Tissue K concentration in relation to the role of the kidney in hibernation and the cause of periodic arousal

1971 ◽  
Vol 39 (3) ◽  
pp. 437-445 ◽  
Author(s):  
J.S. Willis ◽  
S.S. Goldman ◽  
Rachel F. Foster
Keyword(s):  
K Concentration ◽  
Periodic Arousal

scholarly journals Potential role of luminal potassium in tubuloglomerular feedback.

1997 ◽  
Vol 8 (12) ◽  
pp. 1831-1837 ◽  
Author(s):  
V Vallon ◽  
H Osswald ◽  
R C Blantz ◽  
S Thomson
Keyword(s):  
Potential Role ◽  
Macula Densa ◽  
Tubuloglomerular Feedback ◽  
K Channel ◽  
Thick Ascending Limb ◽  
Retrograde Perfusion ◽  
Luminal Membrane ◽  
K Concentration ◽  
Tubular Flow

Transport through the Na+-2Cl(-)-K+ cotransporter in the luminal membrane of macula densa cells is considered critical for tubuloglomerular feedback (TGF). Although various studies could support the importance of luminal Na+ and Cl-, the role of luminal K+ in TGF has not been thoroughly addressed. The study presented here examines this issue in nephrons with superficial glomeruli of anesthetized male Munich-Wistar-Frömter rats. Ambient Na+ concentration in early distal tubular fluid was approximately 22 mM, suggesting collection sites relatively close to the macula densa segment. First, it was found that ambient early distal tubular K+ concentration is approximately 1.3 mM, i.e., close to the K+ affinity of the Na+-2Cl(-)-K+ cotransporter in the thick ascending limb. Second, it was observed that a change in late proximal tubular flow rate, i.e., a maneuver that is known to induce a TGF response, significantly alters early distal tubular K+ concentration. Third, previous experiments failed to show an inhibition in TGF response during retrograde perfusion of the macula densa with K+-free solutions. Because of a potential K+ influx into the lumen between the perfusion site and the macula densa, however, the K+ channel blocker U37883A was added to the K+-free perfusate. TGF response was assessed as the fall in nephron filtration rate in response to retrograde perfusion of the macula densa segment from early distal tubular site. It was observed that luminal U37883A (100 microM) significantly attenuated TGF. Because adding 5 mM KCl to the perfusate restored TGF in the presence of U37883A and because the inhibitory action of U37883A on tubular K+ secretion was confirmed, the effect of U37883A on TGF was most likely caused by inhibition of K+ influx into the perfused segment, which decreased luminal K+ concentration at the macula densa. The present findings support a potential role for luminal K+ in TGF, which is in accordance with a transmission of the TGF signal across the macula densa via Na+-2Cl(-)-K+ cotransporter.

Difference in the Na affinity of Na(+)-K(+)-ATPase along the rabbit nephron: modulation by K

1990 ◽  
Vol 259 (2) ◽  
pp. F246-F250 ◽  
Author(s):  
C. Barlet-Bas ◽  
L. Cheval ◽  
C. Khadouri ◽  
S. Marsy ◽  
A. Doucet
Keyword(s):  
Atpase Activity ◽  
Thick Ascending Limb ◽  
Kidney Cells ◽  
Nephron Segments ◽  
Adaptive Property ◽  
Collecting Tubule ◽  
Pump Activity ◽  
K Concentration ◽  
Cortical Collecting Tubule

The sensitivity of Na(+)-K(+)-ATPase to Na was determined in single segments of rabbit nephron isolated by microdissection. In the cortical collecting tubule (CCT), Na(+)-K(+)-ATPase was threefold more sensitive to Na (apparent K0.5 approximately 3 mM) than in proximal convoluted tubule and cortical thick ascending limb (apparent K0.5 approximately 10 mM). Furthermore, increasing K concentration from 5 to greater than 100 mM markedly reduced the affinity of the pump for Na in all three nephron segments. In fact, the main shift in Na affinity occurred when K changed from 100 to 120 mM; in the CCT, increasing K concentration from 100 to 120 mM while maintaining Na concentration at 10 mM reduced Na(+)-K(+)-ATPase activity by greater than 35%. These findings confirm that, in kidney cells as in other cells, intracellular Na limits the rate of Na(+)-K(+)-ATPase. Thus any alteration of intracellular Na concentration modifies the pump activity in a way that contributes to the restoration of intracellular Na homeostasis. This adaptive property is particularly efficient in the collecting tubule in which the apparent K0.5 of the pump for Na is close to normal intracellular Na concentration. Furthermore, changes in intracellular K concentration, which usually accompany those of Na so as to maintain the total cation concentration constant, potentiate the regulatory role of Na through modifications of its affinity for the pump.

