scholarly journals Voltage-gated divalent currents in descending vasa recta pericytes

2010 ◽  
Vol 299 (4) ◽  
pp. F862-F871 ◽  
Author(s):  
Zhong Zhang ◽  
Hai Lin ◽  
Chunhua Cao ◽  
Sandeep Khurana ◽  
Thomas L. Pallone
Keyword(s):  
Charge Carrier ◽  
Charge Carriers ◽  
Slow Inactivation ◽  
Ang Ii ◽  
Patch Clamp Technique ◽  
Voltage Gated ◽  
Vasa Recta ◽  
Maximal Activation ◽  
Voltage Dependent ◽  
Glomerular Arterioles

Multiple voltage-gated Ca2+ channel (CaV) subtypes have been reported to participate in control of the juxtamedullary glomerular arterioles of the kidney. Using the patch-clamp technique, we examined whole cell CaV currents of pericytes that contract descending vasa recta (DVR). The dihydropyridine CaV agonist FPL64176 (FPL) stimulated inward Ca2+ and Ba2+ currents that activated with threshold depolarizations to −40 mV and maximized between −20 and −10 mV. These currents were blocked by nifedipine (1 μM) and Ni2+ (100 and 1,000 μM), exhibited slow inactivation, and conducted Ba2+ > Ca2+ at a ratio of 2.3:1, consistent with “long-lasting” L-type CaV. In FPL, with 1 mM Ca2+ as charge carrier, Boltzmann fits yielded half-maximal activation potential ( V1/2) and slope factors of −57.9 mV and 11.0 for inactivation and −33.3 mV and 4.4 for activation. In the absence of FPL stimulation, higher concentrations of divalent charge carriers were needed to measure basal currents. In 10 mM Ba2+, pericyte CaV currents activated with threshold depolarizations to −30 mV, were blocked by nifedipine, exhibited voltage-dependent block by diltiazem (10 μM), and conducted Ba2+ > Ca2+ at a ratio of ∼2:1. In Ca2+, Boltzmann fits to the data yielded V1/2 and slope factors of −39.6 mV and 10.0 for inactivation and 2.8 mV and 7.7 for activation. In Ba2+, V1/2 and slope factors were −29.2 mV and 9.2 for inactivation and −5.6 mV and 6.1 for activation. Neither calciseptine (10 nM), mibefradil (1 μM), nor ω-agatoxin IVA (20 and 100 nM) blocked basal Ba2+ currents. Calciseptine (10 nM) and mibefradil (1 μM) also failed to reverse ANG II-induced DVR vasoconstriction, although raising mibefradil concentration to 10 μM was partially effective. We conclude that DVR pericytes predominantly express voltage-gated divalent currents that are carried by L-type channels.

P1597Two novel mutations in SCN5A gene cause enhanced inactivation and lead to Brugada syndrome

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A Zaytseva ◽  
A V Karpushev ◽  
A V Karpushev ◽  
Y Fomicheva ◽  
Y Fomicheva ◽  
...  
Keyword(s):  
Steady State ◽  
Sodium Channel ◽  
Brugada Syndrome ◽  
Slow Inactivation ◽  
Fast Inactivation ◽  
Novel Mutations ◽  
Patch Clamp Technique ◽  
Inactivation Curve ◽  
Voltage Gated ◽  
Cardiac Sodium Channel

