Talk:Calcium channel blocker

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Start[edit]

"Many calcium channel blockers also slow 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). This is known as a negative dromotropic effect."

Maybe this sentence should be changed. My understanding of dromotropism is that it specifically refers to trasnmission through the AV node. User:boruchfishman May 20, 2008 —Preceding unsigned comment added by 169.132.18.249 (talk) 12:58, 20 May 2008 (UTC)


"With low blood pressure, the heart does not have to work as hard, this can ease problems with cardiac myopathy and coronary disease."

Maybe the above sentence should be removed, given that calcium channel blockers have a relative contraindication in the setting of ischemic heart disease? Ksheka 16:29, Jun 19, 2004 (UTC)


i think that there is a mistake in this article "The resulting increase in intracellular calcium has different effects in different types of cells." according to Kaplan book on page 95 (pharma) it clearly state that CCB's DECREASE IC ca++ level. photocopyj@gmail.com

Why no mention of male contraceptive effect?[edit]

The article on male contraceptives says that calcium channel blocker drugs act as a male contraceptive by "interfering with the sperms’ ability to swim properly or preventing sperm from recognizing or binding to an egg". Why is this not mentioned in this article? --Cohen the Bavarian 19:40, 18 June 2006 (UTC)


Because it is not true, nothing has been published showing any contraceptive effect of calcium channel blockers.

How about azelnidipine, the new CCB that is approved in Japan?[edit]

How about Osthol? Elsewhere on Wikipedia it says "Osthol is a calcium channel blocker which is found in the plants Cnidium monnieri and Angelica pubescens."[edit]

Magnesium[edit]

The part about the pharmaceutical industry taking over this website is not necessary and adds nothing to the page. There is no reference given to support the use of Magnesium in lowering heart rate. It is not relevant to this page. 86.132.104.167 17:07, 2 April 2007 (UTC)

Indeed. I've commented out the section, hopefully it will be rewritten with proper sources in due time. Fvasconcellos 19:47, 2 April 2007 (UTC)

I am a patient treated for hypertension for a very long time (> 17 years). The early symtoms of hypertension were left untreated out of ignorance. I used however verious supplements such as garlic (raw), garlic tablets and later discovered magnesium tablets (had already began a mild hypertension treatment). I found the magnesium very useful for lowering the heart frequency especially that related to stress and excessive nervosity). It has to be taken in a very special way in order to work: empty stomach or well outside meals and well away from any cause of nervous excitement (best is to take it and go to your bedroom and lay in bed for 10-15 minutes thinking of nothing at all if possible). In the latter case the result is great. Even now I use this method though rarely since I am also taking beta blockers and CCBs. --178.254.123.232 (talk) 09:29, 20 September 2013 (UTC) dleonte@mylife.lu

The material in this article appears to be copyright infringing[edit]

Although neither the Wikipedia page nor the other webpage I noted which seem to have nearly identical text list any sources, it is hard to say who is stealing from whom. Of course, if Dr. Klabunde is lifting from Wikipedia that is legal, but if whoever wrote the Wikipedia entry cut and pasted from Dr. Klabunde's page, we have a problem. It is beyond me to understand how this is decided or handled.

http://www.cvpharmacology.com/vasodilator/CCB.htm

Tetrandrine[edit]

According to the article, tetrandrine is a calcium channel blocker. Should it not be listed in this article? 99.228.1.190 (talk) 07:01, 11 January 2009 (UTC)

Ca Blocker[edit]

Plendil (Felodipine) is also a dihydropyridine CCB, please add to the list. Thanks HCC Rph CA Selective inhibition of heart rate by calcium blockers remains inferior to beta blockade.--lbeben 02:02, 13 January 2009 (UTC) —Preceding unsigned comment added by Lbeben (talkcontribs)

First line[edit]

That first line reads like a ESOL student wrote it. The next paragraph starts off with "It", despite talking about a plural in the first sentence. —Preceding unsigned comment added by 118.90.39.22 (talk) 04:35, 16 February 2011 (UTC)

I take that back - most of the article reads terribly! I'll try to update it one day. 118.90.39.22 (talk) 04:40, 16 February 2011 (UTC)


Second Line[edit]

Also on the subject of grammar, in the SECOND sentence: "blood vessels, or neurons." It is more clear and more correct to say "and" rather than "or." --JimRodgers (talk) 21:46, 1 May 2011 (UTC)

Third Line[edit]

"Drugs used to target neurons are used as antiepileptics and are not covered in this article." Perhaps we all could agree the phrase "Drugs used to target neurons" is extremely nebulous. And perhaps we could agree on the minimalistic fix thus by not saying "drugs used to target neurons" and by being a bit more general as follows: "Other drugs that target neurons, such as Antiepileptics, are not covered in this article."

