Regulation of cellular volume in rabbit ventricular myocytes: bumetanide, chlorothiazide, and ouabain

Drewnowska, K.; Baumgarten, Clive M.

doi:10.1152/ajpcell.1991.260.1.c122

Cited by 138 publications

(152 citation statements)

References 19 publications

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“…First, if BUM blocked CI-and K + efflux, it should increase cell volume. As shown here and previously (Clemo and Baumgarten, 1991a;Drewnowska and Baumgarten, 1991), BUM significantly decreased cell volume. Second, BUM decreases intracellular CI-activity (Baumgarten and Duncan, 1987;Liu et al, 1987).…”

Section: Does Cgmp Reduce Cell Volume By Inhibiting Na+/k+/2cl -Cotrasupporting

confidence: 91%

“…3 B). Previously we showed that the volume of rabbit myocytes remains stable in hypotonic solutions rather than THE JOURNAL OF GENERAL PHYSIOLOGY " VOLUME 100 " 1992 undergoing a regulatory volume decrease (Drewnowska and Baumgarten, 1991). To eliminate the chance that BUM-induced shrinkage prevented ANF's effect, the study was repeated in cells preswollen in 0.8T media for 10 min.…”

Section: Cgmp Blocks Na+ /K+ /2cl -Cotransportmentioning

confidence: 99%

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Modulation of rabbit ventricular cell volume and Na+/K+/2Cl- cotransport by cGMP and atrial natriuretic factor.

Clemo

Feher

Baumgarten

1992

The Journal of General Physiology

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Previously we showed that atrial natriuretic factor (ANF) decreases cardiac cell volume by inhibiting ion uptake by Na+/K+/2CI-cotransport. Digital video microscopy was used to study the role of guanosine 3',5'-monophosphate (cGMP) in this process in rabbit ventricular myocytes. Each cell served as its own control, and relative cell volumes (volumetest/volumeco,trol) were determined. Exposure to 10 IxM 8-bromo-cGMP (8-Br-cGMP) reversibly decreased cell volume to 0.892 -0.007; the EDs0 was 0.77 +-0.33 tzM. Activating guanylate cyclase with 100 IxM sodium nitroprusside also decreased cell volume to 0.889 ---0.009. In contrast, 8-bromo-adenosine 3',5'-monophosphate (8-Br-AMP; 0.01-100 tzM) neither altered cell volume directly nor modified the response to 8-Br-cGMP. The idea that cGMP decreases cell volume by inhibiting Na+/K+/2C1-cotransport was tested by blocking the cotransporter with 10 I~M bumetanide (BUM) and removing the transported ions. After BUM treatment, 10 IxM 8-Br-cGMP failed to decrease cell volume. Replacement of Na ÷ with N-methyl-D-glucamine or C1-with methanesulfonate also prevented 8-Br-cGMP from shrinking cells. The data suggest that 8-Br-cGMP, like ANF, decreases ventricular cell volume by inhibiting Na+/K+/2C1-cotransport. Evidence that ANF modulates cell volume via cGMP was also obtained. Pretreatment with 10 IzM 8-Br-cGMP prevented the effect of 1 IzM ANF on cell volume, and ANF suppressed 8-Br-cGMP-induced cell shrinkage. Inhibiting guanylate cyclase with the quinolinedione LY83583 (10 tzM) diminished ANF-induced cell shrinkage, and inhibiting cGMP-specific phosphodiesterase with M&B22948 (Zaprihast; 100 IzM) amplified the volume decrease caused by a low dose of ANF (0.01 I~M) approximately fivefold. In contrast, neither 100 I~M 8-Br-cAMP nor 50 tzM forskolin affected the response to ANF. The effects of ANF, LY83583, and M&B29948 on cGMP levels in isolated ventricular myocytes were confirmed by 125I-cGMP radioimmunoassay. These data argue that ANF shrinks cardiac cells by increasing intracellular cGMP, thereby inhibiting Na+/K+/2C1-cotransport. Basal cGMP levels also appear to modulate cell volume.

