Smoke composition and predicting relationships for international commercial cigarettes smoked with three machine-smoking conditions.

The study objectives were to determine the effects of smoking machine puffing parameters on mainstream smoke composition and to express those effects as predicting relationships. Forty-eight commercial Philip Morris USA and Philip Morris International cigarettes from international markets and the 1R4F reference cigarette were machine-smoked using smoking conditions defined by the International Organization of Standardization (ISO), the Massachusetts Department of Public Health (MDPH), and Health Canada (HC). Cigarette tobacco fillers were analyzed for nitrate, nicotine, tobacco-specific nitrosamines (TSNA), and ammonia. Mainstream yields for tar and 44 individual smoke constituents and "smoke pH" were determined. Cigarette constituent yields typically increased in the order ISO

Mainstream smoke constituent yields and predicting relationships from a worldwide market sample of cigarette brands: ISO smoking conditions.

The study objective is evaluation of a benchmark approach for predicting mainstream smoke constituent machine-yields for conventional cigarette brands from worldwide markets. Results for ISO smoke yields support the validity of benchmarking when brands, for which yields are to be predicted, have design characteristics within boundaries established by the exploratory brands. Yields of ISO-method mainstream smoke constituents were generally well described by weighted least squares regression relationships with ISO tar (R2>0.80 and coefficient p values <0.05). The impact of the varied chemical composition of cigarette tobaccos from different regions on smoke constituent yields was recognized. Mainstream smoke nitrogen oxides and tobacco-specific nitrosamine (TSNA) yield prediction relationships improved by including tobacco nitrate or TSNA concentration factors in respective independent parameters. For carbon-filter brands, inclusion of a carbon factor improved the predicting relationships for several vapor-phase constituents. Relationships were validated with a subset of additional validation brands. Greater than 90% of the validation brands' smoke chemistry yields were within the 95% prediction intervals. Average differences between measured and predicted yields were generally within the range of one to two measurement standard deviations. The estimation methods proposed relate to machine-smoking conditions and are not intended to reflect the actual exposure of any given consumer to smoke constituents.

Differences in K+ current components in mesenteric artery myocytes from WKY and SHR.

Previous studies have documented increased K+ permeability of arterial smooth muscle in hypertension and suggested a role in altered arterial contractile function. To characterize the mechanisms responsible for these alterations, we determined the contribution of K+ current (IK) components to whole cell IK in freshly dispersed myocytes and tetraethylammonium (TEA)-induced contractile responses in mesenteric arteries of Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Tetraethylammonium produced a larger tonic contractile response in SHR with a lower threshold compared to WKY (ie, 0.1 v 1 mmol/L), which was due in part to the larger Ca2+ current in SHR. Whole cell IK recorded by perforated patch methods was similar at a holding potential (HP) of -60 mV (IK60), but were larger in SHR when recorded from a HP of -20 mV (IK20). The selective blocker iberiotoxin (IbTX) was used to separate the contribution of voltage- (Kv) and calcium-dependent (KCa) components of IK60. The IK60 and IK20 component inhibited by 100 nmol/L IbTX (ie, KCa) was larger in SHR than in WKY myocytes, whereas the IbTX-insensitive IK60 component (ie, Kv) was larger in WKY. In the presence of IbTX, 1 and 10 mmol/L TEA inhibited a larger fraction of IK60 in SHR myocytes compared with WKY. The activation properties of the TEA-sensitive and TEA-insensitive Kv components determined by fitting a Boltzmann activation function to the current-voltage data, exhibited both group and treatment differences in the half maximal activation voltage (V0.5). The V0.5 of the TEA-sensitive Kv component was more positive than that of the TEA-insensitive component in both groups, and values for the V0.5 of both TEA-sensitive and TEA-insensitive components were more negative in SHR than WKY. These results show that SHR myocytes have larger KCa and smaller Kv current components compared with WKY. Furthermore, SHR myocytes have a larger TEA-sensitive Kv component. These differences may contribute to the differences in TEA contractions, resting membrane potential, Ca2+ influx, and KCa current reported in hypertensive arteries.

Differential expression of voltage-gated K(+) channel genes in arteries from spontaneously hypertensive and Wistar-Kyoto rats.

