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Biomedical subjects

A Den Hertog

Publications and source records attributed to A Den Hertog.

49 records · Page 3Linked to original sources
PubMed1981

Calcium and the alpha-action of catecholamines on guinea-pig taenia caeci.

1. The involvement of calcium in the alpha-action of adrenaline on guinea-pig taenia caeci was studied by measuring the changes in membrane potential and muscle contraction, using the sucrose-gap method, and by determining the (42)K efflux, in the presence of a beta-blocker (propranolol, 1.8 x 10(-6)m).2. In the presence of extracellular calcium, the hyperpolarization caused by adrenaline (3 x 10(-6)m) was sustained during the period of its application (5 min), both in active preparations (at 36 degrees C) and in quiescent muscle (22 degrees C). In the absence of calcium, adrenaline caused a transient hyperpolarization which was smaller at 36 degrees C than at 22 degrees C and passed off within 5 min, while adrenaline was present.3. Both the sustained and the transient hyperpolarization were associated with an increase in (42)K efflux which had a similar time course. (42)K flux measurements were made in depolarized tissue (52.8 mm-potassium), in which the effect was consistent and more pronounced than in polarized muscle (2.8 mm-potassium).4. The transient hyperpolarization which is resistant to calcium removal and EGTA (0.1-2.0 mm) could be evoked only once but, following a short exposure to calcium (2.5 mm) for 20 sec and readmission of calcium-free medium, it was restored.5. The sustained and the transient hyperpolarization and the increase in (42)K efflux were abolished by the alpha-antagonist phentolamine (10(-5)m); their amplitude was dependent on the adrenaline concentration in the range 10(-7) to 3 x 10(-6)m, and both responses persisted in the absence of sodium or chloride.6. The hyperpolarization and the increase in (42)K efflux were greater at higher external calcium concentrations (0.3-2.5 mm).7. Cobalt (0.6 mm), D600 (2.5 x 10(-5)m) and the bee toxin apamin (10(-7)m) reduced the alpha-response.8. In the presence of apamin, in calcium-containing solution, the sustained hyperpolarization caused by adrenaline was preceded by, or converted to, depolarization, spike discharge and contraction.9. The depolarizing effect of adrenaline in the presence of apamin persisted in sodium-free or chloride-free medium, but was blocked in the absence of calcium and diminished by cobalt and D600.10. It is concluded that the alpha-response of guinea-pig taenia caeci consists of two components, both involving calcium. First, the activation of alpha-receptors increases calcium entry, which leads to the opening of potassium channels, a sustained hyperpolarization and inhibition of muscle activity. Secondly, in the absence of external calcium, a transient hyperpolarization is revealed, presumably due to the release of bound calcium from a limited cellular store which can be replenished by addition of external calcium, and this leads to an increase in potassium permeability.

Animals↗
PubMed1980

The action of apamin on guinea-pig taenia caeci.

Apamin (10(-7) M), a substance extracted from bee venom (apis mellifica) causes stimulation of the taenia caeci as seen from an increase in spike activity. The inhibitory effect of ATP or adrenaline (Adr) was reflected by hyperpolarization of the muscle cell, cessation of spike activity and relaxation of the muscle. The 42K efflux and the membrane conductance were enhanced in the presence of these substances. Apamin converted the hyperpolarization caused by ATP or Adr into a transient depolarization which produced contraction of the muscle cells. The changes in membrane conductance and 42K efflux were diminished by the bee toxin. Furthermore, the potassium-dependent phase of the action potential was lengthened by apamin. Reduction of the extracellular chloride or sodium concentration, blockade of the nervous system by TTX (3 x 10(-7) M) or inhibition of spike activity by D600 (3 x 19(-6) M) did not affect the excitatory and blocking action of apamin. A high concentration of the calcium antagonist D600 (10(-4) M) or omission of extracellular calcium was needed to reduce the transient depolarization evoked by ATP or Adr in the presence of apamin. It is concluded that apamin prevents the opening of the ATP- and Adr-sensitive and voltage-dependent potassium channels in guinea-pig taenia caeci.

Action Potentials↗
PubMed1980

Inhibition of fundic strips from guinea-pig stomach: the effect of theophylline on responses to adenosine, ATP and intramural nerve stimulation.

The effect of theophylline on the ATP response, the adenosine response and the inhibitory junction potential was studied on circular smooth muscle preparations of the guinea-pig stomach. The amplitude of the inhibitory junction potential evoked after stimulation of the non-cholinergic, non-adrenergic nervous system was not affected by a moderate concentration of theophylline (5 x 10(-6)-10(-5) M). At higher concentrations (5 x 10(-5)-10(-3) M) theophylline relaxed the muscle hyperpolarized the cell membrane and reduced the inhibitory junction potential slightly. ATP and adenosine (5 x 10(-6)-10(-3) M) also caused relaxation of the smooth muscle cells and hyperpolarization of the cell membrane. Theophylline (5 x 10(-6)-10(-3) M) did not antagonize these effects; in the presence of theophylline (5 x 10(-5)-10(-3) M) additional relaxations produced by ATP and adenosine were limited in view of the muscle tone. These results indicate that theophylline does not inhibit either the effect of the non-adrenergic inhibitory transmitter on the smooth muscle cells of the guinea-pig stomach or the actions of ATP and adenosine. This suggests that the existence of theophylline-sensitive adenosine receptors in the stomach-muscle cell membrane is unlikely and that theophylline is not the drug of choice to support the purinergic nerve hypothesis.