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Section: Does Cgmp Reduce Cell Volume By Inhibiting Na+/k+/2cl -Cotrasupporting

confidence: 91%

Section: Cgmp Blocks Na+ /K+ /2cl -Cotransportmentioning

confidence: 99%

Modulation of rabbit ventricular cell volume and Na+/K+/2Cl- cotransport by cGMP and atrial natriuretic factor.

Clemo

Feher

Baumgarten

1992

The Journal of General Physiology

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“…A combination of commercial (SigmaScan Pro, SPSS; Chicago, IL) and custom programs were used to determine cell width, length, and the planar area of the image. Changes in cell width and thickness are proportional (9). Taking each cell as its own control, relative cell volume was calculated as vol t/volc ϭ (areat ϫ widtht)/(areac ϫ widthc), where t and c refer to test (e.g., 0.6T) and control (1T) solutions, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…The calculated values are independent of assumptions regarding the geometric shape of the cross section of the myocyte as long as the shape does not change. These methods provide estimates of relative cell volume that are reproducible to Ͻ1% (7,9).…”

Section: Methodsmentioning

confidence: 99%

Biphasic effects of cell volume on excitation-contraction coupling in rabbit ventricular myocytes

Zhang

Satin

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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.-We studied the effects of osmotic swelling on the components of excitation-contraction coupling in ventricular myocytes. Myocyte volume rapidly increased 30% in hyposmotic (0.6T) solution and was constant thereafter. Cell shortening transiently increased 31% after 4 min in 0.6T but then decreased to 68% of control after 20 min. In parallel, the L-type Ca 2ϩ current (ICa-L) transiently increased 10% and then declined to 70% of control. Similar biphasic effects on shortening were observed under current clamp. In contrast, action potential duration was unchanged at 4 min but decreased to 72% of control after 20 min. Ca 2ϩ transients were measured with fura 2-AM. The emission ratio with excitation at 340 and 380 nm (f 340/f380) decreased by 12% after 3 min in 0.6T, whereas shortening and I Ca-L increased at the same time. After 8 min, shortening, I Ca-L, and the f340/f380 ratio decreased 28, 25, and 59%, respectively. The results suggest that osmotic swelling causes biphasic changes in I Ca-L that contribute to its biphasic effects on contraction. In addition, swelling initially appears to reduce the Ca 2ϩ transient initiated by a given ICa-L, and later, both I Ca-L and the Ca 2ϩ transient are inhibited.osmolarity; action potential duration; calcium current; calcium transient; cell shortening SWELLING OF CARDIAC MYOCYTES is a prominent aspect of the response to ischemia-reperfusion and elective cardioplegia and also may arise in renal insufficiency and syndromes with inappropriate secretion of antidiuretic hormone. Altered myocyte hydration has important functional consequences. Osmotic perturbations modulate both electrical activity (for reviews, see 34,38,42) and the ability of cardiac muscle to contract (5,16,17). Although facets of the contractile response to osmotic swelling are known from studies on multicellular preparations, little mechanistic information is available at the single cell level to explain the implications of myocyte swelling for excitation-contraction (E-C) coupling. Moreover, the effect of swelling on L-type Ca 2ϩ current (I Ca-L ), a critical aspect of E-C coupling, remains controversial. Under ruptured patch voltage-clamp conditions, for example, swelling is reported to enhance I Ca-L in rabbit atrial and sinoatrial node cells (22), depress I Ca-L in rat ventricular cells (4), and to have no significant effect in guinea pig (13, 31) and canine (44) ventricular cells. A swelling-induced enhancement of I Ca-L also has been claimed based on fura 2 measurements of diltiazem-sensitive Ca 2ϩ influx (36). It is unclear whether these differences in the response of I Ca-L to myocyte swelling arise from species differences or from methodological issues, such as the composition of the patch pipette solution, the effectiveness of cell dialysis, or the variable extent of myocyte swelling under ruptured-patch conditions (6, 33). Several other species differences in E-C coupling, including the sensitivity of contraction to inhibition of the sarcoplasmic reticulum (SR), are well known (2).The present stu...

