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PubMed1990

Membrane hyperpolarization is a mechanism of endothelium-dependent cerebral vasodilation.

Acetylcholine (ACh)-induced hyperpolarization of cerebral arteries requires a functional endothelium. The hyperpolarization is reversed by potassium-channel blockers. The goal of this study was to determine whether the hyperpolarization is causally related to endothelium-dependent dilation of isolated cerebral arteries. ACh hyperpolarized rabbit middle cerebral arteries by up to 19 mV. The hyperpolarizations were sustained and did not occur in arteries without endothelial cells or in the presence of potassium-channel inhibitors (3 x 10(-6) M glibenclamide or 5 x 10(-5) M BaCl2). ACh-induced dilator responses were inhibited but not abolished by glibenclamide or BaCl2. Methylene blue also inhibited the dilator responses, and a combination of glibenclamide or BaCl2 and methylene blue greatly diminished the dilation. Nitric oxide relaxed but did not hyperpolarize the vascular smooth muscle cells, and BaCl2 had no effect on the nitric oxide-induced relaxations. These data indicate that the overall cerebral arterial dilator response to ACh is determined by the combined effects of membrane hyperpolarization, which closes voltage-dependent calcium channels, and the actions of a second endothelial factor, probably endothelium-derived relaxing factor.

Acetylcholine↗
PubMed1993

Similarities between dynamic elastance of left ventricular chamber and papillary muscle of rabbit heart.

The frequency-dependent dynamic elastance of the left ventricle (LV) of isolated rabbit heart was determined and compared with dynamic stiffness of excised rabbit papillary muscle. Comparison was made in three states: 1) relaxed, 2) BaCl2 contracture, and 3) rigor. Dynamic chamber elastance was determined by pressure-to-volume ratio at 12 frequencies of sinusoidal volume variation between 0.1 and 30 Hz. Dynamic elastance during BaCl2 contracture was distinctly different from that during either relaxed or rigor states. Characteristics of BaCl2 contracture were 1) as frequency increased, polar plot of real and imaginary elastance showed a progressively opening clockwise spiral that tended eventually to become tangent to the apogee of a semi-circle by 30 Hz; 2) modulus spectrum exhibited asymptotes at low and high frequencies with an intervening dip to a minimum at 1.25 Hz; and 3) phase showed a sharp transition at dip frequency from small negative values at lower frequencies to large positive values at intermediate frequencies and then declined at highest frequencies. There was little dependence of dynamic elastance on frequency in both relaxed and rigor states. Dynamic muscle stiffness exhibited all features of dynamic chamber elastance in all three states. We concluded that dynamic elements responsible for myofiber stiffness were also responsible for LV chamber elastance. Furthermore, it was possible to describe and interpret dynamic chamber elastance and muscle stiffness with a common model based on muscle cross-bridge theory. This model did a reasonable job of reproducing all important features of experimentally observed LV chamber elastance and muscle stiffness. Thus dynamic homologies between chamber and muscle were established in experimental data and in the fact that a single interpretive model served equally well for both chamber elastance and muscle stiffness.

Animals↗
PubMed1997

Development of inwardly rectifying K+ channel family in rat ventricular myocytes.

The ATP-sensitive K+ current (I(K,ATP)), the inward rectifier K+ current (I(K1)), and the acetylcholine-activated K+ current (I(K,ACh)) were recorded in fetal, neonatal, and adult rat ventricular myocytes using the patch-clamp technique. The density (pA/pF) of I(K1) increased from gestation day 10 through neonatal day 1 and then decreased after neonatal day 30. The density of I(K,ATP) activated maximally by metabolic inhibition changed in parallel with the I(K1) density, and the density of I(K,ATP) channel distribution was 1.3 times higher than that of I(K1) throughout the development. We failed to observe developmental changes in the single-channel conductance and the mean open time of I(K1) and I(K,ATP) channels. However, the open probability of the I(K,ATP) channel was lower in fetuses, and the sensitivity to ATP was highest in 1-day neonates. I(K,ACh) were present in the ventricle at all stages of development but at a much lower density than in atrium. The relationship between the resting membrane potential and the development of the inwardly rectifying K-channel family is discussed.