Adenosine↗
PubMed1980

The effect of the phenyl phosphonate N-0164 on prostaglandin action and on post inhibitory excitation in the taenia of guinea-pig caecum.

In the taenia of guinea-pig caecum, electrical stimulation of the non-adrenergic inhibitory nerves caused relaxation which was followed by an after-contraction. The purinergic compount ATP (10(-5) M) also produced muscle relaxation while wash-out was associated with an after-contraction. The role of prostaglandins (E1, E2, F1 alpha, F2 alpha; 10(-9)--10(-6 M) in these contractions was studied. The prostaglandin responses reflected by membrane depolarization (E type) and muscle contraction (E and F type) were inhibited by the phenyl phosphonate N-0164 (10(-5) M). This substance did not affect the membrane potential or the nerve-mediated non-adrenergic inhibitory junction potential (IJP). The effect of N-0164 on the muscle cells could account for the limited reduction of the after-depolarization and contraction following electrical stimulation. The ATP after-contraction, however, could be inhibited completely by N-0164. The results are consistent with the possibility that the ATP after-contraction was produced by E type prostaglandins, while involvement of prostaglandins in post inhibitory excitation following nerve stimulation seems unlikely.

Adenosine Triphosphate↗
PubMed1979

The effect of apamin on the smooth muscle cells of the guinea-pig taenia coli.

The polypeptide apamin caused a small depolarization of the muscle cell membrane of the guinea-pig taenia coli accompanied by enhancement of spike activity and a concomitant muscle contration. The membrane hyperpolarization evoked by intramural stimulation of the non-adrenergic inhibitory nerves (inhibitory junction potential) was reduced by apamin; the antagonism being non-competitive in nature. The rebound depolarization and contraction following the inhibitory junction potential was enhanced by apamin. The membrane hyperpolarization induced by the purinergic compound ATP and by the sympathomimetic adrenaline was converted to a depolarization in the presence of apamin. This depolarization resulted in an increased spike activity and muscle contraction. This was followed by membrane hyperpolarization and muscle relaxation after washout of the drugs. These findings indicate that apamin is a non-competitive, non-specific antagonist of the non-adrenergic inhibitory transmitter and that the inhibitory junction potential and the rebound are mutually independent phenomena.

Animals↗
PubMed1979

Inhibition of fundic strips from guinea-pig stomach: the effect of theophylline on the membrane potential, muscle contraction and ion fluxes.

The effect of theophylline on the smooth muscle cells of the fundic part of the stomach of the guinea pig was investigated. Theophylline hyperpolarized the membrane, inhibited spike discharges and slow waves and produced relaxation of the muscle cells. Furthermore, the theophylline-induced relaxation was not affected in low sodium solution or during inhibition of the sodium pump. Partial inhibition of the theophylline relaxation was seen in muscle depolarized by a high potassium solution and also when ATP was the relaxant. The potassium efflux was enhanced by ATP, but was not markedly changed by theophylline. A change in calcium efflux in the presence of theophylline could not be measured in quiescent preparations. The calcium influx was not changed by theophylline in Krebs, by low Ca, or by high K solution. Furthermore, the tissue content of cyclic AMP was increased by 59.6% in the presence of theophylline (2 x 10(-3) M). The conclusion is reached that the most likely mode of action of theophylline is a suppression of spontaneous activity and an extensive calcium binding to internal sites.

Animals↗
PubMed1976

Potassium induced potential changes in rat diaphragm muscle.

The effect of different potassium concentrations on the membrane potential and membrane resistance of rat diaphragm muscle fibres was measured by means of a double sucrose gap method and a microelectrode technique. Concentration measurements showed that the muscle fibres gained sodium and lost potassium in the equilibration period. In the absence of external chloride changing the external potassium concentration from 2.8 mM to potassium-free caused a depolarization of the membrane of about 30 mV and a small increase in membrane resistance. This K-dependent potential change (K-response) was induced by ouabain, K-strophanthin, 2,4-dinitrophenol and cyanide, indicating that an energy requiring process is involved. The temperature dependence of the K-response found is consistent with this assumption. Variation in potassium permeability in the absence and presence of external potassium could account for only 13% of the K-response. The K-response amplitude appeared to depend on the external potassium and the internal sodium concentration. Hyperpolarization of the membrane could not only be produced after readmission of potassium but also after addition of thallium, the latter being more potent. Raising the external chloride concentration resulted in a decrease of the K-response and membrane resistance. The current, generating the K-response was shown to be hardly influenced by conditional polarization of the membrane. It is concluded from these results that the K-response is mainly due to the operation of an electrogenic sodium pump.

Animals↗