scholarly journals Role of calcium channel blocker in excessive mast cell degranulation

2021 ◽  
Author(s):  
Sagarika Datta
Keyword(s):  
Mast Cell ◽  
Calcium Channel ◽  
Channel Blocker ◽  
Mast Cell Degranulation ◽  
Channel Blockers ◽  
Case Presentation ◽  
H2 Blocker ◽  
Throat Infection ◽  
Stomach Acid

Abstract Background:I present a case of a female patient, age 45 years, for whom the uncontrolled mast cell degranulation created many issues related to allergy like, skin rash, itching, breathing discomfort, frequent throat infection, GERD, migraine, fibromyalgia, peripheral neuropathy, depression, anxiety disorder, constipation etc. For the patient, it was observed that calcium channel blockers seem to control the unnecessary and uncontrolled mast cell degranulation. CCB seemed to have a role to play in mast cell degranulation.Case presentation:When the patient is taking either Flunarizine or Pregabalin or both together, the need for antihistamine and montelukast are very low. The patient suffers less throat infection while Flunarizine or Pregabalin are being taken. More the dose of Pregabalin less the occurrence of any type of allergy (food, pollen, dust etc.). The requirement of corticosteroid inhaler for breathing discomfort is also less. Frequency of body pain, migraine is minimal. Occurrence of stomach acid or GERD or digestion disorder is also very less. In terms of mood or anxiety, body is stable too. So, per day when 3 Pregabalin (75mg) were taken with 1 Amitriptyline (50mg) and 1 Duloxetine (60mg) health is completely stable with no need for H1 Blocker, H2 Blocker, Montelukast and Corticosteroid inhaler. Conclusion:CCB, specifically L-type CCB must have role in controlling the degranulation of mast cells, thus reducing all problem together at the root. But there are disadvantages like aggravated IBS (lazy gut), aggravated RLS and fluid retention (swelling of palm).We must check the use of Gabapentin and Sodium cromoglycate too. They should also control the unnecessary mast cell degranulation. Thus, fixing the problem at the root.

scholarly journals Role of calcium channel blocker in excessive mast cell degranulation

2021 ◽  
Vol 5 (7) ◽  
Author(s):  
Sagarika Datta
Keyword(s):  
Mast Cell ◽  
Peripheral Neuropathy ◽  
Anxiety Disorder ◽  
Calcium Channel ◽  
Female Patient ◽  
Calcium Channel Blockers ◽  
Channel Blocker ◽  
Mast Cell Degranulation ◽  
Channel Blockers

Here, I present a case of a female patient, age 45 years, for whom the uncontrolled mast cell degranulation created many issues related to allergy like, skin rash, itching, breathing discomfort, frequent throat infection, GERD, migraine, fibromyalgia, peripheral neuropathy, depression, anxiety disorder, constipation etc. For the patient, it was observed that calcium channel blockers seem to control the unnecessary and uncontrolled mast cell degranulation. CCB seemed to have a role to play in mast cell degranulation.

Electroanalytical Methods for Determination of Calcium Channel Blockers

2019 ◽  
Vol 15 (3) ◽  
pp. 207-218 ◽  
Author(s):  
Fatma Ağın
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Channel Blocker ◽  
Heart Diseases ◽  
Dosage Forms ◽  
Channel Blockers ◽  
Electroanalytical Methods ◽  
Pharmaceutical Dosage Forms ◽  
Ischemic Heart Diseases