Adenosine Triphosphate↗
PubMed1997

Effects of ionic channel antagonists barium, cesium, and UL-FS-49 on vagal slowing of atrial rate in dogs.

In response to a brief vagal stimulus, the atrial rate initially slows, then transiently accelerates, and slows a second time. We determined the effects of three antagonists to two ionic channels on this characteristic triphasic pacemaker response. Brief bursts of vagal stimulation were delivered to anesthetized dogs, and atrial cycle lengths were recorded. Either barium, cesium, or UL-FS-49 was administered. Barium, which primarily blocks the acetylcholine-sensitive potassium current (IK,ACh), attenuated the initial vagally induced bradycardia by > 50% without affecting the subsequent acceleration or the secondary slowing. Cesium and UL-FS-49 [both of which primarily block the pacemaker current (If)] did not affect the initial vagal slowing of atrial rate but abolished the acceleratory portion of the response. The secondary slowing was abolished by cesium but not by UL-FS-49. We conclude that the initial rapid atrial response to acetylcholine is mediated mainly by the IK,ACh, with little contribution from the If. The subsequent acceleration is mediated by activation of the If.

Acetylcholine↗
PubMed2000

Nonlinear changes of transmembrane potential caused by defibrillation shocks in strands of cultured myocytes.

Organization of cardiac tissue into cell strands and layers has been implicated in changes of transmembrane potential (DeltaV(m)) during defibrillation. To determine the shock-induced DeltaV(m) in such structures, cell strands of variable width [strand width (SW) = 0.15-2 mm] were grown in culture. Uniform-field shocks with variable strength [shock strength (SS) = 2-50 V/cm] were applied across strands during the action potential (AP) plateau, and DeltaV(m) were measured optically. Three different types of DeltaV(m) were observed. Small DeltaV(m) [<40%AP amplitude (APA)] were linearly dependent on SS and SW and were symmetrically distributed about a strand centerline with maximal positive and negative DeltaV(m) on opposite strand sides being equal. Intermediate DeltaV(m) (<200%APA) were strongly asymmetric with negative DeltaV(m) > positive DeltaV(m) because of a negative time-dependent shift of V(m) at the depolarized side of the strands. For large DeltaV(m) (>200%APA), a second time-dependent shift of V(m) to more positive levels was observed in the hyperpolarized portions of strands, causing reduction of the DeltaV(m) asymmetry. We conclude that during application of shocks to cell strands during the AP plateau, passive changes of V(m) were followed by two voltage- and time-dependent shifts of V(m), possibly reflecting changes of ionic currents or membrane electroporation.

Animals↗
PubMed2000

ATP-sensitive potassium channels may participate in the coupling of neuronal activity and cerebrovascular tone.

K(+) dilate and constrict cerebral vessels in a dose-dependent fashion. Modest elevations of abluminal K(+) cause vasodilatation, whereas larger extracellular K(+) concentration ([K(+)](out)) changes decrease cerebral blood flow. These dilations are believed to be mediated by opening of inward-rectifier potassium channels sensitive to Ba(2+). Because BaCl(2) also blocks ATP-sensitive K(+) channels (K(ATP)), we challenged K(+) dilations in penetrating, resistance-size (<60 mmu) rat neocortical vessels with the K(ATP) channel blocker glibenclamide (1 microM). Glibenclamide reduced K(+) responses from 138 +/- 8 to 110 +/- 0.8%. K(+) constrictions were not affected by glibenclamide. The Na(+)-K(+)-pump inhibitor ouabain (200 microM) did not significantly change resting vessel diameter but decreased K(+) dilations (from 153 +/- 9 to 99 +/- 2%). BaCl(2) blocked K(+) dilations with a half-maximal dissociation constant of 2.9 microM and reduced dilations to the specific K(ATP) agonist pinacidil with equal potency. We conclude that, in resistance vessels, K(+) dilations are mediated by K(ATP); we hypothesize that [K(+)](out) causes activation of Na(+)-K(+) pumps, depletion of intracellular ATP concentration, and subsequent opening of K(ATP). This latter hypothesis is supported by the blocking effect of ouabain.

