Release of creatine kinase from frog muscle by osmotic changes

1982 ◽  
Vol 242 (5) ◽  
pp. C398-C403 ◽  
Author(s):  
G. Suarez-Kurtz
Keyword(s):  
Creatine Kinase ◽  
Release Rate ◽  
Ringer Solution ◽  
Step Change ◽  
Frog Muscle ◽  
Base Line ◽  
Irreversible Loss ◽  
Glycerol Treatment ◽  
Tubular Membranes ◽  
Stimulation Of

The rate of creatine kinase (CK) release from isolated frog extensor longus digiti IV (,toe”) muscle increased on transfer from the control Ringer solution (referred to as 1.0 T) to a hyperosmotic solution (1.0 T plus 400 mM glycerol) or to hypertonic solutions (1.5–2.5 T) prepared by addition of NaCl or sucrose to 1.0 T. On return to 1.0 T, CK release rate was further elevated, reaching peak values (14.4- and 12-fold above the basal value, respectively, with the glycerol treatment and with solution 2.5 T) within 10–15 min and declining subsequently toward base line. Although the stimulation of CK release by changes in external tonicity increased with the magnitude of the osmotic step change, there was no enhancement of release when the tonicity changes were performed gradually in 0.1-T steps at 1-min intervals. The stimulation of CK release by tonicity changes cannot be ascribed to irreversible loss of functional integrity of the surface or tubular membranes or to CK diffusion through aqueous pores. The possibility that an exocytosislike process is involved is discussed.

THE ROLE OF LACTATE IN THE STIMULATION OF THE OXYGEN CONSUMPTION OF FROG MUSCLE BY INSULIN

1964 ◽  
Vol 42 (1) ◽  
pp. 139-151 ◽  
Author(s):  
D. R. H. Gourley ◽  
Kenneth C. Fisher
Keyword(s):  
Oxygen Consumption ◽  
Major Effect ◽  
Ringer Solution ◽  
Frog Muscle ◽  
Complete Oxidation ◽  
Rate Of Oxygen Consumption ◽  
Lactate Utilization ◽  
Stimulation Of ◽  
Extra Oxygen

Lactate, citrate, succinate, or acetate added to isolated muscles suspended in Ringer solution in a Warburg flask produced an increase in the rate of oxygen consumption by the muscles. At a given molar concentration of these substances the increase was greatest with lactate and was progressively less with the addenda in the order given. When the concentration of each substance was adjusted so that the rate of oxygen consumption was the same with all of them, the addition of insulin produced an increase in the oxygen uptake which was of the same magnitude in each case. Evidence is presented which suggests that by causing spontaneous activity in the muscle, the acetate, succinate, and citrate may bring about a production of lactate.The extra oxygen consumed upon the addition of lactate could account for the complete oxidation of only a small part of the lactate which actually disappeared in an experiment. By assuming that all of this extra oxygen was used in the complete oxidation of lactate, it was calculated from the total lactate utilization in the presence or absence of insulin that the major effect of insulin was on the fraction of utilized lactate which was oxidized. This conclusion was also suggested by experiments with monoiodoacetate.

scholarly journals The vasopressin mRNA poly(A) tract is unusually long and increases during stimulation of vasopressin gene expression in vivo.

1988 ◽  
Vol 8 (6) ◽  
pp. 2267-2274 ◽  
Author(s):  
E J Carrazana ◽  
K B Pasieka ◽  
J A Majzoub
Keyword(s):  
Gene Expression ◽  
Osmotic Stress ◽  
Genetic Regulation ◽  
Tail Length ◽  
Rnase H ◽  
The Body ◽  
Base Line ◽  
Tract Length ◽  
Stimulation Of

We developed a method, termed an H-blot, by which the poly(A) tract of any specific mRNA may be detected by RNA filter hybridization after its removal from the body of the mRNA by a RNase H-catalyzed endonucleolytic cleavage in the 3' untranslated region. Using this method, we studied the modulation of the length of the poly(A) tract of rat vasopressin mRNA in vivo during changes in the levels of this mRNA resulting from a physiologic stimulus, osmotic stress. The poly(A) tract of hypothalamic vasopressin mRNA in hydrated rats was, quite remarkably, approximately 250 nucleotides in length, in contrast to that of somatostatin mRNA, which was approximately 30 nucleotides long. Vasopressin mRNA poly(A) tail length increased progressively from approximately 250 to approximately 400 nucleotides with the application of the hyperosmotic stimulus and declined to base line after its removal; somatostatin mRNA poly(A) tail length did not change during osmotic stress. The poly(A) tract length of total hypothalamic mRNA was between 35 and 140 nucleotides and also did not change with osmotic stress. Modulation of poly(A) tract length of specific mRNAs during stimulation of gene expression may provide an additional level of genetic regulation.