Background:Calcium Channel Blockers (CCBs) are widely used in the treatment of cardiovascular and ischemic heart diseases in recent years. They treat arrhythmias by reducing cardiac cycle contraction and also benefit ischemic heart diseases. Electroanalytical methods are very powerful analytical methods used in the pharmaceutical industry because of the determination of therapeutic agents and/or their metabolites in clinical samples at extremely low concentrations (10-50 ng/ml). The purpose of this review is to gather electroanalytical methods used for the determination of calcium channel blocker drugs in pharmaceutical dosage forms and biological media selected mainly from current articles.Methods:This review mainly includes recent determination studies of calcium channel blockers by electroanalytical methods from pharmaceutical dosage forms and biological samples. The studies of calcium channel blockers electroanalytical determination in the literature were reviewed and interpreted.Results:There are a lot of studies on amlodipine and nifedipine, but the number of studies on benidipine, cilnidipine, felodipine, isradipine, lercanidipine, lacidipine, levamlodipine, manidipine, nicardipine, nilvadipine, nimodipine, nisoldipine, nitrendipine, diltiazem, and verapamil are limited in the literature. In these studies, DPV and SWV are the most used methods. The other methods were used less for the determination of calcium channel blocker drugs.Conclusion:Electroanalytical methods especially voltammetric methods supply reproducible and reliable results for the analysis of the analyte. These methods are simple, more sensitive, rapid and inexpensive compared to the usually used spectroscopic and chromatographic methods.

scholarly journals Platelet and Erythrocyte Extravasation across Inflamed Corneal Venules Depend on CD18, Neutrophils and Mast Cell Degranulation

2021 ◽  
Vol 22 (14) ◽  
pp. 7360
Author(s):  
Angie De La Cruz ◽  
Aubrey Hargrave ◽  
Sri Magadi ◽  
Justin A. Courson ◽  
Paul T. Landry ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Types ◽  
Mast Cell Degranulation ◽  
Wild Type ◽  
Delayed Wound Healing ◽  
Corneal Epithelial ◽  
Corneal Abrasion ◽  
Low Levels ◽  
Endothelial Pores

Platelet extravasation during inflammation is under-appreciated. In wild-type (WT) mice, a central corneal epithelial abrasion initiates neutrophil (PMN) and platelet extravasation from peripheral limbal venules. The same injury in mice expressing low levels of the β2-integrin, CD18 (CD18hypo mice) shows reduced platelet extravasation with PMN extravasation apparently unaffected. To better define the role of CD18 on platelet extravasation, we focused on two relevant cell types expressing CD18: PMNs and mast cells. Following corneal abrasion in WT mice, we observed not only extravasated PMNs and platelets but also extravasated erythrocytes (RBCs). Ultrastructural observations of engorged limbal venules showed platelets and RBCs passing through endothelial pores. In contrast, injured CD18hypo mice showed significantly less venule engorgement and markedly reduced platelet and RBC extravasation; mast cell degranulation was also reduced compared to WT mice. Corneal abrasion in mast cell-deficient (KitW-sh/W-sh) mice showed less venule engorgement, delayed PMN extravasation, reduced platelet and RBC extravasation and delayed wound healing compared to WT mice. Finally, antibody-induced depletion of circulating PMNs prior to corneal abrasion reduced mast cell degranulation, venule engorgement, and extravasation of PMNs, platelets, and RBCs. In summary, in the injured cornea, platelet and RBC extravasation depends on CD18, PMNs, and mast cell degranulation.

scholarly journals L-type calcium channel blocker increases VEGF concentrations in retinal cells and human serum

2021 ◽  
Author(s):  
Anmol Kumar ◽  
Stefan Mutter ◽  
Erika Parente ◽  
Valma Harjutsalo ◽  
Raija Lithovius ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Human Serum ◽  
Channel Blocker ◽  
Channel Blockers ◽  
Vascular Endothelial ◽  
Retinal Cells ◽  
Diabetic Eye Disease ◽  
Design And Methods ◽  
Endothelial Growth Factor

