Sodium metabolism in rat resistance vessels.

Aalkjær, Christian; Mulvany, Michael J.

doi:10.1113/jphysiol.1983.sp014883

Cited by 29 publications

(20 citation statements)

References 20 publications

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“…22Na+ flux 22Na+ influx was determined as described previously (Aalkjaer & Mulvany, 1983). In brief, for determination of 22Na+ influx the media volume was first determined from measurements of media thickness and vessel circumference in 2-3 mm long artery segments mounted in the myograph.…”

Section: Ph and Isometric Contractionsmentioning

confidence: 99%

Intracellular pH regulation in resting and contracting segments of rat mesenteric resistance vessels.

Aalkjær

Cragoe

1988

The Journal of Physiology

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125

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SUMMARY1. The pH-sensitive dye 2',7'-bis-(2-carboxyethyl)-5 (and -6)-carboxyfluorescein (BCECF) was used to measure intracellular pH (pHi) in segments of rat resistance vessels (internal diameter about 200 ,tm) with the vessels mounted in a myograph for simultaneous measurements of isometric contraction.2. BCECF loaded slowly into the vessels over 1 h and did not affect the maximal contractility of the vessels. There was a loss of dye with time which, however, was very slow when the segments were only excited for 2 s/min, suggesting that the loss was mainly due to dye bleaching with only a very slow leak.3. The ratio of the emissions (at 540 nm) with excitation at 495 and 450 nm was calibrated in terms of pH using the K+-H+ ionophore nigericin. This calibration gave a pHi value of 7-15 +0'02 (n = 20), suggesting that hydrogen ions are not in electrochemical equilibrium in these vascular smooth muscles which have a membrane potential of about -60 mV.4. Addition of 10 mM-NH4Cl caused a transient alkalinization and wash-out of 10 mM-NH4Cl a transient acidification. Increasing CO2 with maintained bicarbonate caused a rapid acidification followed by an incomplete recovery. Removal of CO2 and bicarbonate (HEPES-buffered solution) with constant extracellular pH caused a transient alkalinization but steady-state pHi was not significantly altered.5. In bicarbonate-free buffer the Na+-H+ exchange blocker 5-(N-ethyl-Nisopropyl) amiloride (EIPA) and sodium-free conditions caused a slow acidification. In bicarbonate buffer (PSS) EIPA had no detectable effect after 10 min but the anion exchange blocker diisothio-cyanatostilbenedisulphonic acid (DIDS) caused a small acidification over that time course.6. The rate of recovery after an acid load was about 50 % lower in HEPES buffer compared to PSS and it was inhibited by EIPA. In PSS amiloride and EIPA each had a small inhibitory effect on the pH recovery after an acid load. DIDS also inhibited the recovery from an acid load in PSS and this effect was additive to that of EIPA. DIDS and EIPA also had additive inhibitory effects on the 22Na+ influx stimulated by the acid loading, while in HEPES buffer DIDS had no effect on either pH recovery or 22Na+ influx. These results suggest that a Na+-H+ exchange and an C. AALKJ?ER AND E. J. CRAGOE influx of bicarbonate coupled to sodium influx are of importance for pHi control in these vessels.7. Noradrenaline-induced contractions in HEPES buffer were associated with a fall in pHi while in PSS pHi was not significantly altered. Contraction induced by high-K+ solutions was associated with an acidification which was larger in HEPESbuffered solution than in PSS. The acidification in high-K+ solutions was only partly explained by the reduction of Na+. 8. These results suggest that the bicarbonate influx is of importance for maintaining pHi during a contraction and since pHi falls during a noradrenaline contraction in HEPES buffer they also suggest that a possible noradrenaline-induced resetting of the Na+-H+ exchange cannot prevent a fall in pH...

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Section: Ph and Isometric Contractionsmentioning

confidence: 99%

Intracellular pH regulation in resting and contracting segments of rat mesenteric resistance vessels.

Aalkjær

Cragoe

1988

The Journal of Physiology

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125

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“…The sodium metabolism was adjusted either by alterations of the sodium concentration of the bathing solution, or by exposing the vessels to ouabain. In all experiments, the ouabain concentration used was 1 rnM, this high concentration being necessary to obtain full inhibition of the Na-K pump in rat vessels (Garay et al, 1978;Aalkjaer and Mulvany, 1983). In some experiments, the results of altered sodium metabolism were investigated by testing the effects of drugs thought to interfere specifically with potential-dependent channels (Bolton, 1979) in the vascular smooth muscle membrane: felodipine (Bostrom et al, 1981;Nyborg and Mulvany, 1984) and methoxyverapamil (D600, Van Breemen and Siegel, 1980).…”

Section: T Petersenmentioning

confidence: 99%

“…The procedures used are presented in detail elsewhere (Aalkjaer and Mulvany, 1983). In brief, these were as follows.…”

Section: Sodium Metabolismmentioning

confidence: 99%

Intracellular sodium, membrane potential, and contractility of rat mesenteric small arteries.