Release and reloading of intracellular Ca stores after cholinergic stimulation of the parietal cell

1988 ◽  
Vol 254 (4) ◽  
pp. C498-C504 ◽  
Author(s):  
P. A. Negulescu ◽  
T. E. Machen
Keyword(s):  
Plasma Membrane ◽  
Parietal Cell ◽  
Base Line ◽  
Cholinergic Stimulation ◽  
Gastric Glands ◽  
Cholinergic Agonist ◽  
Intracellular Ca ◽  
Lanthanum Ion ◽  
Intact Rabbit ◽  
Stimulation Of

Microspectrofluorimetry was used to measure cytosolic free Ca, Cai, in single parietal cells of intact rabbit gastric glands loaded with the Ca-sensitive fluorescent dye, fura-2. Cells were repeatedly stimulated with the cholinergic agonist carbachol to gain insights into the membrane mechanisms involved in hormonally stimulated Ca metabolism. In either Ca-containing or Ca-free solutions, carbachol (100 microM) caused a rapid (within 30 s) elevation of Cai from a resting level of 100 nM to greater than 600 nM. After the spike, Cai decreased within 3 min to a lower level that was somewhat elevated (greater than 200 nM) over base line. This plateau was dependent on both carbachol and extracellular Ca (Cao) and could be blocked by the addition of atropine (1 microM) or lanthanum ion (La, 50 microM). The spike is due to the release of Ca from internal stores, whereas the plateau is due to Ca entry across the plasma membrane through agonist-controlled, La-inhibitable channels. After a carbachol stimulation of 3 min or longer, reloading of the internal store was absolutely dependent on Cao. Under these conditions, reloading occurred through a La-sensitive (but nifedipine- and verapamil-insensitive) pathway in the plasma membrane. No significant change in Cai was detectable during the reloading. In contrast to the longer treatments, if carbachol stimulation was terminated with atropine while Cai was still elevated, significant reloading occurred from the cytosol.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of synergism between glucose and cAMP on stimulation of insulin release

1984 ◽  
Vol 247 (6) ◽  
pp. E701-E708 ◽  
Author(s):  
W. Phang ◽  
L. Domboski ◽  
Y. Krausz ◽  
G. W. Sharp
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Ringer Solution ◽  
Intracellular Camp ◽  
Cyclic Monophosphate ◽  
Rat Pancreatic Islets ◽  
Individual Effects ◽  
The Individual ◽  
Isolated Rat ◽  
Stimulation Of

The mechanism of synergism between glucose and adenosine 3',5'-cyclic monophosphate (cAMP) on insulin release has been studied. Synergism may result from 1) inhibition of Na+-Ca2+ exchange by glucose and 2) a cAMP-induced sensitization of the release machinery to Ca2+. To distinguish between these two possibilities, isolated rat pancreatic islets were perifused with agents that raise intracellular levels of cAMP [3-isobutyl-1-methylxanthine (IBMX) and forskolin] and others that increase intracellular concentrations of Ca2+ either by blocking Na2+-Ca2+ exchange (ouabain and choline-Ringer solution) or by causing increased Ca2+ influx (KCl, carbachol, and 10 mM Ca2+). The results indicate that both the combination of cAMP and increased Ca2+ influx or blocked Na2-Ca2+ exchange and increased Ca2+ influx potentiated insulin release. When the relative potentiating abilities of cAMP and blocked Na2+-Ca2+ exchange were compared by determining the individual effects of IBMX and 1 mM ouabain (a concentration that causes similar inhibition of 45C2+ efflux as 16.7 mM glucose) in the presence of carbachol, cAMP was only 1.4 times more potent as a potentiating agent than blocked Na+-Ca2+ exchange. The greatest potentiation of insulin release was observed when Na+-Ca2+ exchange was blocked in the presence of increased levels of intracellular cAMP.

