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Results for “calcium channel”

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At least 19 recordsLinked to original sources
PubMed1978

Calcium entry leads to inactivation of calcium channel in Paramecium.

Under depolarizing voltage clamp of Paramecium an inward calcium current developed and subsequently relaxed within 10 milliseconds. The relaxation was substantially slowed when most of the extracellular calcium was replaced by either strontium or barium. Evidence is presented that the relaxation is not accounted for by a drop in electromotive force acting on calcium, or by activation of a delayed potassium current. Relaxation of the current must, therefore, result from an inactivation of the calcium channel. This inactivation persisted after a pulse, as manifested by a reduced calcium current during subsequent depolarization. Inactivation was retarded by procedures that reduce net entry of calcium, and was independent of membrane potential. The calcium channel undergoes inactivation as a consequence of calcium entry during depolarization. In this respect, inactivation of the calcium channel departs qualitatively from the behavior described in the Hodgkin-Huxley model of the sodium channel.

Animals↗
PubMed1977

Calcium channels in Paramecium aurelia.

Reversal of swimming direction in paramecium is dependent on the calcium influx through the excitable-membrane calcium channels. Several mutants of Paramecium aurelia have been selected on the basis of their resistance to the paralyzing effect of barium. The mutants have reduced reversal behavior and are in the same three pawn genes as discovered by Kung (16, 17). Also, in barium solutions, the pawns live longer than the wild-type; however, pwB mutants are more resistant to barium toxicity than pwA mutants. These results suggest that the selection picked up mutants in the calcium channel. Electrophysiological studies demonstrate this point directly, showing defective calcium activation in all pawns, but also defective anomalous rectification in pwB mutants. A model is presented which accounts for the differences between pwA and pwB mutants. It ascribes the depolarization-sensitive "gate" function to the pwA gene product and the "pore" function to the pwB gene product. Additionally, the stability of the channel structure is demonstrated, channel half-life being from five to eight days.

Animals↗
PubMed1978

Voltage-sensitive calcium channels regulate guanosine 3',5'-cyclic monophosphate levels in neuroblastoma cells.

Veratridine or high potassium concentration increased guanosine 3',5'-cyclic monophosphate (cGMP) levels in neuroblastoma cells of clone N1E-115 without affecting levels of adenosine 3',5'-cyclic monophosphate (cAMP). The increases in cGMP appear to be a direct result of the depolarizing action of these agents and not due to the action of substances released from the cells upon depolarization. The increase in cGMP produced by depolarization was dependent upon extracellular calcium and could be prevented by the calcium channel blockers D600 and cobalt. Carbachol, acting on muscarinic acetylcholine receptors, also caused a calcium-dependent increase in cGMP in these cells. The carbachol and potassium effects were additive from 5 to 100 mM potassium and from 1 to 3 mM calcium. The carbachol response was nearly as sensitive as the potassium response to inhibition by D600 but was much less sensitive to inhibition by cobalt. The results suggest that depolarization increases cGMP levels in these cells by opening voltage-sensitive calcium channels and that activation of muscarinic receptors opens separate, voltage-insensitive calcium channels.

Carbachol↗
PubMed1978

[Separation of potassium and calcium channels in the nerve cell soma membrane].

Calcium inward and potassium outward currents were studied on internally dialysed isolated neurons of the snail Helix pomatia. Different sensitivity of the corresponding channels to changes in external pH was found. This difference was used for separation of their activation regions on the potential axis so that the characteristics of the inward and outward currents could be studied with minimal overlap. It is shown that the outward current channels possess a definite permeability to Tris ions (PTris :PK=0.05). This explains the impossibility to switch off this current by substituting Tris for internal potassium. The channels for the inward calcium current inactivate slowly with a first order kinetic; their instantaneous current-voltage characteristic reveals considerable Goldman-type rectification. The selectivity of the calcium channels to other bivallent cations is Ba:Sr:Ca:Mg=2.8:2.6:1.0:0.2.

Animals↗
PubMed1977

Permeation of manganese, cadmium, zinc, and beryllium through calcium channels of an insect muscle membrane.

Larval muscle fibers of a beetle, Xylotrupes dichotomus, produce calcium spikes that are maintained when the fibers are bathed in saline solutions containing manganese, cadmium, zinc, or beryllium instead of calcium. This indicates that these cations permeate the calcium channels of the muscle fiber. By contrast, cobalt, nickel, and magnesium are nonpermeating and behave as competitive inhibitors of the permeation of the other divalent cations. Some of the permeating cations suppress delayed rectification.

Action Potentials↗
PubMed1979

Calcium channels in the high resistivity axonal membrane of photoreceptors of the giant barnacle.