Adenosine Triphosphate↗
PubMed2000

Role of inwardly rectifying K(+) channels in K(+)-induced cerebral vasodilatation in vivo.

We tested whether activation of inwardly rectifying K(+) (Kir) channels, Na(+)-K(+)-ATPase, or nitric oxide synthase (NOS) play a role in K(+)-induced dilatation of the rat basilar artery in vivo. When cerebrospinal fluid [K(+)] was elevated from 3 to 5, 10, 15, 20, and 30 mM, a reproducible concentration-dependent vasodilator response was elicited (change in diameter = 9 +/- 1, 27 +/- 4, 35 +/- 4, 43 +/- 12, and 47 +/- 16%, respectively). Responses to K(+) were inhibited by approximately 50% by the Kir channel inhibitor BaCl(2) (30 and 100 microM). In contrast, neither ouabain (1-100 microM, a Na(+)-K(+)-ATPase inhibitor) nor N(G)-nitro-L-arginine (30 microM, a NOS inhibitor) had any effect on K(+)-induced vasodilatation. These concentrations of K(+) also hyperpolarized smooth muscle in isolated segments of basilar artery, and these hyperpolarizations were virtually abolished by 30 microM BaCl(2). RT-PCR experiments confirmed the presence of mRNA for Kir2.1 in the basilar artery. Thus K(+)-induced dilatation of the basilar artery in vivo appears to partly involve hyperpolarization mediated by Kir channel activity and possibly another mechanism that does not involve hyperpolarization, activation of Na(+)-K(+)-ATPase, or NOS.

Acetylcholine↗
PubMed1998

Ca2+ and K+ currents regulate accommodation and firing frequency in guinea pig bronchial ganglion neurons.

Intracellular microelectrode recordings were obtained from neurons located in adult guinea pig bronchial parasympathetic ganglia in situ to determine the calcium and potassium currents regulating repetitive action potential activity and firing rates by these neurons. Neurons in these ganglia respond to prolonged suprathreshold depolarizing current steps with either a burst of action potentials at the onset of the stimulus (accommodating or phasic neurons) or repetitive action potentials throughout the stimulus (nonaccommodating or tonic neurons). Instantaneous and adapted firing rates during prolonged threshold and suprathreshold stimuli were lower in tonic than in phasic neurons, indicating a longer interspike interval between repetitive action potentials in tonic neurons. In tonic neurons, blockade of A-type current with 4-aminopyridine increased accommodation; 4-aminopyridine or apamin decreased the interspike interval in tonic neurons. Calcium-free buffer, cadmium ions, or omega-conotoxin GVIA also increased accommodation in tonic neurons but did not affect the interspike interval; nifedipine or verapamil did not affect the tonic firing pattern. Accommodation in phasic neurons could be decreased by a conditioning hyperpolarization step of the resting potential, which could be subsequently blocked by 4-aminopyridine or calcium-free buffer. Accommodation in phasic neurons could also be decreased by apamin or barium ions: the repetitive action potentials observed during these treatments could be reversed by cadmium ions or calcium-free buffer. These results indicate that tonic and phasic neurons in guinea pig bronchial parasympathetic ganglia have similar types of calcium currents, but potassium channels may ultimately regulate the accommodation pattern, the firing rate, and, consequently, the output from these neurons.

4-Aminopyridine↗
PubMed2001

Developmental expression of neurokinin A and functional neurokinin-2 receptors in lung.