scholarly journals THE PENETRATION OF AMMONIA INTO FROG MUSCLE

1944 ◽  
Vol 28 (1) ◽  
pp. 53-77 ◽  
Author(s):  
Wallace O. Fenn ◽  
Lorraine F. Haege ◽  
Eugenia Sheridan ◽  
John B. Flick
Keyword(s):  
Smooth Muscle ◽  
Blood Plasma ◽  
Chloride Content ◽  
Ringer Solution ◽  
Frog Muscle ◽  
Rate Of Penetration ◽  
Ringer’S Solution ◽  
Muscle Ph ◽  
And Control ◽  
Made In

1. A study was made of the electrolyte changes which occur when frog muscles are immersed in a Ringer solution with 1/5 of the Na replaced by NH4Cl. Analyses were made in the solution and in the muscles for K and NH3, and the muscles were also analyzed for Cl, HCO3, and Na. Control muscles were immersed in normal Ringer's solution and similarly analyzed. 2. The amount of ammonia taken up was about equal to the K and Na lost. There was also a small increase in chloride content. The bicarbonate content was the same in both experimental and control muscles, indicating no change in the muscle pH due to the NH3 which penetrated. An increased loss of K due to the penetration of NH3 was also demonstrated by the use of radioactive K. 3. After 5 hours, the concentration of ammonia per gram of muscle is about the same as the concentration in the solution. After 4 or 5 days, the concentration in the muscle is about 1.5 times that in the solution. The inside to outside NH3 ratio is about equal to the corresponding H ion ratio, but is much less than the K ratio. 4. The rate of penetration of the NH3 is increased by a rise of temperature, by stirring the solution, and by decrease in the concentration of Na, K, Ca, or Mg in the solution; it is decreased by increasing the size of the muscles or by killing them with chloroform or boiling. 5. Liver, smooth muscle, skin, and kidney, in a few experiments, behaved much like muscle except that there was a formation of urea in the case of liver. 6. The injection of NH4Cl into anesthetized cats causes an increase in the level of K in the blood plasma.

Ca(2+)- and pH-dependent halothane stimulation of Ca2+ release in sarcoplasmic reticulum from frog muscle

1996 ◽  
Vol 271 (2) ◽  
pp. C540-C546 ◽  
Author(s):  
M. Beltran ◽  
R. Bull ◽  
P. Donoso ◽  
C. Hidalgo
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Release Kinetics ◽  
Frog Muscle ◽  
Time Range ◽  
Frog Skeletal Muscle ◽  
Open Probability ◽  
Filtration System ◽  
Stimulation Of

The effect of halothane on calcium release kinetics was studied in triad-enriched sarcoplasmic reticulum vesicles from frog skeletal muscle. Release from vesicles passively equilibrated with 3 mM 45CaCl2 was measured in the millisecond time range by use of a fast-filtration system. Halothane (400 microM) increased release rate constants at pH 7.1 and 7.4 as a function of extravesicular pCa. In contrast, halothane at pH 6.8 produced the same stimulation of release from pCa 7.0 to 3.0; no release took place in these conditions in the absence of halothane. Halothane shifted the calcium activation curve at pH 7.1, but not at pH 7.4, to the left and increased channel open probability at pH 7.1 in the cis pCa range of 7.0 to 5.0. These results indicate that cytosolic pCa and pH modulate the stimulatory effects of halothane on calcium release. Furthermore, halothane stimulated release in frog skeletal muscle at low pH and resting calcium concentration, indicating that in frog muscle halothane can override the closing of the release channels produced by these conditions, as it does in malignant hyperthermia-susceptible porcine muscle.