Mulvany¹,

Aalkjær²,

Petersen³

1984

Circulation Research

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SUMMARY. We have investigated effects of altered extracellular sodium, intracellular sodium concentration, and membrane potential on the contractile responses of rat isolated mesenteric small arteries (internal diameter ca. 200 fim), when mounted as ring preparations on an isometric myograph. To avoid possible neural effects, all vessels were denervated in vitro using 6-hydroxydopamine. In unstimulated vessels, exposure to low-Na + solutions (25 mM sodium, sucrose, or choline-subsrituted) did not cause any response nor did exposure to ouabain (1 mM) for 1 hour [when intracellular sodium concentration increased to 64 mmol/(liter-cell)]. However, a response was obtained if ouabain-exposed vessels were subjected to low-sodium solutions (ca. 15% of maximal response). The magnitude of the response was dependent on the ratio of intracellular to extracellular sodium and was not inhibitable by the calcium blockers, felodipine (1 nM) or D600 (10 MM). This response could therefore be explained in terms of a Na-Ca exchange mechanism. The responses of activated vessels to ouabain and to low-sodium solutions were also investigated. The responses of vessels to submaximal doses of noradrenaline or potassium were potentiated acutely by ouabain (by 10-30% of the maximal response), even if the extracellular sodium was reduced to 25 mM. In all cases, the potentiation by ouabain was accompanied by a depolarization (3-12 mV). However, only in the case of noradrenaline-activated vessels with normal extracellular sodium was the potentiation accompanied by an increase in intracellular sodium [by ca. 7 mmol/(liter-cell)]. Moreover, the latter response was inhibited by felodipine and D600. The results suggest that Na-Ca exchange mechanisms may be present in these vessels but that they only play a role under extreme conditions; under normal conditions the effect of ouabain on activated vessels seems to be primarily due to its depolarizing effect, and not to its effect on intracellular sodium. (CircRes 54:740-749, 1984)

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“…A detailed description of determination of 22Na+-efflux has been given elsewhere (Aalkjaer & Mulvany, 1983). In brief, vessels were preincubated for 1 h in physiological salt solution, loaded in 22Na' salt solution for 30 min and then washed through a series of vials containing physiological salt solution at 370C.…”

Section: Na+-effluxmentioning

confidence: 99%

Atrial natriuretic factor causes specific relaxation of rat renal arcuate arteries

Aalkjær

Mulvany²,

Nyborg

1985

British J Pharmacology

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1 We have investigated the effect of a synthetic 'atrial natriuretic factor' (ANF) on induced tone in rat isolated renal arcuate arteries (lumen diameter ca. 250 Im), and compared this with the effects of synthetic ANF on resistance vessels of similar size taken from the mesenteric, femoral, cerebral and coronary vasculature. 2 Synthetic ANF was found to cause relaxation of the renal vessels when these were sub-maximally activated with K+, noradrenaline or 5-hydroxytryptamine, but had no effect on the responses of the other vessels to these agonists. Synthetic ANF had a near maximal effect (65% relaxation) at 100 nM, with an IC50 of 7.9 nm. The relaxant effect of synthetic ANF on the renal vessels was fully maintained for at least 15 min.3 Hydrallazine (100 gM) caused relaxation of renal vessels (47%) and coronary vessels (42%), but had no effect on the other vessel types. By contrast, sodium nitroprusside (1 gM) relaxed all vessel types.4 The relaxant action of synthetic ANF on the renal vessels was seen in the presence of ouabain (1 mM), propranolol (1 JM), phentolamine (1 LM), atropine (1 JM) and felodipine (1 nM). 5 In the renal vessels, synthetic ANF had no effect on membrane potential, measured with intracellular electrodes, despite the simultaneously measured relaxation.6 Synthetic ANF had no effect on the efflux of 22Na' in either renal or mesenteric vessels.7 The results demonstrate that synthetic ANF has a specific and prolonged relaxant effect on renal small arteries, and are consistent with this effect being mediated through specific receptors.

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Sodium metabolism in rat resistance vessels.

Cited by 29 publications

References 20 publications

Intracellular pH regulation in resting and contracting segments of rat mesenteric resistance vessels.

Intracellular pH regulation in resting and contracting segments of rat mesenteric resistance vessels.

Intracellular sodium, membrane potential, and contractility of rat mesenteric small arteries.

Atrial natriuretic factor causes specific relaxation of rat renal arcuate arteries

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