Peribronchial smooth muscle constriction causes airway stretch, an important mechanical force in developing lung. Little is known about factors influencing these spontaneously active muscle elements. We measured contractile activity of neurokinin (NK) receptors on fetal intrapulmonary smooth muscle by tracheal perfusion assay (n = 11). Injecting either capsaicin or the NK(2) receptor agonist [NLE(10)]NKA resulted in significant (P < 0.05) bronchoconstriction. A specific NK(2) receptor antagonist inhibited constriction caused by endogenous tachykinins released by capsaicin. We then examined NK(2) receptor (n = 44) and NKA (n = 23) ontogeny in human lung. NKA immunostaining was identified in peribronchial nerves in samples with gestational age >12 wk. NK(2) receptor protein was identified in peribronchial and perivascular smooth muscle. These results indicate that endogenous tachykinins released by the developing lung act via NK(2) receptors to cause smooth muscle constriction. We speculate that tachykinins could modulate lung development.

Adult↗
PubMed1991

Spontaneously hypertensive rats demonstrate increased renal vascular alpha 1-adrenergic receptor responsiveness.

To determine alpha 1-adrenergic receptor responsiveness of the renal vasculature in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR), phenylephrine (2.5 or 5.0 micrograms.kg-1.min-1 iv) or saline was infused. Effective renal blood flow (ERBF) and glomerular filtration rate were determined by p-aminohippuric acid and inulin clearances, respectively. Peritubular capillary, proximal tubular, and stop-flow pressures (SFP) were measured by micropuncture. Phenylephrine decreased ERBF (6.27 +/- 0.48 to 4.55 +/- 0.65 ml.min-1.g-1; P less than 0.05) and increased arterial pressure and SFP (31.5 +/- 0.9 to 34.2 +/- 1.0 mmHg) in SHR. It only increased arterial pressure and ERBF in WKY without changing SFP. Afferent arteriolar resistance (RA) and glomerular capillary pressure (PG) remained unchanged, whereas efferent resistance (RE) decreased in WKY; in contrast, RA, RE, and PG increased in SHR (RA 21.2 +/- 2.0 to 38.1 +/- 7.1 mmHg.ml-1.min.g, RE 6.9 +/- 0.6 to 13.9 +/- 3.8 mmHg.ml-1.min.g; and PG 49.6 +/- 0.9 to 53.7 +/- 1.1 mmHg; all P less than 0.05). These data demonstrated increased SHR afferent and efferent arteriolar responsiveness; WKY efferent arteriolar hyperresponsiveness was not observed. The findings support the concept of augmented intrarenal vascular alpha 1-adrenergic responsiveness in hypertension that may predispose to subsequent glomerular hypertension.

Animals↗
PubMed1996

Activation of GABAB receptors increases a potassium conductance in rat bulbospinal neurons of the C1 area.

In anesthetized rats, iontophoresis of the gamma-aminobutyric acid (GABAB)-receptor agonist and antispastic drug baclofen inhibits the bulbospinal vasomotor neurons of the rostral ventrolateral medulla (RVLM). The present study was carried out to determine whether C1 adrenergic and other bulbospinal neurons of the RVLM have postsynaptic GABAB receptors. Retrogradely labeled RVLM bulbospinal neurons (n = 52) were recorded in 120-micron-thick slices from neonatal rat brain (3-10 days old). Most neurons (48/52) were tonically active (3 +/- 0.6 spikes/s). Twenty-six neurons were recovered histologically, and 18 of them were immunoreactive for tyrosine hydroxylase (TH). In current clamp, baclofen (0.3-10 microM) hyperpolarized RVLM bulbospinal cells in a dose-dependent manner (16 +/- 0.5 mV hyperpolarization by 3 microM baclofen; n = 19) and decreased input resistance by 40% (n = 10). In voltage clamp (1 microM tetrodotoxin present; holding potential: -40 to -60 mV), 3 microM baclofen induced an outward current of 21 +/- 2 pA (n = 29). This current exhibited inward rectification and reversed polarity close to the K+ equilibrium potential (external K+ from 2.5 to 10 mM). The current induced by baclofen was reduced 90% by 0.1-0.2 mM BaCl2 (n = 6) and was blocked reversibly by the selective GABAB-receptor antagonist CGP-55845A (0.5-1 microM; n = 6). All histologically verified TH-immunoreactive cells (n = 18) were sensitive to baclofen. In summary, RVLM bulbospinal neurons including C1 adrenergic cells possess GABAB receptors. Activation of these receptors increases an inwardly rectifying K+ conductance. This effect reduces the intrinsic firing frequency of RVLM vasomotor neurons "in vitro" and may contribute to the sympatholytic action of baclofen "in vivo."