Voltage-gated K(+) currents play an important role in determining membrane potential, intracellular Ca(2+), and contraction in arterial smooth muscle. In this study, the expression of genes encoding voltage-gated K(+) channels of the Kv1.X family was compared in arteries from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Expression of Kv1.X in thoracic aorta, mesenteric arteries, tail artery, and heart was determined, both qualitatively and quantitatively, by reverse transcription-polymerase chain reaction. Our results demonstrate distinct but overlapping patterns of expression in vascular tissues. In general, Kv1.2 and Kv1.5 were most highly represented, and the levels of Kv1.2 were significantly larger in all tissues from SHR. Levels of Kv1.5 in arteries did not differ significantly between strains but were greater in SHR heart. Moderate levels of Kv1.3 and Kvbeta1.1 expression were also found in all tissues and were larger in SHR. Kv1.1 expression was not different between the 2 strains, and no significant expression of Kv1.4 (except in heart and aorta), Kv1.6, or Kvbeta2.1 was observed in either strain. Kv1.2 and Kv1.5 transcripts represent approximately 1 to 2 parts/10(5) of total mesenteric arterial RNA with approximately 2- to 5-fold lower levels in aorta and tail artery. Whole-cell voltage-gated K(+) channel currents, recorded from mesenteric arterial myocytes, were larger in SHR than WKY (eg, at 0 mV: 7.3+/-0.8 versus 10.9+/-1.2 pA/pF). The voltage dependence of activation was more negative in SHR (V(0.5): -20+/-4 mV versus -32+/-3 mV) but that of availability was not different. These results indicate that Kv1.X genes are differentially expressed between WKY and SHR (especially Kv1.2 and Kvbeta1.1). These differences in gene expression are associated with a greater voltage-gated K(+) channel current density in SHR and shifted voltage-dependent activation compared with WKY. These differences may be a compensatory mechanism related to the membrane potential depolarization in SHR or some manifestation thereof.

Effect of exercise and medium-chain fatty acids on postprandial lipemia.

The purpose of this study was to evaluate the effect of medium-chain triglycerides (MCT) with and without exercise on postprandial lipemia (PPL). Subjects were 25 young men and women. Each subject performed three trials: 1) control (fat meal only, 1.5 g fat/kg) 2) MCT (substitution of MCT oil, 30% of fat calories), and 3) MCT + Ex (exercise 12 h before the MCT meal). Before each trial, the subject underwent consistent dietary preparation. Blood was collected on 2 separate days for baseline measurements of postheparin lipases and, in each trial, at 0 h (premeal), at 2, 4, 6, and 8 h after the fat meal for triglycerides and cholesterol ester transfer protein (CETP), and at 8 h for postheparin lipoprotein lipase (LPL) and hepatic lipase activities (HL). ANOVA indicated that the partial substitution of MCT oil to the fat meal did not affect the PPL response. However, the PPL was significantly lower after the MCT + Ex trial vs. the other trials. LPL activity was significantly elevated after all trials compared with baseline, whereas HL was lower in the MCT + Ex trial only. CETP mass was significantly lower at 4 and 8 h than 0 h during all trials but relatively higher in the MCT + Ex trial vs. the nonexercise trials. These results suggest that MCT does not affect the TG response to a fat meal. LPL and CETP are affected by a fat meal with or without exercise, but HL is affected only when exercise is included.

Effects of exercise and n-3 fatty acids on postprandial lipemia.

Because n-3 fatty acid ingestion and aerobic exercise each has been associated with diminished postprandial lipemia (PPL), the purpose of this study was to evaluate the effect of a combination of these two factors on PPL. Sedentary men underwent a standard dietary preparation, including a 12-h fast before each trial. Six subjects performed a control trial (fat meal, 100 g fat) and an n-3 fatty acid trial (fat meal after 3 wk of n-3 fatty acid supplementation at 4 g/day). In a parallel experiment, six different subjects underwent a control trial and n-3 fatty acid supplementation + 60 min of exercise before ingestion of the fat meal. Supplementation with n-3 fatty acid significantly decreased baseline triglyceride (TG) concentrations but did not significantly affect PPL. The combination of n-3 fatty acid and exercise had no effect on the postprandial TG response. The present study suggests that n-3 fatty acid supplementation lowers resting TG concentrations but inhibits the beneficial effect of aerobic exercise on the postprandial TG response.