Abstract Background Mutations in gene SCN5A, encoding cardiac potential-dependent sodium channel Nav1.5, are associated with various arrhythmogenic disorders among which the Brugada syndrome (BrS) and the Long QT syndrome (LQT) are the best characterized. BrS1 is associated with sodium channel dysfunction, which can be reflected by decreased current, impaired activation and enhanced inactivation. We found two novel mutations in our patients with BrS and explored their effect on fast and slow inactivation of cardiac sodium channel. Purpose The aim of this study was to investigate the effect of BrS (Y739D, L1582P) mutations on different inactivation processes in in vitro model. Methods Y739D and L1582P substitutions were introduced in SCN5A cDNA using site-directed mutagenesis. Sodium currents were recorded at room temperature in transfected HEK293-T cells using patch-clamp technique with holding potential −100 mV. In order to access the fast steady-state inactivation curve we used double-pulse protocol with 10 ms prepulses. To analyze voltage-dependence of slow inactivation we used two-pulse protocol with 10s prepulse, 20ms test pulse and 25ms interpulse at −100mV to allow recovery from fast inactivation. Electrophysiological measurements are presented as mean ±SEM. Results Y739D mutation affects highly conserved tyrosine 739 among voltage-gated sodium and calcium channels in the segment IIS2. Mutation L1582P located in the loop IVS4-S5, and leucine in this position is not conserved among voltage-gated channels superfamily. We have shown that Y739D leads to significant changes in both fast and slow inactivation, whereas L1582P enhanced slow inactivation only. Steady-state fast inactivation for Y739D was shifted on 8.9 mV towards more negative potentials compare with that for WT, while L1582P did not enhanced fast inactivation (V1/2 WT: −62.8±1.7 mV; Y739D: −71.7±2.3 mV; L1582P: −58.7±1.4 mV). Slow inactivation was increased for both substitutions (INa (+20mV)/INa (−100mV) WT: 0.45±0.03; Y739D: 0,34±0.09: L1582P: 0.38±0.04). Steady-state fast inactivation Conclusions Both mutations, observed in patients with Brugada syndrome, influence on the slow inactivation process. Enhanced fast inactivation was shown only for Y739D mutant. The more dramatic alterations in sodium channel biophysical characteristics are likely linked with mutated residue conservativity. Acknowledgement/Funding RSF #17-15-01292

scholarly journals Voltage-gated transient currents in bovine adrenal fasciculata cells. I. T-type Ca2+ current.

1993 ◽  
Vol 102 (2) ◽  
pp. 217-237 ◽  
Author(s):  
B Mlinar ◽  
B A Biagi ◽  
J J Enyeart
Keyword(s):  
Time Constant ◽  
Low Voltage ◽  
Zona Fasciculata ◽  
Patch Clamp Technique ◽  
Time Constants ◽  
Voltage Gated ◽  
Wide Range ◽  
Boltzmann Function ◽  
Voltage Dependent ◽  
Ca2 Channels

The whole cell version of the patch clamp technique was used to identify and characterize voltage-gated Ca2+ channels in enzymatically dissociated bovine adrenal zona fasciculata (AZF) cells. The great majority of cells (84 of 86) expressed only low voltage-activated, rapidly inactivating Ca2+ current with properties of T-type Ca2+ current described in other cells. Voltage-dependent activation of this current was fit by a Boltzmann function raised to an integer power of 4 with a midpoint at -17 mV. Independent estimates of the single channel gating charge obtained from the activation curve and using the "limiting logarithmic potential sensitivity" were 8.1 and 6.8 elementary charges, respectively. Inactivation was a steep function of voltage with a v1/2 of -49.9 mV and a slope factor K of 3.73 mV. The expression of a single Ca2+ channel subtype by AZF cells allowed the voltage-dependent gating and kinetic properties of T current to be studied over a wide range of potentials. Analysis of the gating kinetics of this Ca2+ current indicate that T channel activation, inactivation, deactivation (closing), and reactivation (recovery from inactivation) each include voltage-independent transitions that become rate limiting at extreme voltages. Ca2+ current activated with voltage-dependent sigmoidal kinetics that were described by an m4 model. The activation time constant varied exponentially at test potentials between -30 and +10 mV, approaching a voltage-independent minimum of 1.6 ms. The inactivation time constant (tau i) also decreased exponentially to a minimum of 18.3 ms at potentials positive to 0 mV. T channel closing (deactivation) was faster at more negative voltages; the deactivation time constant (tau d) decreased from 8.14 +/- 0.7 to 0.48 +/- 0.1 ms at potentials between -40 and -150 mV. T channels inactivated by depolarization returned to the closed state along pathways that included two voltage-dependent time constants. tau rec-s ranged from 8.11 to 4.80 s when the recovery potential was varied from -50 to -90 mV, while tau rec-f decreased from 1.01 to 0.372 s. At potentials negative to -70 mV, both time constants approached minimum values. The low voltage-activated Ca2+ current in AZF cells was blocked by the T channel selective antagonist Ni2+ with an IC50 of 20 microM. At similar concentrations, Ni2+ also blocked cortisol secretion stimulated by adrenocorticotropic hormone. Our results indicate that bovine AZF cells are distinctive among secretory cells in expressing primarily or exclusively T-type Ca2+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Slow inactivation of L-type calcium current distorts the measurement of L- and T-type calcium current in Purkinje myocytes.

