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Ca channel blockers

Discussion in 'The EMF Rx' started by NeilBB, Oct 11, 2013.

  1. Jack Kruse

    Jack Kruse Administrator

    Lasers are something I use on myself to optimize myself. I do not talk about it much. Photons all have different energy levels. High energy level photons are perceived as blue and those with lesser energies get perceived as red. When photons crash into matter they get re routed or absorbed. This interaction is a big deal in the brain. The most common molecule in and around the brain is water. Water molecules selectively absorb low energy photons, which is why water appears blue to us. When water absorbs photons the particle knocks out an electron in DHA and moves it to a higher energy state. The resulting charge excites and electron in the pi electron cloud of DHA in a neuronal membrane causing the DC current to flow. This is the current Robert O Becker found in the 1960's and could not explain its origin. I can. The semiconductors in us then are used to amplify the electrical signal from every DHA photodiode. This is how the brain collects environmental native EMF and deciphers things.
     
    Alex97232 likes this.
  2. PaulG

    PaulG New Member

    The vielight come in three models (633, 655 and 810nm wavelengths), with the claim that the latest one that pulses at 10hz 810nm laser penetrates and affects the brain more optimally. What is the recommendation here?
     
  3. explains every torn rotator cuff, achilles tendinopathy and plantar fasciitis i see in all the crossfit retards that come into my clinic
     
  4. Clayton

    Clayton New Member

    810 (IR light) causes the most exclusion zone growth
     
  5. Jack Kruse

    Jack Kruse Administrator

    ^^^THIS but if you dehydrated any level of red light helps water recover electrons quickly as I mentioned in the Q & A.
     
    David Limacher likes this.
  6. Stella

    Stella New Member

  7. SeaHorse

    SeaHorse Gold

    from Wiki article: Part 1



    Mechanism of action[edit]

    [​IMG]
    [​IMG]

    A calcium channel embedded in a cell membrane.
    In the body's tissues, the concentration of calcium ions (Ca2+) outside of cells is normally about ten-thousand-fold higher than the concentration inside of cells. Embedded in the membrane of some cells are calcium channels. When these cells receive a certain signal, the channels open, letting calcium rush into the cell. The resulting increase in intracellular calcium has different effects in different types of cells. Calcium channel blockers prevent or reduce the opening of these channels and thereby reduce these effects.

    There are several types of calcium channels, and a number of classes of calcium channel blockers, but almost all of them preferentially or exclusively block the L-type voltage-gated calcium channel.[5]

    L-type calcium channels are responsible for excitation-contraction coupling of skeletal, smooth, and cardiac muscle and for hormonesecretion in endocrine cells. In the heart they are also involved in the conduction of the pacemaker signals. CCBs used as medications primarily have three effects:

    • by acting on vascular smooth muscle they reduce contraction of the arteries and cause an increase in arterial diameter, a phenomenon called vasodilation (CCBs do not work on venous smooth muscle)
    • by acting on cardiac muscles (myocardium), they reduce the force of contraction of the heart
    • by slowing down the conduction of electrical activity within the heart, they slow down the heart beat.
    Since blood pressure is determined by cardiac output and peripheral resistance, CCBs reduce blood pressure. With relatively low blood pressure, the afterload on the heart decreases; this decreases how hard the heart must work to eject blood into the aorta, and so the amount of oxygen required by the heart decreases accordingly. This can help ameliorate symptoms of ischaemic heart disease such as angina pectoris.

    Reducing the force of contraction of the myocardium is known as the negative inotropic effect of calcium channel blockers. Slowing down the conduction of electrical activity within the heart, by blocking the calcium channel during the plateau phase of the action potential of the heart (see: cardiac action potential), results in a negative chronotropic effect, or a lowering of heart rate. This can increase the potential for heart block. The negative chronotropic effects of calcium channel blockers make them a commonly used class of agents in individuals with atrial fibrillation or flutter in whom control of the heart rate is generally a goal. Negative chronotropy can be beneficial when treating a variety of disease processes because lower heart rates represent lower cardiac oxygen requirements. Elevated heart rate can result in significantly higher "cardiac work," which can result in symptoms of angina.

    The class of CCBs known as dihydropyridines mainly affect arterial vascular smooth muscle and lower blood pressure by causing vasodilation. The phenylalkylamine class of CCBs mainly affect the cells of the heart and have negative inotropic and negative chronotropic effects. The benzothiazepine class of CCBs combine effects of the other two classes.

    It is because of the negative inotropic effects that the nondihydropyridine calcium channel blockers should be avoided (or used with caution) in individuals with cardiomyopathy.[6]

    Unlike beta blockers, calcium channel blockers do not decrease the responsiveness of the heart to input from the sympathetic nervous system. Since moment-to-moment blood pressure regulation is carried out by the sympathetic nervous system (via the baroreceptor reflex), calcium channel blockers allow blood pressure to be maintained more effectively than do beta blockers. However, because dihydropyridine calcium channel blockers result in a decrease in blood pressure, the baroreceptor reflex often initiates a reflexive increase in sympathetic activity leading to increased heart rate and contractility.