Interaction of charybdotoxin S10A with single maxi-K channels: kinetics of blockade depend on the presence of the beta 1 subunit.

The maxi-K channel from bovine aortic smooth muscle consists of a pore-forming alpha subunit and a regulatory beta1 subunit that modifies the biophysical and pharmacological properties of the alpha subunit. In the present study, we examine ChTX-S10A blocking kinetics of single maxi-K channels in planar lipid bilayers from smooth muscle or from tsA-201 cells transiently transfected with either alpha or alpha+beta 1 subunits. Under low external ionic strength conditions, maxi-K channels from smooth muscle showed ChTX-S10A block times, 48 +/- 12 s, that were similar to those expressing alpha+beta 1 subunits, 51 +/- 16 s. In contrast, with the alpha subunit alone, ChTX-S10A block times were much shorter, 5 +/- 0.6 s, and were qualitatively similar to previously reported values for the skeletal muscle maxi-K channel. Increasing the external ionic strength caused a decrease in ChTX-S10A block times for maxi-K channel complexes of alpha+beta 1 subunits but not of alpha subunits alone. These findings indicate that it may be possible to predict the association of beta 1 subunits with native maxi-K channels by monitoring the kinetics of ChTX blockade of single channels, and they suggest that maxi-K channels in skeletal muscle do not contain a beta 1 subunit like the one present in smooth muscle. To further test this hypothesis, we examined the binding and cross-linking properties of [(125)I]-IbTX-D19Y/Y36F to both bovine smooth muscle and rabbit skeletal muscle membranes. [(125)I]-IbTX-D19Y/Y36F binds to rabbit skeletal muscle membranes with the same affinity as it does to smooth muscle membranes. However, specific cross-linking of [(125)I]-IbTX-D19Y/Y36F was observed into the beta 1 subunit of smooth muscle but not in skeletal muscle. Taken together, these data suggest that studies of ChTX block of single maxi-K channels provide an approach for characterizing structural and functional features of the alpha/beta 1 interaction.

Ca(2+) influx inhibits voltage-dependent and augments Ca(2+)-dependent K(+) currents in arterial myocytes.

These experiments were performed to determine the effects of reducing Ca(2+) influx (Ca(in)) on K(+) currents (I(K)) in myocytes from rat small mesenteric arteries by 1) adding external Cd(2+) or 2) lowering external Ca(2+) to 0.2 mM. When measured from a holding potential (HP) of -20 mV (I(K20)), decreasing Ca(in) decreased I(K) at voltages where it was active (>0 mV). When measured from a HP of -60 mV (I(K60)), decreasing Ca(in) increased I(K) at voltages between -30 and +20 mV but decreased I(K) at voltages above +40 mV. Difference currents (DeltaI(K)) were determined by digital subtraction of currents recorded under control conditions from those obtained when Ca(in) was decreased. At test voltages up to 0 mV, DeltaI(K60) exhibited kinetics similar to control I(K60), with rapid activation to a peak followed by slow inactivation. At 0 mV, peak DeltaI(K60) averaged 75 +/- 13 pA (n = 8) with Cd(2+) and 120 +/- 20 pA (n = 9) with low Ca(2+) concentration. At test voltages from 0 to +60 mV, DeltaI(K60) always had an early positive peak phase, but its apparent "inactivation" increased with voltage and its steady value became negative above +20 mV. At +60 mV, the initial peak DeltaI(K60) averaged 115 +/- 18 pA with Cd(2+) and 187 +/- 34 pA with low Ca(2+). With 10 mM pipette BAPTA, Cd(2+) produced a small inhibition of I(K20) but still increased I(K60) between -30 and +10 mV. In Ca(2+)-free external solution, Cd(2+) only decreased both I(K20) and I(K60). In the presence of iberiotoxin (100 nM) to inhibit Ca(2+)-activated K(+) channels (K(Ca)), Cd(2+) increased I(K60) at all voltages positive to -30 mV while BAY K 8644 (1 microM) decreased I(K60). These results suggest that Ca(in), through L-type Ca(2+) channels and perhaps other pathways, increases K(Ca) (i.e., I(K20)) and decreases voltage-dependent K(+) currents in this tissue. This effect could contribute to membrane depolarization and force maintenance.