1993 ◽  
Vol 102 (5) ◽  
pp. 859-869 ◽  
Author(s):  
N B Datyner ◽  
I S Cohen
Keyword(s):  
Patch Clamp ◽  
Calcium Current ◽  
Slow Inactivation ◽  
Total Calcium ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Whole Cell Patch Clamp ◽  
Voltage Curve ◽  
Voltage Dependent ◽  
Method Of Measurement

We have examined slow inactivation of L-type calcium current in canine Purkinje myocytes with the whole cell patch clamp technique. Slow inactivation is voltage dependent. It is negligible at -50 mV but can inactivate more than half of available iCaL at -10 mV. There are two major consequences of this slow inactivation. First, standard protocols for the measurement of T-type current can dramatically overestimate its contribution to total calcium current, and second, the position and steepness of the inactivation versus voltage curve for iCaL will depend on the method of measurement. Given the widespread attempts to identify calcium current components and characterize them biophysically, an important first step should be to determine the extent of slow inactivation of calcium current in each preparation.

Membrane currents in a calcitonin-secreting human C cell line

1992 ◽  
Vol 263 (5) ◽  
pp. C986-C994 ◽  
Author(s):  
B. A. Biagi ◽  
B. Mlinar ◽  
J. J. Enyeart
Keyword(s):  
Cell Line ◽  
Time Constant ◽  
Membrane Currents ◽  
Human Thyroid ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Voltage Gated ◽  
Voltage Dependent ◽  
Tt Cells ◽  
K Currents

The whole cell version of the patch-clamp technique was used to identify and characterize voltage-gated Ca2+, Na+, and K+ currents in the calcitonin-secreting human thyroid TT cell line. Ca2+ current consisted of a single low-voltage-activated rapidly inactivating component. The current was one-half maximally activated at a potential of -27 mV, while steady-state voltage-dependent inactivation was one-half complete at -51 mV. The Ca2+ current inactivated with a voltage-dependent time constant that reached a minimum of 16 ms at potentials positive to -15 mV. Deactivation kinetics could also be fit with a single voltage-dependent time constant of approximately 2 ms at -80 mV. Replacing Ca2+ with Ba2+ reduced the maximum current by 18 +/- 5% (n = 6). The dihydropyridine Ca2+ agonist (-)BAY K 8644 did not affect the Ca2+ current, but 50 microM Ni2+ reduced it by 81 +/- 0.8% (n = 5). TT cells also possessed tetrodotoxin-sensitive voltage-gated Na+ channels and tetraethylammonium-sensitive delayed rectifier type K+ currents. These results indicate that TT cells possess membrane currents necessary for the generation of action potentials. T-type Ca2+ channels are the sole pathway for voltage-dependent Ca2+ entry into these cells and may couple electrical activity to calcitonin secretion.

scholarly journals Slow Inactivation Does Not Affect Movement of the Fast Inactivation Gate in Voltage-gated Na+ Channels

1998 ◽  
Vol 111 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Vasanth Vedantham ◽  
Stephen C. Cannon
Keyword(s):  
Na Channel ◽  
Slow Inactivation ◽  
Na Channels ◽  
Fast Inactivation ◽  
Voltage Gated ◽  
Cytoplasmic Face ◽  
Voltage Dependent ◽  
Tightly Coupled ◽  
Exclusive Processes ◽  
A Site