The core problem is the use of the phrase "target neurons" here; it is simply bad writing. It may bespeak bad science or an ESOL author as suggested above.

--JimRodgers (talk) 21:47, 1 May 2011 (UTC)


Mechanism of Action[edit]

The article states "Since blood pressure is determined by cardiac output and peripheral resistance, blood pressure drops." This is a widely held misbelief. The relationship exists if you define the terms for it, but it is NOT CAUSAL. The vertibrate circulatory systems are mechanically CIRCULATORY systems; thus, there are feedback loops. When feedback exists, the individual component behaviors are not deterministic of system behavior. This is a basic scientific fact that underlies every system. Peripheral resistance is a lumped parameter used in special abbreviated models; it is the inverse of the sum of all the systemic arterial fluid conductances. It is not physically real. Even the simplist of computer models (lumped parameters, average values, no pulmonary circuit) clearly show that systemic arterial pressure is directly related to blood volume and neither "cardiac output" nor "peripheral resistnce." Now add the autonomic neurohormonal feedback systems, and you are WAY past worrying about controlling BP by either PR or CO. This is what we scientists call "Ohms Law." It IS true; however, changing one will always change the other — if "changing" PR even has meaning anyway.

The so-called Starling/Franck Law of the Heart reveals that the heart is a transconductance amplifier. If laymen's terms, CO is a linear function of input pressure (~CVP). The autonomic neurohormonal control system may have many effector mechanisms; but, obviously, the key control modality is changing the slope (and intercept) of the hearts I/O function. Retail medicine has gone far afield of these facts. In Scientific terms, things went quickly awry in the 1960's after Ciba-Geigy engaged Frank Netter to make those famous pictures of hypertrophied arterioles in their campaign to sell Apresoline, a peripheral vasodilator. Peripheral vasodilation, if successful, will raise the CO by lowering the PR while AP is controlled by the CNS. This can cause increased load on the heart and increase the death rate. I believe studies finally have shown this to be true, but I do not have the references handy. I apologize. Nevertheless, vasodilation in general may help alleviate hypertension in many ways like increasing perfusion in the kidneys, thus reducing excess blood volume, which is the core cause of essential hypertension. When animal experimenters want to induce hypertension, they damage the kidneys.

A calcium channel blocker will appear to act as both an adrenergic blocker (lowering the strength of contraction AND heart rate) and a diuretic by vasodilation in the kidneys. This is a powerful effect. Using a simpler diuretic could raise the heart rate, mitigating the effect. Adding a smoothe muscle relaxer that did not as substantially suppress heart rate (THC? Atenolol?) would more substantially lower the AP — and the increased heart rate would not be able to make up for it. This resembles shock. Too much CaChBlckr will really bring down the AP as there are perhaps no mechanisms remaining to keep it up.

The reason AP comes down in the presence of the autonomic neurohormonal control is two-fold: (1) Some of the effectors are disabled or weakened, and (2) The remaining effectors form a Class Zero control system which exhibits a steady state position error; that is, the AP must fall SOME to kick in the remaining effector(s).

I hope this Systems Theory treatment of the subject is helpful. It is based on my experience with simulation at the Pennsylvania State University Hybrid Computer Laboratory, and from studies under my father, a cardiologist and an unpublished experimenter at Emory University School of Medicine in 1945-47.

--JimRodgers (talk) 22:39, 1 May 2011 (UTC)

"CCBs do not work on venous smooth muscle"[edit]

Can you explain why?? and why Vein disease is worse when patients take these drugs? Edema, painful and red legs, aggravation of their varicous veins? Theses symptoms disapear in around 10 days after medication arrest Nini00 (talk) 14:02, 29 December 2012 (UTC)

removed this line[edit]

"One type of calcium channel blocker is used experimentally to prevent migraine, and another one is used as a powerful painkiller." Since this isn't specific at all, and is not referenced, I will remove it. — Preceding unsigned comment added by 98.70.62.140 (talk) 23:10, 4 December 2013 (UTC)

Elephant in Room![edit]

The lede states that CCBs have failed to show a decrease in mortality. If this means that people taking them share the same risk of death as those who don't, then this is serious and deserves expanded discussion. I suggest a new section on "Treatment Effects". It would include the studies on the mortality, morbidity, alleviation of symptoms, and quality of life improvement. I presume these drugs have some (positive) effect on at least one of those categories and aren't just used to enrich doctors, pharmacists, and drug manufacturers...? I find it difficult to believe that they are the first line treatment in the U.K. and yet lack any solid studies on mortality or morbidity or quality of life.Abitslow (talk) 23:14, 26 January 2015 (UTC)