Effect of catecholamines on Na/H exchange in vascular smooth muscle cells.

Owen, N. E.

doi:10.1083/jcb.103.5.2053

Cited by 44 publications

(14 citation statements)

References 26 publications

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“…This increased wall to lumen ratio could itself sustain hypertension [33]. Vascular agonists such as angiotensin II and catecholamines and growth factors such as epidermal growth factor and platelet derived growth factor could not only stimulate Na+/H + antiport activity but also act as trophic stimuli for vascular smooth muscle cells [34,35]. Further support for this notion comes from the increased smooth muscle cellular proliferation when cells are isolated from blood vessels of spontaneously hypertensive rats [37] and increased thymidine incorporation in blood vessels in vivo even in the pre-hypertensive stage [38].…”

Section: Discussionmentioning

confidence: 99%

Leucocyte Na+/H+ antiport activity in Type 1 (insulin-dependent) diabetic patients with nephropathy

Simmons²,

Frighi³

et al. 1990

Diabetologia

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Section: Discussionmentioning

confidence: 99%

Leucocyte Na+/H+ antiport activity in Type 1 (insulin-dependent) diabetic patients with nephropathy

Simmons²,

Frighi³

et al. 1990

Diabetologia

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“…Angiotensin II and norepinephrine have been demonstrated to stimulate Na+-H+ exchange and elevate intracellular pH in vitro. 55,56 Endothelin has also been demonstrated to cause intracellular alkalinization. 57 The results of the present study suggest that intracellular alkalinization could elevate cytosolic calcium indirectly, by inhibiting calcium sequestration.…”

Section: Calcium Sequestrationmentioning

confidence: 99%

H(+)-induced vasodilation of rat aorta is mediated by alterations in intracellular calcium sequestration.

Loutzenhiser

Matsumoto

Okawa

et al. 1990

Circulation Research

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Acidosis induces vasodilation both in vivo and in vitro. Although it is commonly surmised that acidosis alters contractility by affecting contractile proteins and calcium entry, the exact role of these mechanisms in acidosis-induced vasodilation has not been determined. In the present study, we demonstrated that a novel mechanism, involving increased calcium sequestration into intracellular sites sensitive to norepinephrine, mediates the vasodilation associated with relatively modest decreases in pH. The effects of changing pH from 7.4 to 7.0 on tension development, 45Ca fluxes, and the norepinephrine-releasable intracellular calcium stores were studied in isolated rat aorta. Acute acidification produced marked endothelium-independent dilations of aortic rings that had been precontracted with norepinephrine. In contrast, this maneuver had only modest effects on contractions elicited by 80 mM KCI or phorbol ester. Acidification in this range did not alter basal or norepinephrine-stimulated unidirectional 45Ca influx, nor did it reduce the norepinephrine-induced net gain in 45Ca content. Furthermore, neither norepinephrine-stimulated 45Ca efflux nor the peak contractile response to norepinephrine in calcium-free buffer was affected, although in this setting, the duration of the phasic contractile response was shortened. When calcium was restored to tissues exposed to norepinephrine in calcium-free buffer, acidification slowed the rate of tension development without altering 45Ca uptake, thus changing the relation between tension development and calcium entry. These effects of acidification were shown to be associated with an increase in the amount of calcium sequestered into the norepinephrine-sensitive intracellular calcium store. These findings clearly indicate that acidification, within a range that has no effect on other aspects of smooth muscle activation, elicits vasodilation by stimulating intracellular calcium sequestration. This action may represent a predominant mechanism whereby acidosis alters vascular smooth muscle contractility. (Circulation Research 1990;67:426-439) Several lines of evidence suggest that a decrease in pH is associated with a decrease in vascular smooth muscle tone. Severe acidosis is often accompanied by a decreased pressor response to catecholamines."2 Furthermore, the external application of CO2 is known to produce local vasodilation,34 presumably by increasing tissue PCO2.' Similarly, in vitro studies indicate that the contractile response of blood vessels is reduced if the pH of the

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“…The information on the control of pHi in vascular smooth muscles (VSM) has been obtained from studies of cultured smooth muscle cells from large arteries (Smith & Brock, 1983;Owen, 1986;Weissberg et al 1987), while the regulation of and importance of pHi of VSM in situ in small arteries (with internal diameters of about 200,um), which take part in the control of peripheral resistance, are not known.…”

mentioning

confidence: 99%

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

Aalkjær

Cragoe

1988

The Journal of Physiology

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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Effect of catecholamines on Na/H exchange in vascular smooth muscle cells.

Cited by 44 publications

References 26 publications

Leucocyte Na+/H+ antiport activity in Type 1 (insulin-dependent) diabetic patients with nephropathy

Leucocyte Na+/H+ antiport activity in Type 1 (insulin-dependent) diabetic patients with nephropathy

H(+)-induced vasodilation of rat aorta is mediated by alterations in intracellular calcium sequestration.

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

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