Order of scale administration and concurrent validity of the Anxiety Rating Scale.

The Anxiety Rating Scale-2 and the Competitive State Anxiety Inventory-2 were administered to 100 male university intramural volleyball players 15 min. before a match began. For 50 participants, the above order of presentation was used; for the other 50 the order was reversed. Correlations for cognitive anxiety, somatic anxiety, and self-confidence between the two inventories were .47, .63, and .67, respectively, for scores from Order 1 and .56, .75, and .84 for Order 2.

Voltage-gated sodium channels in human aortic smooth muscle cells.

Whole-cell, voltage clamp methods were used to study inward currents in human aortic smooth muscle cells in culture. Cells were plated on glass coverslips, cultured in supplemented M-199 media with 5% serum and studied as primary cells and at passages 2-5. Inward currents were measured with a pipette solution containing Cs+ and TEA+ to block K+ currents and with 2.5 mM [Ca2+]0 in the perfusate. Inward currents activated at about -50 mV, peaked at about -15 mV and reversed at about +30 mV. Values of peak inward current averaged 14. 7 +/- 3.3 pA/pF and cell capacitance averaged 124 +/- 10 pF (n = 35). These currents activated rapidly with a time-to-peak current of 2.4 +/- 0.3 ms at a test potential of -10 mV from a holding potential of -80 mV. The current also inactivated rapidly with a time course that could be described by two components with time constants of 1.8 +/- 0.2 and 17.8 +/- 3.5 ms at -10 mV. The currents decreased when extracellular Na+ was reduced and were completely inhibited by 50 nM tetrodotoxin (TTX), suggesting that they represented voltage-gated Na+ currents (INa). Activation curves were characterized with a V0.5 = -16.6 +/- 2.4 mV and a slope factor k = -5.2 +/- 0.2 mV while inactivation curves were characterized with a V0.5 = -60.9 +/- 1.7 mV and a slope factor k = 8.8 +/- 0.4 mV. Lowering external [Ca2+] to zero increased the maximum INa, shifted its voltage dependence in the hyperpolarizing direction and increased the rate of INa inactivation. Increasing external [Ca2+] or [Mg2+]decreased INa and slowed its rate of inactivation. These studies demonstrate the presence of voltage-gated Na+ channels with high TTX sensitivity that are modulated by extracellular divalent cations in human aortic smooth muscle cells maintained in cell culture. Window currents were found in the voltage range of -50 to -20 mV, suggesting that these channels could contribute to the resting membrane potential.

Sex, sport, situation, and competitive state anxiety.

Within a multivariate design, the relationship between sex, sport, and competitive situation with state anxiety was examined. The Competitive State Anxiety Inventory-2 was administered to selected intramural basketball and volleyball teams (ns = 266 and 226) prior to round-robin and play-off competition. Multivariate analysis of variance yielded a significant interaction of sport by sex and a significant main effect for sport. Follow-up tests indicated that basketball players scored higher somatic and cognitive state anxiety than volleyball players. Women scored higher on somatic and cognitive state anxiety than men prior to play-off games. Results are discussed in terms of importance of a multivariate approach to studying competitive anxiety.

Augmented contributions of voltage-gated Ca2+ channels to contractile responses in spontaneously hypertensive rat mesenteric arteries.

The observation that organic Ca2+ channel blockers are more effective in lowering blood pressure and peripheral resistance in hypertensive compared to normotensive subjects suggests that there is a greater contribution from voltage-gated Ca2+ channels (CaL) to vascular force maintenance in hypertensive arteries. This study tests this hypothesis by comparing the effects of Bay k 8644 and nisoldipine on basal force development, contractile responses to norepinephrine and serotonin, and Ca2+ currents (ICa) in mesenteric artery (MA) from Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). MA rings were used to record isometric contractions at Lmax. Single cells were isolated by collagenase plus elastase for measurement of CaL properties by patch-clamp methods. Contractile responses to Bay k 8644 were larger and more sensitive in SHR than WKY, and were larger in endothelium-denuded compared to intact rings. In SHR, the addition of 10 nmol/L Bay k 8644 increased contractile sensitivity to norepinephrine (NE) and serotonin (5HT), and increased maximum response to 5HT. In WKY, 10 nmol/L Bay k 8644 produced a small increase in 5HT sensitivity with no effect on maximum response, and had no effect on NE responses. In the presence of 1 mumol/L nisoldipine, the maximum response and the sensitivity to both NE and 5HT were decreased in both WKY and SHR with the inhibitory effects of nisoldipine being larger in SHR than WKY. Peak ICa was larger in SHR, and current-voltage curves were shifted toward more negative voltages compared to WKY. Bay k 8644 increased ICa in both WKY and SHR myocytes with no apparent difference in the magnitude of its effect when expressed as a percent of control ICa. These results suggest that CaL contribute significantly to tonic force maintenance as well as to agonist responses in MA from both WKY and SHR, but with a much larger contribution in SHR. Differences in the sensitivity of CaL to Bay k 8644 were not responsible for the differences in contractile responses to this agonist.