Voltage-gated Na+ channels exhibit two forms of inactivation, one form (fast inactivation) takes effect on the order of milliseconds and the other (slow inactivation) on the order of seconds to minutes. While previous studies have suggested that fast and slow inactivation are structurally independent gating processes, little is known about the relationship between the two. In this study, we probed this relationship by examining the effects of slow inactivation on a conformational marker for fast inactivation, the accessibility of a site on the Na+ channel III–IV linker that is believed to form a part of the fast inactivation particle. When cysteine was substituted for phenylalanine at position 1304 in the rat skeletal muscle sodium channel (μl), application of [2-(trimethylammonium)ethyl]methanethiosulfonate (MTS-ET) to the cytoplasmic face of inside-out patches from Xenopus oocytes injected with F1304C RNA dramatically disrupted fast inactivation and displayed voltage-dependent reaction kinetics that closely paralleled the steady state availability (h∞•) curve. Based on this observation, the accessibility of cys1304 was used as a conformational marker to probe the position of the fast inactivation gate during the development of and the recovery from slow inactivation. We found that burial of cys1304 is not altered by the onset of slow inactivation, and that recovery of accessibility of cys1304 is not slowed after long (2–10 s) depolarizations. These results suggest that (a) fast and slow inactivation are structurally distinct processes that are not tightly coupled, (b) fast and slow inactivation are not mutually exclusive processes (i.e., sodium channels may be fast- and slow-inactivated simultaneously), and (c) after long depolarizations, recovery from fast inactivation precedes recovery from slow inactivation.

Membrane potential controls calcium entry into descending vasa recta pericytes

2002 ◽  
Vol 283 (4) ◽  
pp. R949-R957 ◽  
Author(s):  
Zhong Zhang ◽  
Kristie Rhinehart ◽  
Thomas L. Pallone
Keyword(s):  
Membrane Potential ◽  
Channel Blocker ◽  
Calcium Entry ◽  
Ang Ii ◽  
Channel Blockade ◽  
Voltage Gated ◽  
Vasa Recta ◽  
Intracellular Ca ◽  
Bayk 8644

We tested the hypothesis that constriction of descending vasa recta (DVR) is mediated by voltage-gated calcium entry. K+ channel blockade with BaCl2 (1 mM) or TEACl (30 mM) depolarized DVR smooth muscle/pericytes and constricted in vitro-perfused vessels. Pericyte depolarization by 100 mM extracellular KCl constricted DVR and increased pericyte intracellular Ca2+ ([Ca2+]i). The KATP channel opener pinacidil (10−7-10−4 M) hyperpolarized resting pericytes, repolarized pericytes previously depolarized by ANG II (10−8 M), and vasodilated DVR. The DVR vasodilator bradykinin (10−7 M) also reversed ANG II depolarization. The L-type Ca2+ channel blocker diltiazem vasodilated ANG II (10−8 M)- or KCl (100 mM)-preconstricted DVR, and the L-type agonist BayK 8644 constricted DVR. The plateau phase of the pericyte [Ca2+]i response to ANG II was inhibited by diltiazem. These data support the conclusion that DVR vasoreactivity is controlled through variation of membrane potential and voltage-gated Ca2+ entry into the pericyte cytoplasm.

scholarly journals A novel calcium current in dysgenic skeletal muscle.

1989 ◽  
Vol 94 (3) ◽  
pp. 429-444 ◽  
Author(s):  
B A Adams ◽  
K G Beam
Keyword(s):  
Skeletal Muscle ◽  
Charge Carrier ◽  
Calcium Channel ◽  
Calcium Current ◽  
Primary Cultures ◽  
High Sensitivity ◽  
Calcium Currents ◽  
Patch Clamp Technique ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent

The whole-cell patch-clamp technique was used to study voltage-dependent calcium currents in primary cultures of myotubes and in freshly dissociated skeletal muscle from normal and dysgenic mice. In addition to the transient, dihydropyridine (DHP)-insensitive calcium current previously described, a maintained DHP-sensitive calcium current was found in dysgenic skeletal muscle. This current, here termed ICa-dys, is largest in acutely dissociated fetal or neonatal dysgenic muscle and also in dysgenic myotubes grown on a substrate of killed fibroblasts. In dysgenic myotubes grown on untreated plastic culture dishes, ICa-dys is usually so small that it cannot be detected. In addition, ICa-dys is apparently absent from normal skeletal muscle. From a holding potential of -80 mV. ICa-dys becomes apparent for test pulses to approximately -20 mV and peaks at approximately +20 mV. The current activates rapidly (rise time approximately 5 ms at 20 degrees C) and with 10 mM Ca as charge carrier inactivates little or not at all during a 200-ms test pulse. Thus, ICa-dys activates much faster than the slowly activating calcium current of normal skeletal muscle and does not display Ca-dependent inactivation like the cardiac L-type calcium current. Substituting Ba for Ca as the charge carrier doubles the size of ICa-dys without altering its kinetics. ICa-dys is approximately 75% blocked by 100 nM (+)-PN 200-110 and is increased about threefold by 500 nM racemic Bay K 8644. The very high sensitivity of ICa-dys to these DHP compounds distinguishes it from neuronal L-type calcium current and from the calcium currents of normal skeletal muscle. ICa-dys may represent a calcium channel that is normally not expressed in skeletal muscle, or a mutated form of the skeletal muscle slow calcium channel.