Action Potentials↗
PubMed1996

Stimulation of Na(+)-K(+)-2Cl- cotransport in rat medullary thick ascending limb by dopamine.

Dopamine receptors are present in the medullary thick ascending limb (mTAL) of Henle, but their effect on ion transport in this nephron segment has not been tested. Therefore, we studied the short-term effects of dopamine on Na(+)-K(+)-2Cl- cotransport (assessed by 100 microM bumetanide-sensitive 86Rb uptake) in rat mTAL tubular suspensions. Dopamine (1 microM) stimulated bumetanide-sensitive 86Rb uptake (72.1 +/- 10.6% vs. control, n = 5) by increasing total 86Rb uptake and by decreasing bumetanide-insensitive 86Rb uptake; this effect was concentration dependent. The dopamine-induced stimulation of Na(+)-K(+)-2Cl- cotransport activity was mimicked by calyculin A, a protein phosphatase (PP) inhibitor, and Sp isomer of adenosine 3',5'-cyclic monophosphothioate (Sp-cAMP[S]), a protein kinase A (PKA) agonist, and blocked by Rp isomer of 8-(4-chlorophenylthio)-cAMP[S] (Rp-8-CPT-cAMP[S]), a PKA inhibitor (n = 5). Dopamine did not increase the stimulatory effect of the PP inhibitor. However, the stimulatory effect of the PP inhibitor and PKA agonist was additive and approached the stimulatory effect of dopamine. The stimulatory effects of dopamine, PP inhibitor, and PKA agonist persisted even when intracellular sodium was clamped by 5 microM monensin. When K+ channels were blocked by 1 mM BaCl2, the effects of dopamine and calyculin A on the cotransport were no longer apparent, although the stimulatory effect of the PKA agonist was attenuated. We conclude that dopamine stimulates Na(+)-K(+)-2Cl- cotransport activity. This action is mediated mainly by PKA-dependent phosphorylation/dephosphorylation processes and modulated by dopamine actions on K+ channels.

Animals↗
PubMed1998

Inward rectifier potassium channels in the rat middle cerebral artery.

Inward rectifier K+ channels (Kirs) were studied in the isolated perfused rat middle cerebral artery (MCA). The addition of 15 mM K+ (KCl) to the extraluminal bath dilated the MCAs. These dilations were blocked by selective inhibitors for the Kirs (40 microM BaCl2 or 40 mM CsCl) but not selective inhibitors for other K+ channels (glibenclamide, tetraethylammonium, or 4-aminopyridine). Neither removal of the endothelium nor treatment with the nitric oxide synthase inhibitor (NG-nitro-L-arginine methyl ester, 10 microM) affected the K(+)-induced dilation. The addition of BaCl2 to resting MCAs produced a dose-dependent constriction of 8-12%, indicating that, during resting conditions, Kirs aid in setting or determining the resting tone. The magnitude of the dilations produced by the addition of K+ or constrictions produced by BaCl2 were independent of pressure over a range of 40-100 mmHg. We conclude that Kirs, which produce a dilation when activated, exist on the vascular smooth muscle of the rat MCA. These Kirs aid in determining the resting tone of the vessel, and their function is independent of pressure over physiological pressure ranges.