Effects of age on Ca2+ currents in small mesenteric artery myocytes from Wistar-Kyoto and spontaneously hypertensive rats.

The purpose of this study was to test the hypothesis that differences in voltage-gated Ca2+ channels increase with age during the development of sustained hypertension in the spontaneously hypertensive rat (SHR). Using patch-clamp methods, we measured whole-cell Ca2+ currents in freshly isolated myocytes from small mesenteric arteries of juvenile (5 to 7 weeks), young (10 to 12 weeks), and mature (19 to 23 weeks) Wistar-Kyoto rats (WKY) and SHR. Indirect tail artery systolic pressure increased progressively with age in SHR (from 125 +/- 5 to 159 +/- 5 to 192 +/- 5 mm Hg) but only in the younger WKY (from 107 +/- 6 to 130 +/- 4 to 136 +/- 4 mm Hg). Peak Ca2+ current density (current per cell capacitance) was larger in SHR than WKY myocytes at all ages (at 6 weeks, 3.5 +/- 0.4 versus 2.3 +/- 0.2 pA/pF; at 12 weeks, 3.8 +/- 0.2 versus 3.1 +/- 0.2; at 20 weeks. 4.9 +/- 0.4 versus 3.3 +/- 0.4). Cell capacitance (surface area) was significantly smaller in 12-week-old SHR than WKY (25.2 +/- 1.1 versus 31.8 +/- 1.6 pF), but no differences were found in the 6- or 20-week-old groups. There were significant differences in Ca2+ current with strain, age, and voltage but no significant age-strain interactions. The ratio of peak Ca2+ current for SHR to that of WKY declined linearly with voltage at all ages suggesting differences in the voltage dependence of Ca2+ current activation. The voltage dependence of Ca2+ current was shifted to the left in SHR compared with WKY at all ages. Activation curves were shifted significantly in the negative-voltage direction only in 20-week-old SHR myocytes. We have found differences with age in Ca2+ current density and its voltage dependence in SHR compared with WKY during the phase of development in which blood pressure becomes established in the SHR. The net effect of these differences predicts a larger Ca2+ current in SHR at voltages in the physiological range of membrane potential.

NH2-terminal-inserted myosin II heavy chain is expressed in smooth muscle of small muscular arteries.

We demonstrate, using reverse transcriptase-polymerase chain reaction, that, whereas abdominal aorta from rabbit consists almost entirely of myosin heavy chain (MHC) mRNA with no insert at the 5'-terminal coding region, the distributing arteries (femoral and saphenous) begin to show MHC mRNA with the 21-nucleotide insert that encodes seven amino acids in the ATP-binding region located in the myosin head. The femoral/iliac artery contains > 50% inserted mRNA, whereas the more distal saphenous artery contains > 80% inserted mRNA. This insert is also present in the smooth muscle from rat tail artery but is absent in the smooth muscle from rat aorta. The actin-activated ATPase activity of myosin from the rabbit femoral/saphenous artery is 1.7-fold higher than that of the myosin from the aorta. A concomitant increase (about twofold) in the maximum shortening velocity of the saphenous artery, compared with that of the aorta, indicates that the preponderance of the inserted myosin is associated with both an increase in the actin-activated ATPase activity and a larger maximum velocity of shortening. Furthermore, analysis of the 17-kDa essential light chain from the aorta reveals near equal quantities of the 17-kDa light chain isoforms a and b, whereas the myosin from the femoral/ saphenous artery contains predominantly the 17-kDa light chain a isoform. Together, these data indicate that the smooth muscle cells from the small distributing arteries are similar to those of visceral smooth muscle with respect to the expression of myosin isoforms, actin-activated myosin ATPase activity and contractility.

