Calcium dependence of effects of endothelin on rat mesenteric microvessels

1991 ◽  
Vol 69 (6) ◽  
pp. 798-804 ◽  
Author(s):  
Li Yuan Deng ◽  
Ernesto L. Schiffrin
Keyword(s):  
Calcium Channel ◽  
Channel Blocker ◽  
Extracellular Fluid ◽  
Channel Blockers ◽  
Active Tension ◽  
Calcium Dependence ◽  
Rat Mesentery ◽  
Resistance Vessels ◽  
Voltage Dependent ◽  
Mesenteric Microvessels

We investigated the calcium dependence of the effects of endothelin (ET) on resistance vessels (less than 300 μm lumen diameter) from the mesenteric vascular bed of the rat, mounted on a wire myograph. ET-1 induced a potent sustained contraction with an ED50 of 12 nmol/L. The response to ET-3 and big ET at the maximum concentrations used (100 nmol/L) was less than 40% of that to ET-1, with an estimated ED50 of 45 nmol/L. Relaxation of the ET-1-induced contraction was slow, and resulted in a reduction of the maximum response to a second challenge with ET-1 to 60% of the initial contraction after 3 h. Long-lasting tachyphylaxis to arginine vasopressin (AVP) induced contraction also occurred. The response to 100 nmol/L ET-1 produced an active tension 88% greater than that induced by 124 mmol/L KCl, and similar to that produced by norepinephrine and AVP. The response to 100 nmol/L ET-1 in the absence of calcium + 1 mmol/L EGTA in the medium for 30 min resulted in a maximum contraction of 43% of the response in the presence of calcium, followed by a faster relaxation rate. The addition of calcium produced a further contraction, and stimulation with 100 nmol/L ET-1 at this point did not result in further response. The calcium channel blocker nitrendipine in concentrations of 1–10 μmol produced increasing reductions of the responses to 100 nmol/L ET-1 to 35% at the higher concentration. Nitrendipine (3 μmol/L) partially blocked the response to calcium after ET-1 was added in the absence of calcium. We conclude that resistance microvessels of the rat mesentery are more sensitive to ET-1 than ET-3 or big ET, which were also much less potent. These microvessels have a sensitivity to AVP 20 times greater than that to ET-1. The response to ET-1 may be mediated in part by the release of intracellular calcium, but the influx of calcium from the extracellular fluid through plasma membrane voltage-dependent channels is necessary for completing approximately 60% of the initial contraction and for the persistence of a sustained response.Key words: mesenteric arterioles, vasopressin, norepinephrine, nitrendipine, calcium channel blockers.

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 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.

Effect of nifedipine on calcium-induced contractions to potassium in the aorta and mesenteric arteries of spontaneously hypertensive and normotensive rats

1986 ◽  
Vol 64 (3) ◽  
pp. 310-314 ◽  
Author(s):  
M. S. Kannan ◽  
A. E. Seip ◽  
D. J. Crankshaw
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Effective Concentration ◽  
Mesenteric Arteries ◽  
Induced Responses ◽  
Shr Rats ◽  
Free Medium ◽  
Spontaneously Hypertensive ◽  
Calcium Dependence

Graded contractions to cumulative additions of calcium in the presence of KCl were obtained in strips of aorta and mesenteric arteries of normotensive (WKY) and spontaneously hypertensive (SHR) rats. In calcium-free medium, a maximally effective concentration of KCl produced a response that was larger in the mesenteric arteries (43–51% of control) than in the aorta (12–14% of control). The calcium channel blocker nifedipine (NFD, up to 10−7 M) did not significantly alter these calcium-insensitive responses. The Ca2+-induced responses were inhibited by NFD, in a concentration-dependent fashion, in both vessel types of WKY and SHR rats. The aortic responses were more sensitive to inhibition by NFD than the responses of mesenteric arteries. Moreover, the aortic responses of WKY were inhibited to a greater extent than those of the SHR. The results suggest: (a) a differential calcium dependence of contractions to KCl in the vessels studied; (b) that aortic responses are dependent on NFD-sensitive voltage-sensitive Ca2+ channels to a greater extent than the responses of mesenteric arteries; and (c) that hypertension results in a decreased sensitivity of the aorta Ca2+ channels to NFD.