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“…In contrast to APD, the mechanism of hypoxic cell swelling is not completely understood. Although the ATP-dependent Na + /K + pump was suppressed on incubation with 1 μM ouabain, no significant change occurred in the cell volume of rabbit ventricular cells (5). A recent report revealed that the coordinated action of the ATP-dependent plasma membrane calcium pump and Na + /Ca 2+ exchanger substitutes for the Na + /K + pump in extruding Na + from the cells during ouabain exposure (16).…”

mentioning

confidence: 98%

OSU-03012, a novel celecoxib derivative, induces cell swelling and shortens action potential duration in mouse ventricular cells

Yamamoto¹,

Iyoda²,

Kita³

et al. 2010

Biomed. Res.

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OSU03012, a novel celecoxib derivative, has been shown to inhibit proliferation and induce apoptosis in numerous cancer cell lines. However, not much is known about its influence on cell volume regulation and cardiac function in the mammalian heart. We examined the effects of OSU-03012 on cell volume and action potentials in mouse ventricular cells. Video image analysis showed that cell volume increased on application of OSU-03012 in a dose-dependent manner. The action potential duration (APD) at 50% and 90% repolarization (APD 50 and APD 90 respectively) as well as the resting membrane potential (RMP) were measured in current-clamp experiments. OSU-03012 had little effect on APD 50 and RMP but induced approximately 30% shortening of APD 90 . These results for cell volume and AP are similar to those in cells under ischaemia/hypoxia, and we confirmed that the shortening of APD 90 was almost completely recovered by glibenclamide, a potent inhibitor of ATP-sensitive potassium channels. We concluded that OSU-03012 may lead to cell swelling and shortening of AP via reduced ATP production in mouse ventricular cells.OSU-03012 has been shown to be a potent phosphoinositide-dependent kinase-1 (PDK1) inhibitor derived from the selective cyclooxygenase-2 (COX-2) inhibitor celecoxib, but it does not possess COX-2 inhibitory activity (10,22). Celecoxib is used for preventing an increase in the number of cancer cells, which may be due to moderate apoptosis through blocking of PDK1/Akt signalling (22). OSU-03012 was shown to be a more potent inhibitor of cancer cell growth than celecoxib, and it inhibited both recombinant PDK1 activity and PC-3 cell viability with IC 50 values of about 5 μM (22). This new compound is currently undergoing preclinical development under the Rapid Access to Intervention Development Program at the National Cancer Institute. Until date, several mechanisms have been reported for OSO-03012-induced cell death. Zhang et al. (21) showed that the loss of mitochondrial membrane potential may be involved in OSU-03012-induced cell death in multiple myeloma cells. Furthermore, genomic inhibition of PDK1 was reported to suppress cardiac functions in the mouse heart (3, 8, 11), however, severe cardiac side effects of OSU-03012 were not reported at blood concentrations below 20 μM (6, 15). To our knowledge, information on direct effects of OSU-03012 on cardiac function is absent. In the present study, we examined the effect of OSU-03012 on cardiac cell volume and action potential (AP) in an attempt to elucidate the effect of this compound on cardiac function. Fukuoka University Animal Care and Use Committee approved the use and treatment of all animals included in the experiments described here. Single ventricular cells from mice (18-25 g, C-57BL/6J/ black inbred, male) anaesthetised with sodium pentobarbitone (50 mg/mL, I.P.) were isolated by an enzymatic dispersion technique (20). The stock and A two-tailed probability of < 0.05 indicated statistical significance. Figure 1A and B represent typical vi...

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Regulation of cellular volume in rabbit ventricular myocytes: bumetanide, chlorothiazide, and ouabain

Cited by 138 publications

References 19 publications

Modulation of rabbit ventricular cell volume and Na+/K+/2Cl- cotransport by cGMP and atrial natriuretic factor.

Modulation of rabbit ventricular cell volume and Na+/K+/2Cl- cotransport by cGMP and atrial natriuretic factor.

Biphasic effects of cell volume on excitation-contraction coupling in rabbit ventricular myocytes

OSU-03012, a novel celecoxib derivative, induces cell swelling and shortens action potential duration in mouse ventricular cells

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