Role of circulation in maintaining Na+ and K+ concentration in pelvic patch in Rana catesbeiana

1991 ◽  
Vol 261 (3) ◽  
pp. R686-R689 ◽  
Author(s):  
R. H. Parsons ◽  
R. Schwartz
Keyword(s):  
Water Flow ◽  
Water Uptake ◽  
Rana Catesbeiana ◽  
Salt Content ◽  
Ventral Surface ◽  
Bathing Medium ◽  
Pectoral Region ◽  
K Concentration ◽  
Skin Samples

Skin samples from the pelvic, pectoral, and back areas of frogs were taken from control (C) animals and from dehydrated animals under three conditions: dehydrated and not exposed to a bathing medium (D), dehydrated live and ventral surface exposed to a bathing medium (DL), and dehydrated with heart stopped and ventral surface exposed to a bathing medium (DHS). The skin concentration of Na+ and K+ of the pelvic patch in the absence of circulation was significantly reduced [DHS 286 +/- 22 microM/mg dry wt (n = 6)] compared with control [C 392 +/- 21 microM/mg dry wt (n = 8)]. However, the pelvic skin concentration was maintained in a frog with an intact circulation [DL 381 +/- 26 microM/mg dry wt (n = 7)] even in the presence of a high pelvic water flow [684 +/- 105 cm3.cm-2.s-1.10(-7) (n = 13)]. The water uptake in the pectoral region [231 +/- 54 cm3.cm-2.s-1.10(-7) (n = 13)] was not high enough to predict a dilution, and none was found. The concentrations were 354 +/- 21 (n = 8), 359 +/- 22 (n = 7), 353 +/- 26 (n = 7), and 373 +/- 45 microM/mg dry wt (n = 6) for C, D, DL, and DHS, respectively. Examination of the Na+ and K+ concentrations separately in the pelvic skin shows that the lower salt content in DHS frogs is mainly due to a loss of Na+.(ABSTRACT TRUNCATED AT 250 WORDS)

Stimulation of prolactin release by dopamine withdrawal: role of membrane hyperpolarization

1994 ◽  
Vol 267 (5) ◽  
pp. E781-E788 ◽  
Author(s):  
K. A. Gregerson ◽  
N. Golesorkhi ◽  
R. Chuknyiska
Keyword(s):  
Resting Membrane Potential ◽  
Prolactin Release ◽  
Membrane Hyperpolarization ◽  
Basal Release ◽  
K Concentration ◽  
Hypothalamic Dopamine ◽  
Ca2 Channels ◽  
Stimulation Of ◽  
External K

Hypothalamic dopamine (DA) tonically inhibits prolactin (PRL) release from the anterior pituitary gland, whereas removal of DA markedly augments its release to values exceeding pre-DA rates. We investigated whether electrical events induced by DA contribute to this secretory rebound. In primary cultured lactotropes, spontaneous Ca(2+)-dependent spiking activity was enhanced after recovery from DA-induced hyperpolarization. Voltage clamp studies showed a rapidly and a slowly inactivating Ca2+ current that were both augmented by a hyperpolarizing conditioning potential. We measured PRL release from perifused cells exposed to DA to correlate the electrical with the secretory responses. DA inhibited PRL release by 67%, whereas PRL secretion increased three- to fourfold over basal release after washout of DA. Valinomycin, used to directly hyperpolarize the cell membrane, mimicked the actions of DA, inhibiting PRL release (65%) and, upon washout, augmenting PRL secretion. Blocking the DA- or valinomycin-induced hyperpolarization by elevating external K+ concentration blocked both the inhibition and rebound of PRL release. These novel results demonstrate that hyperpolarization of the lactotrope membrane by DA is critical for the development of PRL rebound after DA withdrawal. We hypothesize the mechanism involves the removal of inactivation from a population of Ca2+ channels, leading to enhanced Ca2+ influx and PRL release upon recovery of the resting membrane potential after DA removal.