Role of K+ channels in adrenal catecholamine secretion in anesthetized dogs

1998 ◽  
Vol 274 (4) ◽  
pp. R1125-R1130 ◽  
Author(s):  
Takahiro Nagayama ◽  
Kimiya Masada ◽  
Makoto Yoshida ◽  
Mizue Suzuki-Kusaba ◽  
Hiroaki Hisa ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Splanchnic Nerve ◽  
Channel Blockers ◽  
Cholinergic Agonists ◽  
Voltage Dependent ◽  
Anesthetized Dogs ◽  
Splanchnic Nerve Stimulation ◽  
Mast Cell Degranulating ◽  
Small Conductance

We examined the role of K+ channels in the secretion of adrenal catecholamine (CA) in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. K+ channel blockers and the cholinergic agonists were infused and injected, respectively, into the adrenal gland. The voltage-dependent K+ channel (KA type) blocker mast cell degranulating (MCD) peptide infusion (10–100 ng/min) enhanced increases in CA output induced by SNS (1–3 Hz), but it did not affect increases in CA output induced by ACh (0.75–3 μg), DMPP (0.1–0.4 μg), or muscarine (0.5–2 μg). The small-conductance Ca2+-activated K+(SKCa) channel blocker scyllatoxin infusion (10–100 ng/min) enhanced the ACh-, DMPP-, and muscarine-induced increases in CA output, but it did not affect the SNS-induced increases in CA output. These results suggest that KA channels may play an inhibitory role in the regulation of adrenal CA secretion in response to SNS and that SKCa channels may play the same role in the secretion in response to exogenously applied cholinergic agonists.

Influence of Nifedipine on the Visual Fields of Patients with Optic-Nerve-Head Diseases

1994 ◽  
Vol 4 (1) ◽  
pp. 24-28 ◽  
Author(s):  
A.Z. Gaspar ◽  
J. Flammer ◽  
PH. Hendrickson
Keyword(s):  
Optic Nerve ◽  
Visual Field ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Optic Nerve Head ◽  
Channel Blocker ◽  
Glaucoma Patient ◽  
Visual Fields ◽  
Visual Field Defects ◽  
Channel Blockers

Calcium-channel blockers have long been employed in coronary disease, and recent investigations have indicated their efficacy in improving the visual field in low-tension glaucoma or presumed vasospasm, possibly by enhancing ocular circulation. We evaluated the short-term influence of a typical calcium-channel blocker, nifedipine, on 59 patients with visual-field defects, some with optic-nerve-head pathology (n = 38) and some with normal-appearing optic nerve heads (n = 21). On the average, a statistically significant improvement of 1.2 dB was observed. Different types of patients, however, behaved quite differently. The younger the patient, the greater the improvement. Patients with normal optic nerve heads improved by 1.54 dB, whereas patients with optic-nerve-head excavation improved by only 0.66 dB. No response was observed in patients with anterior ischemic neuropathy. Marked deterioration was noted in one glaucoma patient with low systemic blood pressure. The visual-field changes were observed in the scotomatous and non-scotomatous areas. Thus, the calcium-channel blocker nifedipine can be effective in some selected diseases whose pathogenesis probably involves vascular dysregulation though it may even be contraindicated in others

scholarly journals Aberrant Exon 8/8a Splicing by Downregulated PTBP (Polypyrimidine Tract-Binding Protein) 1 Increases Ca V 1.2 Dihydropyridine Resistance to Attenuate Vasodilation

2020 ◽  
Vol 40 (10) ◽  
pp. 2440-2453
Author(s):  
Jianzhen Lei ◽  
Xiaoxin Liu ◽  
Miaomiao Song ◽  
Yingying Zhou ◽  
Jia Fan ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Binding Protein ◽  
Expression Patterns ◽  
Mesenteric Arteries ◽  
Channel Blockers ◽  
Polypyrimidine Tract ◽  
Polypyrimidine Tract Binding ◽  
Polypyrimidine Tract Binding Protein