1. The distribution of calcium channels in the cell membrane of the photoreceptor neurone of the giant barnacle, Balanus nubilus, was studied by recording intracellularly in or near the soma, in the axon, and near the presynaptic terminals. The membrane properties of these different regions of the cell could be studied by separately superfusing each region with test salines or by cutting the axon between two regions. 2. In the presence of tetraethylammonium (TEA) or 3-aminopyridine (3-AP), but not in their absence, Ca dependent action potentials could be evoked with depolarizing current pulses in the somatic, axonal, and terminal regions. Consequently, voltage-sensitive Ca channels and TEA-sensitive channels are present in all three regions of the cell. 3. The action potentials recorded from the three regions were similar in their slow times-to-peak (30-300 msec), long durations (0.2-2 sec in 100 mM-TEA), and long-lasting (0.2-10 sec) undershoots. The action potentials were inhibited by extracellular Co. 4. Clear differences were consistently observed between terminal action potentials and axonal or somatic action potentials in TEA. Terminal action potentials displayed a lower voltage threshold, faster rate of rise, and were less sensitive to inhibition by extracellular cobalt, suggesting that the Ca current is greater in the terminal region. 5. Bathing the receptor axon in low Ca or Co solutions led to a greater attenuation of large depolarizing components of the visual signal as they spread to the presynaptic terminals.

Action Potentials↗
PubMed2025

Pharmacogenomic insights into angiotensin converting enzyme inhibitors and calcium channel blockers for personalized hypertension treatment.

Arterial hypertension is a complex disorder influenced by extensive genetic variability, which contributes to interindividual differences in drug response by altering metabolism, transport, and receptor interaction. Current antihypertensive therapies effectively control arterial hypertension in only about half of patients, emphasizing the need for precise strategies. Genetic variation plays a crucial role in modulating drug response, and integrating this knowledge into clinical practice could significantly transform the management of hypertension through personalized medicine. This review examines the impact of genetic factors on the efficacy of antihypertensive drug classes, including angiotensin converting enzyme inhibitors and calcium channel blockers. It also examines advances in pharmacogenomic research that can aid in tailoring drug selection and dose adjustment based on genetic profiles. Beyond genomics, this review also highlights the impact of multiomics approaches, such as proteomics, metabolomics, and microbiomics, in advancing precision medicine and enabling a comprehensive, personalized approach to hypertension management. Pharmacogenomics can help refine hypertension care, improve patient outcomes, and reduce the burden of the disease. The future of hypertension treatment lies in precision medicine, where therapy is tailored to individual needs for effective and personalized management.

Humans↗
PubMed1977

[Effect of calcium channel blockaders (verapamil, D-600 and manganese ions) on mediator release from frog muscle motor nerve endings].

The reduction in the EPPs quantum content produced by manganese ions (0.4-5.0 mM) was observed in the frog sartorius muscle. In contrast to the inhibitory action on the evoked release, manganese ions increased a spontaneous transmitter release. Verapamil (1-10(-6)-5-10(-5) g/ml) and D-600 (2.5-10(-5) g/ml) did not inhibit the evoked release but increased the spontaneous one. All the calcium antagonists studied were able to prevent the facilitatory effect of imidazole (3 mM) on neuromuscular transmission. Verapamil (5-10(-6)-5-10(-5) g/ml) disturbed the action potential generation during the repetitive stimulation of the motor nerve. Manganese ions were ineffective in this respect. A conclusion is made that the calcium ionic channels in the nerve terminals differ from the calcium channels in some other tissues (heart, soma of neurons etc.).

Animals↗
PubMed1979

Regulation of nerve terminal calcium channel selectivity by a weak acid site.

The effects of low pH, and of alkaline earth cations, were examined on calcium uptake by pinched-off nerve terminals (synaptosomes). This uptake appears to be mediated by voltage-sensitive Ca channels (J. Physiol. 247:617, 1975). Ca uptake was measured in low (5 mM) or high (77 mM) potassium media. The extra uptake promoted by depolarizing (K-rich) media was almost maximal at pH 7.5, and decreased as the pH was lowered. Data relating depolarization-induced 45Ca uptake to pH fit a titration curve with a pKa approximately 6. Experiments in which Ca concentration and pH were both varied indicated that Ca2+ and H+ compete for a common binding site. Inhibition of depolarization-induced 45Ca uptake by the alkaline earth cations was studied to determine the apparent binding sequence for these cations in the Ca channels: Ca greater than Sr greater than Ba greater than Mg. This sequence resembles that observed for block of Ca channels in other preparations. The apparent binding sequence of the alkaline earth cations and the apparent pKa (approximately 6) of the Ca-binding site indicate that the Ca channel is a "high field strength" system. Protonation of a Ca channel binding site could explain the inhibitory effect of low pH on Ca-dependent neurotransmitter release (cf. Del Castillo et al., J. Cell. Comp. Physiol. 59:35, 1962).

Animals↗