Molecular mechanism underlying muscle mass retention in hibernating bats: Role of periodic arousal

2010 ◽  
Vol 222 (2) ◽  
pp. 313-319 ◽  
Author(s):  
Kisoo Lee ◽  
Hyekyoung So ◽  
Taesik Gwag ◽  
Hyunwoo Ju ◽  
Ju-Woon Lee ◽  
...  
Keyword(s):  
Molecular Mechanism ◽  
Muscle Mass ◽  
Periodic Arousal

The Disposition of Intravenous Potassium in Normal Man: The Role of Insulin

1981 ◽  
Vol 61 (1) ◽  
pp. 23-28 ◽  
Author(s):  
R. H. Sterns ◽  
J. Guzzo ◽  
P. U. Feig
Keyword(s):  
Plasma Insulin ◽  
Normal Volunteer ◽  
Immunoreactive Insulin ◽  
K Uptake ◽  
Insulin Levels ◽  
Urinary Potassium ◽  
Plasma Insulin Levels ◽  
Normal Man ◽  
K Concentration

1. Potassium infusion causes an increase in immunoreactive insulin levels in dogs, but either a small (30%) or no increase in humans. Since insulin stimulates the uptake of K+ by cells, a regulatory role for K+-induced insulin release has been postulated. To study the role of insulin in regulating cellular K+ uptake, six fasting normal volunteer subjects underwent two K+ infusions on separate days. Both infusions delivered 0.6 mmol h−1 kg−1 for 3 h. In one subject glucose was simultaneously infused at 0.67 mmol h−1 kg−1 (a rate known to increase peripheral insulin levels by 40–100%); the other infusion contained no glucose. 2. Plasma insulin levels did not increase during the glucose-free infusions. During glucose-containing infusions, insulin levels were 40% higher than those during glucose-free infusions. Despite this, neither urinary potassium excretion nor the increment in plasma K+ concentration or the calculated cellular K+ uptake differed significantly during the 3 h of glucose-free and glucose-containing infusions respectively. 3. These data do not support the view that potassium-induced insulin secretion regulates cellular potassium uptake within the physiological range of plasma K+ concentration.

A possible role of inwardly rectifying K+ channels in chick myoblast differentiation

1997 ◽  
Vol 272 (3) ◽  
pp. C894-C900 ◽  
Author(s):  
K. S. Shin ◽  
J. Y. Park ◽  
H. Kwon ◽  
C. H. Chung ◽  
M. S. Kang
Keyword(s):  
Time Course ◽  
Developmental Change ◽  
Myoblast Differentiation ◽  
Resting Membrane Potential ◽  
K Channels ◽  
K Concentration ◽  
Inwardly Rectifying ◽  
K Permeability ◽  
K Currents

We examined the developmental change of inwardly rectifying K+ channels (IRK) and its possible role in myogenesis. Northern blot analysis revealed an increase in the level of IRK mRNA during myogenesis. Accordingly, IRK current was not detectable in replicating myoblasts but first appeared in aligned myoblasts that were competent for fusion and gradually increased thereafter. The time course change of IRK activity was closely related to the increase in resting membrane potential during myogenesis. Application of 0.5 mM Ba2+ to the bath depolarized the membrane and blocked IRK currents dramatically but not outwardly rectifying K+ currents. Myoblasts devoid of IRK had low resting K+ permeability, whereas myotubes that possess IRK had high resting K+ permeability. In some aligned myoblasts, anomalous hyperpolarization was elicited by increasing extracellular K+ concentration, which may be attributable to the increased conductance of IRK. Noteworthy was the fact that maximal fusion was obtained at this range of K+ concentration. These findings imply that IRK is responsible for the change in the K+ permeability during chick myogenesis, which may provide a larger driving force for Ca2+ influx that is a prerequisite for myoblast fusion.

K(+)-induced inhibition of contractile force in rat skeletal muscle: role of active Na(+)-K+ transport

1991 ◽  
Vol 261 (5) ◽  
pp. C799-C807 ◽  
Author(s):  
T. Clausen ◽  
M. E. Everts
Keyword(s):  
Rat Skeletal Muscle ◽  
Uniform Size ◽  
Muscle Work ◽  
Standard Buffer ◽  
High K ◽  
Longus Muscle ◽  
K Concentration ◽  
K Transport ◽  
Contractile Performance

During excitation, K+ is lost from the working muscle fibers, and interfiber K+ may reach 10-15 mM. This, in turn, may lead to depolarization and impairment of contractile performance. The significance of elevated interfiber K+ was assessed by exposing rat muscles of uniform size (25 mg) to buffer containing 12.5-15 mM K+ and studying the decline in contractile performance and its recovery following restoration of the K+ concentration of the standard buffer (5.9 mM). When active Na(+)-K+ transport was partially inhibited by ouabain (10(-6)-10(-5) M leading to relative occupancies of 28 and 84%, respectively), the decrease in force development induced by high K+ in soleus was considerably accelerated and recovery was delayed. Conversely, when active Na(+)-K+ transport was stimulated by epinephrine, the beta 2-agonist salbutamol, or insulin, the exposure to high K+ gave a much slower decline in force. The time until full inhibition was closely correlated to the rate of Na(+)-K+ pump-mediated 86Rb uptake (r = 0.98; P less than 0.005). Significant retardation of K(+)-induced force decline could be detected down to 10(-8) M epinephrine or salbutamol. After restoration of 5.9 mM K+, recovery was promoted by epinephrine and salbutamol but not by insulin. In extensor digitorum longus muscle, insulin reduced the rate of force decline induced by exposure to 15 mM K+. The results indicate that the Na(+)-K+ pump plays a major role in the maintenance of contractility during the physiological acute exposure to high extracellular K+ associated with muscle work.

Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone

1995 ◽  
Vol 268 (4) ◽  
pp. C985-C992 ◽  
Author(s):  
P. Q. Barrett ◽  
E. A. Ertel ◽  
M. M. Smith ◽  
J. J. Nee ◽  
C. J. Cohen
Keyword(s):  
Inhibitory Concentration ◽  
Cell Voltage ◽  
Calcium Currents ◽  
Maximal Response ◽  
Channel Blockers ◽  
Aldosterone Secretion ◽  
K Concentration ◽  
Opposing Effects ◽  
Ca2 Channels

Using Ca2+ channel blockers with different specificities for L- and T-type Ca2+ channels, we have investigated the roles of these two channel types in K(+)-induced aldosterone secretion. In whole cell voltage-clamp experiments, the spider toxin omega-agatoxin-IIIA (omega-Aga-IIIA) completely blocks L-type Ca2+ channels but has no effect on T-type Ca2+ channels. In contrast, Ni2+ and 1,4-dihydropyridines block both L- and T-type Ca2+ channels. Secretion induced by 7 mM extracellular K+ concentration ([K+]o) is unaffected by omega-Aga-IIIA but is strongly inhibited by Ni2+ or the 1,4-dihydropyridine, nitrendipine. This suggests that physiological increases in [K+]o stimulate aldosterone secretion primarily by enhancing Ca2+ entry through T-type Ca2+ channels. Surprisingly, secretion induced by 60 mM [K+]o is enhanced by omega-Aga-IIIA or Ni2+ and is inhibited by the L-type Ca2+ channel activator BAY K 8644. Nitrendipine (1 nM) also stimulates such secretion, although higher concentrations are inhibitory (concentration inhibiting 50% of maximal response approximately 30 nM). If extracellular Ca2+ concentration is reduced from 1.25 to 0.5 mM, secretion induced by 60 mM [K+]o is enhanced, and Ni2+ or low nitrendipine become inhibitory. Together, these results that L-type Ca2+ currents can reduce steroidogenesis and that the role of these currents was previously misconstrued because 1,4-dihydropyridines modify secretion by multiple mechanisms. Thus Ca2+ entry can function as a negative modulator of steroid secretion.

Effect of aminophylline on plasma [K+] and hypoxic ventilatory response during mild exercise in men

1994 ◽  
Vol 77 (4) ◽  
pp. 1763-1768 ◽  
Author(s):  
T. Igarashi ◽  
M. Nishimura ◽  
Y. Akiyama ◽  
M. Yamamoto ◽  
K. Miyamoto ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
Double Blind ◽  
Endogenous Adenosine ◽  
Adenosine Uptake ◽  
Body Activity ◽  
K Concentration ◽  
End Tidal ◽  
Arterial O2 Saturation

To examine the role of endogenous adenosine on the hypoxic ventilatory response (HVR) enhanced during exercise, we measured HVR at rest and during mild exercise (12.5 W) in nine healthy men in a supine position after pretreatment with aminophylline (5 mg/kg), an adenosine receptor blocker, or dipyridamole (0.6 mg/kg), an adenosine uptake blocker, by using a 3-day double-blind placebo-controlled design. Although HVR was enhanced during exercise on all occasions, HVR with aminophylline [0.42 +/- 0.07 (SE) l.min-1.%fall-1 of arterial O2 saturation] was significantly lower than that with placebo (0.64 +/- 0.13 l.min-1.%fall-1) or dipyridamole (0.64 +/– 0.08 l.min-1.%fall-1) during exercise (P < 0.05 for both) at similar end-tidal PCO2 on the 3 days but not at rest. We then examined the changes in plasma K+ concentration ([K+]) and catecholamines, the other possible endogenous potentiators of the carotid body activity. The exercise- and hypoxia-induced increases in plasma [K+] were significantly lower with aminophylline (0.23 +/- 0.09 meq/l) than with the placebo (0.51 +/- 0.10 meq/l) or dypyridamole (0.58 +/- 0.13 meq/l) (P < 0.05 for both). We therefore conclude that aminophylline attenuates the enhancement of HVR during mild exercise and that this might be due to its attenuating effect on exercise- and hypoxia-associated increases in plasma [K+] rather than due to its antagonizing effect on endogenous adenosine.

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