scholarly journals Mitochondria-produced superoxide mediates angiotensin II-induced inhibition of neuronal potassium current

2010 ◽  
Vol 298 (4) ◽  
pp. C857-C865 ◽  
Author(s):  
Jing-Xiang Yin ◽  
Rui-Fang Yang ◽  
Shumin Li ◽  
Alex O. Renshaw ◽  
Yu-Long Li ◽  
...  
Keyword(s):  
Potassium Current ◽  
Biological Significance ◽  
Primary Source ◽  
Oxygen Species ◽  
Ang Ii ◽  
Patch Clamp Technique ◽  
Voltage Gated ◽  
Calmodulin Kinase ◽  
The Central Nervous System ◽  
Stimulation Of

Reactive oxygen species (ROS), particularly superoxide (O2·−), have been identified as key signaling intermediates in ANG II-induced neuronal activation and sympathoexcitation associated with cardiovascular diseases, such as hypertension and heart failure. Studies of the central nervous system have identified NADPH oxidase as a primary source of O2·− in ANG II-stimulated neurons; however, additional sources of O2·−, including mitochondria, have been mostly overlooked. Here, we tested the hypothesis that ANG II increases mitochondria-produced O2·− in neurons and that increased scavenging of mitochondria-produced O2·− attenuates ANG II-dependent intraneuronal signaling. Stimulation of catecholaminergic (CATH.a) neurons with ANG II (100 nM) increased mitochondria-localized O2·− levels, as measured by MitoSOX Red fluorescence. This response was significantly attenuated in neurons overexpressing the mitochondria-targeted O2·−-scavenging enzyme Mn-SOD. To examine the biological significance of the ANG II-mediated increase in mitochondria-produced O2·−, we used the whole cell configuration of the patch-clamp technique to record the well-characterized ANG II-induced inhibition of voltage-gated K+ current ( IKv) in neurons. Adenovirus-mediated Mn-SOD overexpression or pretreatment with the cell-permeable antioxidant tempol (1 mM) significantly attenuated ANG II-induced inhibition of IKv. In contrast, pretreatment with extracellular SOD protein (400 U/ml) had no effect. Mn-SOD overexpression also inhibited ANG II-induced activation of Ca2+/calmodulin kinase II, a redox-sensitive protein known to modulate IKv. These data indicate that ANG II increases mitochondrial O2·−, which mediates, at least in part, ANG II-induced activation of Ca2+/calmodulin kinase II and inhibition of IKv in neurons.

High-voltage-activated calcium currents in basal forebrain neurons during aging

1996 ◽  
Vol 76 (1) ◽  
pp. 158-174 ◽  
Author(s):  
D. Murchison ◽  
W. H. Griffith
Keyword(s):  
Charge Carrier ◽  
High Voltage ◽  
Current Density ◽  
Slow Inactivation ◽  
Peak Current ◽  
Perforated Patch ◽  
Age Related ◽  
Dependent Component ◽  
Voltage Dependent ◽  
Current Densities