Animals↗
PubMed2004

Inhibition of K+ conductance in descending vasa recta pericytes by ANG II.

We tested whether K(+) channel inhibition accompanies ANG II-induced depolarization of descending vasa recta (DVR) pericytes. An increase in extracellular K(+) concentration ([K(+)](o)) from 5 to 100 mM depolarized resting pericytes but had no effect after prolonged (10 nM, 20 min) ANG II exposure. In contrast, reduction of extracellular Cl(-) concentration ([Cl(-)](o)) from 154 to 34 mM had a minor effect on resting membrane potential but strongly depolarized pericytes treated with ANG II. The K(+) channel blockers BaCl(2) (0.1, 1 mM) and tetraethylammonium (TEA; 30 mM) depolarized resting pericytes but did not affect membrane potential of ANG II-treated pericytes. Pericyte whole cell currents were reduced by ANG II and nearly eliminated by combined ANG II exposure and the Cl(-) channel blocker niflumic acid (100 muM). Augmentation of inward current induced by raising [K(+)](O) from 5 to 50 mM was eliminated by preexposure to ANG II. TEA- and BaCl(2)-sensitive outward currents, generated by depolarizing pericytes from -80 to -40 mV, were eliminated by ANG II. We conclude that ANG II depolarizes DVR pericytes by a combination of Cl(-) channel activation and K(+) channel inhibition.

Angiotensin II↗
PubMed1983

Intracellular microelectrode characterization of the rabbit cortical collecting duct.

Cortical collecting ducts of the rabbit were perfused in vitro and the intracellular potential (Vbl) was measured with KCl-filled microelectrodes. The ratio of apical to basolateral membrane resistance (Ra/Rbl) was estimated from the voltage divider ratio using cable analysis. In control tubules Vbl averaged--84.0 +/- 2.5 mV and Ra/Rbl was 0.83 +/- 0.11. Pretreatment of the rabbits with mineralocorticoid caused Vbl to hyperpolarize to--105.8 +/- 3.1 mV and Ra/Rbl to decrease slightly to 0.62 +/- 0.10. A 10-fold increase of the luminal [K+] caused a 40.6 +/- 3.1 mV depolarization of Vbl in control tubules and a 33.0 +/- 4.2 mV depolarization in tubules from DOCA-pretreated rabbits. Concurrently, Ra/Rbl decreased in both groups, consistent with the existence of a conductive K+ channel at the apical cell membrane. This apical K+ channel was not sensitive to amiloride but was blocked by Ba2+. Conductive movement of Na+ across the apical membrane was also apparent in that Ra/Rbl increased with amiloride from 0.61 +/- 0.10 to 1.45 +/- 0.28. A 10-fold increase in the bath [K+] caused a 28.6 +/- 3.8 and a 49.4 +/- 4.4 mV depolarization of Vbl in tubules obtained from control and DOCA-pretreated rabbits, respectively. In both groups Ra/Rbl increased, suggesting that the basolateral cell membrane also contains a conductive K+ channel. Taken together the results support a model in which the transepithelial reabsorption of Na+ and the transepithelial secretion of K+ are driven by the Na+-K+-ATPase located in the basolateral cell membrane, with passive movement of these ions occurring through separate conductive pathways in the apical cell membrane.

Amiloride↗
PubMed1985

Conductive properties of the rabbit outer medullary collecting duct: inner stripe.