    Ionic calcium is antagonized by magnesium ions in the nervous system. Because of this, bioavailable supplements of magnesium, possibly including magnesium chloride,magnesium lactate, and magnesium aspartate, may increase or enhance the effects of calcium channel blockade.[7]

    N-type calcium channels are found in neurons and are involved in the release of neurotransmitter at synapses. Ziconotide is a selective blocker of these calcium channels and acts as an analgesic.
     
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  8. Clayton

    Clayton New Member

    Im on it and I definitely notice a difference
     
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  9. SeaHorse

    SeaHorse Gold

    Here's part 11


    Classes[edit]

    Dihydropyridine[edit]
    Dihydropyridine calcium channel blockers
    are derived from the molecule dihydropyridine and often used to reduce systemic vascular resistance and arterial pressure. Sometimes when they are used to treat angina, the vasodilation and hypotension can lead to reflex tachycardia, which can be detrimental for patients with ischemic symptoms because of the resulting increase in myocardial oxygen demand). Dihydropyridine calcium channel blockers can worsen proteinuria in patients with nephropathy.[8]

    This CCB class is easily identified by the suffix "-dipine".

    Side effects of these drugs may include but are not limited to:

    • Dizziness, headache, redness in the face
    • Fluid buildup in the legs and ankle edema
    • Rapid heart rate
    • Slow heart rate
    • Constipation
    • Gingival overgrowth
    Non-dihydropyridine[edit]
    Phenylalkylamine[edit]
    [​IMG]
    [​IMG]

    Skeletal formula of verapamil


    Phenylalkylamine calcium channel blockers are relatively selective for myocardium, reduce myocardial oxygen demand and reverse coronary vasospasm, and are often used to treat angina. They have minimal vasodilatory effects compared with dihydropyridines and therefore cause less reflex tachycardia, making it appealing for treatment of angina, where tachycardia can be the most significant contributor to the heart's need for oxygen. Therefore, as vasodilation is minimal with the phenylalkylamines, the major mechanism of action is causing negative inotropy. Phenylalkylamines are thought to access calcium channels from the intracellular side, although the evidence is somewhat mixed.[9]

    Benzothiazepine[edit]
    [​IMG]
    [​IMG]

    Structural formula of diltiazem


    Benzothiazepine calcium channel blockers belong to the benzothiazepine class of compounds and are an intermediate class between phenylalkylamine and dihydropyridines in their selectivity for vascular calcium channels. By having both cardiac depressant and vasodilator actions, benzothiazepines are able to reduce arterial pressure without producing the same degree of reflex cardiac stimulation caused by dihydropyridines.

    • Diltiazem (Cardizem) (also used experimentally to prevent migraine)
     
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  10. excitotoxicity, and thus apoptosis is caused by influx, not efflux of calcium when high voltage ca channels such as L type are activated...
    i have never understood why we are always talking about efflux, unless some do it the opposite way??
    or it pumps in then suddenly out again?
     
  11. Stella

    Stella New Member

    Out of curiosity, are you normotensive or taking for hypertension? I'm normotensive but would be interested in beneficial non indicated uses. Got to forward all of these to my doc for a serious discussion at next months appt.
     
  12. Jack Kruse

    Jack Kruse Administrator

    Calcium is tightly bound in the ER and it gets free via efflux to rush into the inner mitochondrial membrane to cause apoptosis. People forget the mitochondria is like a prokaryote inside of our cells.
     
  13. bionaut

    bionaut New Member

    Does Hawthorne act as an effective over the counter calcium channel blocker?
     
  14. Clayton

    Clayton New Member

    Nope normotensive. Taking it strictly for the emf mitigating effects.
     
  15. Jack Kruse

    Jack Kruse Administrator

  16. caroline

    caroline Moderator

  17. PaulG

    PaulG New Member

    The first comment is spot on

    "The experiment can be reproduced consistently in a matter of hours in a petri dish: Give a colony of bacteria an energy source; the colony will expand as quickly as it can utilize the energy source, until either their environment either becomes toxic from waste, or the energy source runs out, whichever comes first. Then, the colony collapses.

    One might hope humans are slightly more intelligent than bacteria in a petri dish, but so far, it isn't looking good. "
     
    Alex97232, Shijin13, Stella and 2 others like this.
  18. RobH

    RobH Gold


    What specifically are you noticing?

    Robh
     
  19. THIS
     
  20. Jack Kruse

    Jack Kruse Administrator

    Go listen to the Australian webinar about what I said about the Great barrier reef.....or in the CO2 and EMF thread......the crumbs are all there.
     
    Shijin13 likes this.

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