Transcendence and imminence in psychotherapy.

The traditional dilemma of the compatibility of religion and psychotherapy is discussed within the context of maturing beyond the language and behavior of the imminent, i.e., the here-and-now. Transcendence is presented as a model for therapist and therapeutic methodology.

Comparison of K+ channel properties in freshly isolated myocytes from thoracic aorta of WKY and SHR.

Altered function of smooth muscle cell K+ channels have been reported in hypertension, but the contribution of various K+ channel types to these changes has not been completely determined. The purpose of this study was to compare the contribution of K+ channel types to whole cell K+ currents recorded from isolated thoracic aorta myocytes of 13 to 15 week old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Cells were isolated by collagenase and elastase digestion, and K+ currents recorded using whole cell voltage clamp methods at room temperature. Cells were superfused with a solution containing (in mmol/ L) 140 NaCl, 5 KCl, 2 CaCl2, 1 MgCl2, 10 HEPES, and 10 glucose. Pipettes were filled with a solution containing (in mmol/L) 120 KCl, 5 NaCl, 5 MgATP, 20 HEPES, and 10 BAPTA. The K+ currents (IK) recorded from a holding potential (HP) of -80 mV were smaller in the SHR compared to those in WKY (for example, at 20 mV: WKY = 6.1 +/- 0.6 pA/pF and SHR = 3.7 +/- 0.2 pA/pF). Values of cell capacitance were not different between the two groups (WKY = 25.2 +/- 3.2 pF and SHR = 26.6 +/- 1.9 pF). A component of IK inhibited by voltage (Kv) over the range from -80 to -20 mV was smaller in SHR. The voltage dependence of Kv availability and activation were not significantly different between the two groups. IK recorded from a HP = -20 mV (KCa) was not different between the two groups. Difference currents calculated from IK measured at HP of -80 and -20 mV (that is, Kv) were smaller in SHR as was the fraction of IK inhibited by 4-aminopyridine. These results suggest that under conditions of low intracellular [Ca2+] there are no differences in KCa currents, but the Kv currents are smaller in SHR. Inhibition of Kv by 4-aminopyridine (0.1 to 10 mmol/L) caused larger increases in basal tone in WKY aorta. These results suggest that Kv channels contribute to resting K+ conductance in both WKY and SHR aorta, but with a relatively larger contribution in the WKY.

Augmented calcium currents in mesenteric artery branches of the spontaneously hypertensive rat.

The greater efficacy of organic channel blockers in lowering peripheral resistance and blood pressure in hypertensive subjects has been suggested to be the result of augmented calcium influx through L-type calcium channels in arterial smooth muscle. These studies were performed to determine whether differences exist in voltage-gated calcium channels of mesenteric artery branches from 20-week-old spontaneously hypertensive rats (SHR) compared with Wistar-Kyoto rats (WKY). Single myocytes were acutely isolated by collagenase and elastase treatment and studied at room temperature (approximately 20 degrees C) with the use of whole-cell, patch-clamp methods. Maximum values of calcium current measured at 0 mV from a holding potential of -90 mV were larger in SHR myocytes (105 +/- 11 versus 149 +/- 15 pA). Values of cell capacitance were smaller in SHR (29.5 +/- 1.3 pF) compared with WKY (35.0 +/- 1.5 pF) myocytes. Cell capacitance measures surface membrane area and, when used to normalize calcium currents, magnified the difference between WKY and SHR to approximately 47%. There was a larger percent reduction of maximum calcium current at holding potentials of -60 and -40 mV in SHR compared with WKY myocytes: for example, at -40 mV calcium current was reduced from values at -90 mV by -73 +/- 2% in SHR compared with -58 +/- 1% in WKY. When divided by the maximum current for each holding potential, the voltage dependence of normalized calcium currents for the two groups was completely superimposed. Difference currents were calculated by subtracting currents measured from holding potentials of -90 and -40 mV. The voltage dependence of difference currents was identical to that of the calcium currents measured from the two values of holding potential.(ABSTRACT TRUNCATED AT 250 WORDS)