Effect of the ionophore A23187 on chloride transport across isolated frog cornea

1977 ◽  
Vol 233 (2) ◽  
pp. F94-F101
Author(s):  
O. A. Candia ◽  
R. Montoreano ◽  
S. M. Podos
Keyword(s):  
Chloride Transport ◽  
Ringer Solution ◽  
Ionophore A23187 ◽  
Free Medium ◽  
Intracellular Ca ◽  
Adrenergic Blockers ◽  
Relative Inhibition ◽  
Stimulation Of ◽  
Frog Cornea ◽  
Cl Permeability

The ionophore A23187 at a concentration of 10(-7) to 10(-5) M stimulated active transport of Cl across the isolated frog cornea. The ionophore had no effect in a Cl-free medium. Both unidirectional Cl fluxes were increased by A23187. The electrical resistance was decreased, and this can be totally accounted for by the increment in passive Cl fluxes. The effect of A23187 on Cl transport and permeability mimicked the effects of cyclic AMP, isoproterenol, and epinephrine. A23187 had no effect when the corneas were fully stimulated by epinephrine or isoproterenol. A23187 produced normal stimulation of the SCC in corneas pretreated with alpha- and beta-adrenergic blockers. The stimulation of the SCC by A23187 was dependent on the presence of Ca in the Ringer solution. Excess Ca (10 mM) resulted in a reduced response. Increasing the Mg concentration in the medium reduced the stimulation of the SCC with Ca concentrations of 0.1-5 mM, but prevented the relative inhibition of 10 mM Ca. Intracellular Ca concentration seemed to regulate Cl permeability of the cornea.

Ca2+- and pH-dependent halothane stimulation of Ca2+ release in sarcoplasmic reticulum from frog muscle

1996 ◽  
Vol 271 (1) ◽  
pp. 1-1
Author(s):  
M. Beltrán ◽  
R. Bull ◽  
P. Donoso ◽  
C. Hidalgo
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Frog Muscle ◽  
Ph Dependent ◽  
Stimulation Of

Pages C540-C546: M. Beltrán, R. Bull, P. Donoso, and C. Hidalgo. “Ca2+- and pH-dependent halothane stimulation of Ca2+ release in sarcoplasmic reticulum from frog muscle.” Page C543, because of a printer's error, Fig. 6 was inadvertently published as a repeat of Fig. 5. The correct Fig. 6 appears below. (See PDF)

Perfused rat intestine for study of norepinephrine release

1988 ◽  
Vol 254 (6) ◽  
pp. H1187-H1193
Author(s):  
A. P. Shepherd ◽  
G. L. Riedel ◽  
T. K. Keeton
Keyword(s):  
Release Rate ◽  
Base Line ◽  
Rat Intestine ◽  
Response Curves ◽  
Resistance Response ◽  
Bicarbonate Buffer ◽  
Alpha Adrenoceptors ◽  
Resistance Vessels ◽  
Perivascular Nerves ◽  
Large Vessels

Previous preparations for studying the neuronal release of norepinephrine (NE) employed relatively large vessels, nonsanguinous perfusates, and the preloading of [3H]NE. To study the stimulated release of endogenous NE and the responses of true resistance vessels, we developed a rat intestine preparation that is pump perfused with canine red blood cells suspended in bicarbonate buffer with 6% albumin. In a pentobarbital-anesthetized rat, the duodenum, colon, and cecum are extirpated to isolate the ileum vascularly. After the superior mesenteric artery and vein are cannulated, the perivascular nerves are isolated to stimulate the postganglionic sympathetic fibers. To evaluate the preparation, we stimulated the sympathetic fibers at 1-10 Hz with supramaximal pulses. Resistance changes were assessed by monitoring perfusion pressure, and the concentration of NE was assayed in the venous effluent by the single-isotope radioenzymatic method. During nerve stimulation, the increases in both resistance and NE release rate were frequency dependent. Repetitions of electrical stimulation yielded reproducible frequency-response curves. Pretreatment with phentolamine (10 microM) abolished the resistance response and enhanced stimulated NE release, which roughly tripled at 10 Hz. Phentolamine at smaller doses (1 microM) eliminated the resistance responses to stimulation but did not enhance NE release. Cocaine alone (30 microM) increased base-line resistance and unstimulated NE release. After cocaine pretreatment, phentolamine at 1 microM enhanced the stimulated NE release rate. We conclude that the isolated rat intestine contains postsynaptic alpha-adrenoceptors that mediate vasconstriction and prejunctional alpha 2-adrenoceptors that mediate the inhibition of NE release. Thus the rat intestine is a responsive preparation for studying the release of endogenous NE and noradrenergic neurotransmission.

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