Segments of outer medullary collecting duct were dissected from the inner stripe of the rabbit kidney (OMCDi) and perfused in vitro. The conductive properties of the tubule epithelium and individual cell membranes were determined by means of cable analysis and intracellular voltage-recording microelectrodes. In 35 tubules the transepithelial voltage (VT) and resistance (RT) averaged 17.2 +/- 1.4 mV, lumen positive, and 58.6 +/- 5.3 k omega X cm, respectively. The basolateral membrane voltage, (Vbl) was -29.2 +/- 2.1 mV (n = 23). The apical cell membrane did not contain appreciable ion conductances, as evidenced by the high values of apical cell membrane fractional resistance (fRa = Ra/Ra + Rb), which approached unity (0.99 +/- 0.01; n = 23). Moreover, addition of amiloride or BaCl2 to the tubule lumen was without effect on the electrical characteristics of the cell, as was a twofold reduction in luminal [Cl-]. The conductive properties of the basolateral cell membrane were assessed with bath ion substitutions. A twofold reduction in bath [Cl-] depolarized Vbl by 14.7 +/- 0.4 mV (theoretical, 17 mV), while a 10-fold increase in bath [K+] resulted in only a 0.9 +/- 0.4 mV depolarization (theoretical, 61 mV). Substituting bath Na+ with tetramethylammonium (from 150 to 75 mM) was without effect. Reducing bath [HCO-3] from 25 to 5 mM (constant PCO2) resulted in a steady-state depolarization of Vbl of 8.4 +/- 0.4 mV that could not be attributed to conductive HCO-3 movement. Thus, the basolateral cell membrane is predominantly Cl- selective.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1985

Effect of barium on cell volume regulation in rabbit proximal straight tubules.

Rabbit proximal straight tubules swell abruptly when exposed to hypotonic medium but then shrink in a few minutes as they approach their base-line volume following loss of solute and water. Potassium, the major intracellular cation, as well as sodium, is lost during this process. In the present experiments, we studied hypotonic cell volume regulation in the presence of barium, an agent reported to decrease potassium permeability. Exposure to BaCl2 significantly prolonged hypotonic volume recovery in a dose-dependent manner. Tubules depleted of potassium and loaded with sodium chloride by exposure to 10(-4) M ouabain for 1 h swelled osmometrically and subsequently volume regulated in dilute medium. Volume regulation in such tubules is a consequence of transbasement membrane hydrostatic forces. By contrast, tubules similarly loaded with sodium, but also exposed to 10(-3) M BaCl2, volume regulated only minimally in dilute medium, suggesting BaCl2 might also affect sodium movement. However, hypotonic volume regulation was restored in sodium-loaded BaCl2-treated tubules when cells were more effectively depleted of potassium by incubation in 0-mM potassium medium. We conclude that barium retards hypotonic volume regulation primarily because of its effect on potassium movement.

Animals↗
PubMed1985

Lack of potassium effect on Na-Cl cotransport in the medullary thick ascending limb.

The effect of potassium on sodium chloride uptake into rabbit renal medullary thick ascending limb of Henle's loop (mTALH) cells was studied to assess whether K participates in the Na-Cl cotransport system. Na uptake into the mTALH cells was inhibited 70% at 3 min by 1 mM furosemide. The total and furosemide-sensitive Na uptake was stimulated by Cl. Additionally, Cl uptake into the mTALH cells was stimulated by Na gradients and inhibited 42% at 3 min by 1 mM furosemide. Na uptake was studied in the presence of 0,5, or 140 mM external K gradients. Na uptake was similar in the absence and presence of K. Additionally, furosemide inhibited Na uptake as effectively in the absence or presence of K. Similar studies were conducted to study the effects of Na on 86Rb uptake. Na did not stimulate 86Rb uptake. The uptake of 86Rb was similar in the presence of 0,5, or 140 mM Na gradients. Furosemide had no significant inhibitory effect on 86Rb uptake. Barium (5 mM), an inhibitor of K conductance pathways, inhibited total 86Rb uptake by 19%. In the presence of 5 mM BaCl2, Na still did not have a stimulatory effect on 86Rb uptake. The results confirm the existence of a Na-Cl cotransport system in mTALH cells, but a direct effect of K on the NaCl cotransport system could not be demonstrated under the experimental conditions we used.

Animals↗