Objective: Calcium channel blockers, such as dihydropyridines, are commonly used to inhibit enhanced activity of vascular Ca V 1.2 channels in hypertension. However, patients who are insensitive to such treatments develop calcium channel blocker-resistant hypertension. The function of Ca V 1.2 channel is diversified by alternative splicing, and the splicing factor PTBP (polypyrimidine tract-binding protein) 1 influences the utilization of mutually exclusive exon 8/8a of the Ca V 1.2 channel during neuronal development. Nevertheless, whether and how PTBP1 makes a role in the calcium channel blocker sensitivity of vascular Ca V 1.2 channels, and calcium channel blocker-induced vasodilation remains unknown. Approach and Results: We detected high expression of PTBP1 and, inversely, low expression of exon 8a in Ca V 1.2 channels (Ca V 1.2 E8a ) in rat arteries. In contrast, the opposite expression patterns were observed in brain and heart tissues. In comparison to normotensive rats, the expressions of PTBP1 and Ca V 1.2 E8a channels were dysregulated in mesenteric arteries of hypertensive rats. Notably, PTBP1 expression was significantly downregulated, and Ca V 1.2 E8a channels were aberrantly increased in dihydropyridine-resistant arteries compared with dihydropyridine-sensitive arteries of rats and human. In rat vascular smooth muscle cells, PTBP1 knockdown resulted in shifting of Ca V 1.2 exon 8 to 8a. Using patch-clamp recordings, we demonstrated a concomitant reduction of sensitivity of Ca V 1.2 channels to nifedipine, due to the higher expression of Ca V 1.2 E8a isoform. In vascular myography experiments, small interfering RNA-mediated knockdown of PTBP1 attenuated nifedipine-induced vasodilation of rat mesenteric arteries. Conclusions: PTBP1 finely modulates the sensitivities of Ca V 1.2 channels to dihydropyridine by shifting the utilization of exon 8/8a and resulting in changes of responses in dihydropyridine-induced vasodilation.

scholarly journals Bio-inspired voltage-dependent calcium channel blockers

2013 ◽  
Vol 4 (1) ◽  
Author(s):  
Tingting Yang ◽  
Lin-Ling He ◽  
Ming Chen ◽  
Kun Fang ◽  
Henry M. Colecraft
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Channel Blockers ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent

scholarly journals Densitas tulang mandibula pengguna obat anti hipertensi calcium channel blocker (CCB) melalui radiograf panoramik

2020 ◽  
Vol 4 (2) ◽  
pp. 1
Author(s):  
Gunawan Gunawan ◽  
Suhardjo Sitam ◽  
Lusi Epsilawati
Keyword(s):  
Bone Density ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Calcium Channel Blockers ◽  
Drug Users ◽  
Channel Blocker ◽  
Antihypertensive Drugs ◽  
Panoramic Radiograph ◽  
Channel Blockers ◽  
Hypertensive Drug

Objectives: The purpose of this research was to describe radiographic density of mandibular bone in calcium channel blocker anti-hypertensive drug users. Bone density in the mandible is assessed from the trabecular. Panoramic radiograph is a routine examination that is often done in dentistry that can be used to assess changes in quality in the form of changes in bone density in users of anti-hypertensive calcium channel blockers Material and Methods: This research is a descriptive study of 21 panoramic radiographs of calcium channel blocker anti-hypertensive drug users aged 40-75 years. Panoramic radiograph archive density checks in the distal region of the foramen mentale and the mandibular angular region using software image j, with the final result was the percentage between bone and marrow. Results: This research showed the average radiographic density in male using calcium channel blocker antihypertensive drugs was 18.81% and the average radiographic density in female was 20.92%. Conclusion: Based on the results of the study found that the average radiographic density of female patients taking antihypertensive drugs calcium channel blockers was higher than male.

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