Objective: Vascular endothelial growth factor (VEGF) plays a key role in diabetic retinopathy (DR). L-type calcium channel blockers (LTCCBs) have been widely used as antihypertensive medication (AHM), but their association with VEGF and DR is still unclear. Therefore, we explored the effect of LTCCBs compared to other AHMs on VEGF concentrations in retinal cells and human serum. Furthermore, we evaluated the association between the use of LTCCBs and the risk of severe diabetic eye disease (SDED). Research design and methods: Muller cells (MIO-M1) were cultured as per recommended protocol and treated with LTCCBs and other AHMs. VEGF secreted from cells were collected at 24 hours intervals. In an interventional study, 39 individuals received LTCCBs or other AHM for four weeks with a four-week wash-out placebo period between treatments. VEGF was measured during the medication and placebo periods. Finally, we evaluated the risk of SDED associated with LTCCB usage in 192 individuals from the FinnDiane Study in an oberservational setting. Results: In the cell cultures, medium VEGF concentration increased time-dependently after amlodipine (p<0.01) treatment, but not after losartan (p>0.01), or lisinopril (p>0.01). Amlodipine, but no other AHM, increased serum VEGF concentration (p<0.05) during the interventional clinical study. The usage of LTCCB was not associated with the risk of SDED in the observational study. Conclusions: LTCCB increases VEGF concentrations in retinal cells and human serum. However, the usage of LTCCBs does not appear to be associated with SDED in adults with type 1 diabetes.

Role of 5-HT3 receptors and afferent fibers in the effects of mast cell degranulation on colonic motility in rats

1994 ◽  
Vol 107 (4) ◽  
pp. 976-984 ◽  
Author(s):  
Nathalie Castex ◽  
Jean Fioramonti ◽  
Marie JoséFargeas ◽  
Jean More ◽  
Lionel Bueno
Keyword(s):  
Mast Cell ◽  
Colonic Motility ◽  
Mast Cell Degranulation ◽  
Afferent Fibers

Severe beta blocker and calcium channel blocker overdose: Role of high dose insulin

2018 ◽  
Vol 36 (4) ◽  
pp. 736.e5-736.e6 ◽  
Author(s):  
Karan Seegobin ◽  
Satish Maharaj ◽  
Ansuya Deosaran ◽  
Pramod Reddy
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Beta Blocker ◽  
Channel Blocker ◽  
High Dose

Arteriolar constriction in skeletal muscle during vascular stunning: role of mast cells

1997 ◽  
Vol 272 (5) ◽  
pp. H2154-H2163 ◽  
Author(s):  
M. W. Keller
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Vascular Reactivity ◽  
Striated Muscle ◽  
Mast Cell Degranulation ◽  
Response Curves ◽  
Maximal Diameter ◽  
Muscle Tissues ◽  
Stimulation Of

Striated muscle becomes stunned during reperfusion after sublethal ischemia. Resistance vessel tone and reactivity are altered in stunned muscle tissues. The hypothesis that adenosine-regulated mast cell degranulation occurs during reperfusion and leads to constriction of resistance arterioles was tested. The hamster cremaster muscle was subjected to 1 h of ischemia followed by reperfusion. Resistance arterioles constricted during reperfusion (74% of maximal diameter at baseline vs. 42% of maximal diameter after 30 min of reperfusion; P < 0.01). Mast cells degranulated in reperfusion concomitant with arteriolar constriction. Stimulation of mast cell degranulation in control animals with compound 48/80 or cold superfusate (21 degrees C) caused vasoconstriction that mimicked that seen in reperfusion. The mast cell stabilizer cromolyn blocked degranulation and constriction. If mast cell granules were depleted by applying compound 48/80 before inducing ischemia, then arterioles failed to constrict during reperfusion. Adenosine A3-antagonist BW-A1433 abolished constriction. These findings suggest that arterioles constrict in reperfusion due to adenosine-regulated mast cell degranulation. Vasodilation in response to sodium nitroprusside and acetylcholine was normal in stunned, constricted arterioles. However, the dose-response curves to adenosine were shifted to the left in arterioles constricted by either stunning, compound 48/80, exposure to cold superfusate, or cromolyn compared with control vessels. Depletion of granular components via stunning, compound 48/80, cold superfusate, or inhibition of secretion with cromolyn results in unopposed A1- or A2-mediated vasodilation in response to adenosine, whereas the dilatory effects of adenosine are blunted by simultaneous release of vasoconstrictors from mast cells in control animals. In summary, it was found that mast cell degranulation occurs during reperfusion and leads to constriction of resistance arterioles and altered vascular reactivity to adenosine. Adenosine is released in ischemia and stimulates mast cell degranulation via the A3 receptor located on mast cells during reperfusion.

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