1. Both conventional whole cell and perforated-patch voltage-clamp recordings were made of high-voltage-activated (HVA) calcium (Ca2+) channel currents in acutely dissociated medical septum and nucleus of the diagonal band neurons from young (1-3.5 mo) and aged (19-26.5 mo) Fischer 344 rats. Barium (Ba2+) was used as the charge carrier to minimize secondary Ca(2+)-induced conductances and Ca(2+)-induced inactivation. 2. When HVA currents generated by voltage ramps from a holding potential (Vh) of-60 mV were recorded within minutes after whole cell formation, no change in peak current density was observed between young (-44.7 +/- 2.5 pA/pF, mean +/- SE, n = 93) and aged (-44.2 +/- 2.1 pA/pF, n = 86) cells. However, currents recorded later with voltage step protocols revealed a reduction in peak current amplitudes and a trend toward larger peak current densities in aged cells. From a Vh of -60 mV and with steps to -10 mV, current densities were -21.5 +/- 1.9 pA/pF in young cells (n = 55) and -25.0 +/- 2.0 pA/pF in aged cells (n = 44). The differences in current densities recorded by the two protocols were explained by nonspecific current rundown and the development of a slow (min) inactivation process. Slow inactivation was different from conventional rundown of HVA currents because it was reversible with the use of perforated-patch recordings. 3. Perforated-patch recordings were used to characterize slow inactivation. There was significantly less slow inactivation in aged cells. When voltage steps (200 ms in duration, from -80 to -10 mV) were delivered at 12-s intervals, slow inactivation reduced the current after 15 min to 63 +/- 7% of control in young cells and 86 +/- 4% in aged cells (P = 0.028). When voltage steps were delivered at 20-s intervals, the current at the 15th step decreased to 93.4 +/- 1.5% of control in aged cells, compared with 86.6 +/- 1.6% in young (P = 0.007). There was less slow inactivation with increased intervals between voltage steps and with shorter step durations. There was also less inactivation with reduced concentration of charge carrier, indicating a current-dependent component to slow inactivation. Additionally, a voltage-dependent component was evident, because slow inactivation was increased at depolarized VhS. 4. Perforated-patch recordings were used to study at least four pharmacologically distinct fractions of HVA currents in both young and aged cells. Nifedipine (10 microM) blocked 16.9 +/- 2.8% and 23.6 +/- 2.5% of the HVA currents in young and aged cells, respectively. omega-Conotoxin GVIA (500 nM) blocked 53.2 +/- 5.8% in young and 53.6 +/- 2.9% in aged cells. In young cells, omega-agatoxin IVA (200-400 nM) blocked 28.4 +/- 2.2% of the HVA current, and it blocked 29.9 +/- 2.8% in aged cells. A fraction of the current (young cells: 13.8 +/- 2.2%; aged cells: 11.4 +/- 1.6%) was resistant to a combination of all three antagonists. Cadmium (100 microM) completely blocked the remaining HVA current. No significant age-related differences in the HVA current fractions were observed. 5. The HVA current density, current-voltage relationship, and voltage-dependent activation were unchanged with age. However, slow inactivation of HVA currents was reduced in aged cells. The age-related difference in HVA Ca2+ currents reported here suggests a possible mechanism by which Ca2+ homeostasis may be altered in aged neurons.

Single K+ channels in adrenal zona glomerulosa cells. II. Inhibition by angiotensin II

1992 ◽  
Vol 263 (4) ◽  
pp. E760-E765 ◽  
Author(s):  
M. V. Kanazirska ◽  
P. M. Vassilev ◽  
S. J. Quinn ◽  
D. L. Tillotson ◽  
G. H. Williams
Keyword(s):  
Angiotensin Ii ◽  
Single Channel ◽  
Zona Glomerulosa ◽  
K Channel ◽  
Delayed Rectifier ◽  
Ang Ii ◽  
Patch Clamp Technique ◽  
K Channels ◽  
Sequence Of Events ◽  
Voltage Dependent

The effects of angiotensin II (ANG II) on single K+ channels were studied in rat and bovine adrenal zona glomerulosa (ZG) cells, using the patch-clamp technique. ANG II (0.1-10 nM) induced substantial inhibition of inward rectifier and delayed rectifier K+ channel activities in rat and bovine ZG cells. Analysis of single-channel activities showed that the ANG II-induced channel-blocking effect involved reductions in the probability of the open state (Po) and the mean open time. The changes in these channel parameters occurred at all test voltages, indicating that the effect of ANG II was voltage independent. ANG II could not interact directly with the extracellular sides of the membranes in these experiments using cell-attached patches. Therefore, the effect of ANG II on K+ channels must occur through an indirect cytosolic transduction pathway. The ANG II-induced block of K+ channels will result in membrane depolarization, which may activate voltage-dependent Ca2+ channels, thereby increasing cytosolic free Ca2+ and stimulating aldosterone secretion. These channel-modulating actions of ANG II may be an important step in the initial sequence of events underlying its transduction mechanism.

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