁺, compared to histamine and angiotensin II.

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Section: Discussionsupporting

confidence: 66%

Intraluminal Flow Preferentially Increases Net Sodium Uptake in the Rabbit Facial Vein

Henrion

Bevan²

1995

J Vasc Res

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“…The increase in intracellular Na+ induced by noradrenaline could also explain why repeated stimulation by high K+ of aortic strips in the presence of subthreshold ouabain does not induce an increase in tone, since Na+ influx associated with high K+-mediated contraction is smaller than that induced by noradrenaline stimulation (Aaronson & Jones, 1988). Furthermore, the mutually antagonistic actions of potassium and digitalis glycosides on the Na+ pump could contribute to the ineffectiveness of high K+ stimulation.…”

Section: Discussionmentioning

confidence: 99%

Effect of subthreshold ouabain on the tone of guinea‐pig aortic strips following repeated noradrenaline stimulation

Bova¹,

Rossi

Luciani³

et al. 1994

British J Pharmacology

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1 The effect of ouabain at a concentration (0.8;pM) that does not induce contractile response in guinea-pig aortic strips has been studied on endothelium-denuded strips repeatedly stimulated with 1 AM noradrenaline or 60 mM K+ applied for 5 min every 30 min. 2 The resting tone (i.e. the tone between one noradrenaline stimulation and the following) of the aortic strips exposed to ouabain increased progressively, whereas the control strips (no ouabain) completely relaxed on washout of the agonist. In the aortic strips stimulated by 60 mM K+, the resting tone did not increase.3 The calcium antagonist, verapamil, did not affect the increase in tone, that was nevertheless strictly dependent on external calcium, since the contracted strips completely relaxed on calcium removal and promptly contracted again on calcium readdition. This finding indicates a mechanism independent of voltage-gated calcium channels. 4 Caffeine-induced contractions, taken as a measure of sarcoplasmic reticulum calcium content, were amplified by the presence of ouabain in aortic strips either stimulated by noradrenaline or unstimulated, with a larger increase in the former. 5 These results suggest that the repeated stimulation of guinea-pig aortic strips by noradrenaline in the presence of ouabain, by raising both intracellular Na+ and Ca2+, decreases the ouabain threshold concentration required for contraction, thus increasing the responsiveness of vascular smooth muscle to the glycoside.

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“…A similar ratio was reported for norepinephrine-stimulated Na influx and Ca efflux from rabbit aorta. 10 In contrast, the proposed stoichiometry for the Na-Ca exchanger was 3 to I. 26 Although agonist stimulation of vascular smooth muscle was reported to stimulate Na-H exchange, 131427 the activity of this exchanger under basal conditions has only been demonstrated in rat aorta that was incubated with ouabain in a HEPESbuffered solution.…”

Section: Discussionmentioning

confidence: 99%

“…A Caregulated nonselective cation channel has been demonstrated in rat myocytes 8 and mouse neuroblastoma cells. 9 A Ca-dependent increase in Na influx has also been reported in arterial smooth muscle 10 and skeletal muscle. 11 Na influx may also be coupled to intracellular Ca via a Na-Ca exchange mechanism, which has been suggested to alter vascular function during hypertension.…”

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confidence: 82%

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Nisoldipine inhibition of sodium influx into aorta from aldosterone-salt-hypertensive rats.

1989

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The purpose of this study was to determine whether increased sodium (Na) influx into the aorta was associated with aldosterone-salt hypertension in the rat and, if present, to determine what mechanisms contributed to the increase. Basal M Na influx was elevated in aorta from the hypertensive rats (2.21+0.10 mmol/1 cell H 2 0/min, n=25) compared with control-salt rats (1.75±0.04 mmol/1 cell H 2 O/min, n=24). The calcium (Ca) antagonist nisoldipine inhibited the Na influx into aorta from hypertensive rats in a concentration-dependent manner. At 10 nM nisoldipine, the Na influx in hypertensive rats (1.52±0.14 mmol/1 ceU H 2 0/min, n=10) was similar to control rats (1.66±0.18 mmol/1 cell H 2 0/min, n=l). The basal Na influx in aorta from hypertensive rats was not altered by dichlorobenzamil or ethylisopropylamiloride, selective inhibitors of Na-Ca and Na-H exchange, respectively. The Na influx was 2.21±0.10, 2.03±0.24, and 2.11 ±0.19 mmol/1 cell H 2 O/min for basal (n=25), dichlorobenzamil (w=4), and ethylisoproisopropylamiloride (n=ll), respectively. Inhibition of Na influx in hypertensive rats by 0.1 fiM nisoldipine (ANa influx=-0.72±0.18 mmol/1 cell H 2 0/min, n=9) was not significantly altered when applied with dichlorobenzamil (-0.72±0.21 mmol/1 cell H 2 O/min, n=4) or ethylisopropylamiloride (-0.55±0.15 mmol/1 cell H 2 O/min, n = l l ) . These agents did not alter Na influx in control aorta. Our results suggest that, in aorta from aldosterone-salt-hypertensive rats, an elevated Na influx exists that is dependent on Ca entry through potential-operated Ca channels. Na-Ca and Na-H exchange do not appear to contribute significantly to the elevated Na influx, which is suggested to result from the activity of a Ca-dependent cationic channel. (Hypertension 1989;13:676-680)

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Ca dependence of Na influx during treatment of rabbit aorta with NE and high K solutions

Cited by 10 publications

References 32 publications

Intraluminal Flow Preferentially Increases Net Sodium Uptake in the Rabbit Facial Vein

Intraluminal Flow Preferentially Increases Net Sodium Uptake in the Rabbit Facial Vein

Effect of subthreshold ouabain on the tone of guinea‐pig aortic strips following repeated noradrenaline stimulation

Nisoldipine inhibition of sodium influx into aorta from aldosterone-salt-hypertensive rats.

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