Responsiveness of Coronary Arteries to Nitroglycerin under Hypoxia: The Importance of the Endothelium

Pharmacology ◽  
2017 ◽  
Vol 99 (5-6) ◽  
pp. 275-280
Author(s):  
Masashi Tawa ◽  
Takashi Shimosato ◽  
Hiroshi Sakonjo ◽  
Tomio Okamura

Background/Aims: Nitroglycerin is widely used as a coronary vasodilator in the treatment of ischemic heart diseases. This study investigated the influence of hypoxia on nitroglycerin-induced relaxation in endothelium-intact and -denuded rabbit, monkey, and porcine coronary arteries. Methods: Helically cut strips of coronary arteries were suspended in organ chambers, and isometric tension was recorded. Results: Nitroglycerin concentration dependently relaxed endothelium-intact rabbit coronary arteries, which were not different under normoxic and hypoxic conditions. On the other hand, nitroglycerin-induced relaxation of endothelium-denuded arteries was significantly attenuated by hypoxia. Similarly, the relaxant response of endothelium-intact monkey coronary arteries to nitroglycerin was not affected by hypoxia, whereas that of endothelium-denuded arteries was impaired. As is the case with rabbit and monkey coronary arteries, exposure to hypoxia resulted in impaired relaxation by nitroglycerin in endothelium-denuded but not endothelium-intact porcine coronary arteries. Conclusion: These findings suggest that coronary endothelium plays a pivotal role in preventing the hypoxia-induced impairment of nitroglycerin responsiveness, regardless of the animal species.

2019 ◽  
Vol 15 (3) ◽  
pp. 207-218 ◽  
Author(s):  
Fatma Ağın

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.


1976 ◽  
Vol 25 (1) ◽  
pp. 271-275 ◽  
Author(s):  
Ulf de Faire

From January 1971 to March 1973 all twin pairs in the Swedish Twin Registry below the age of 70, who became death-discordant, were continuously recorded. A total of 205 (78%) of the surviving cotwins were examined with respect to different manifestations of ischemic heart diseases (IHD) and several “environmental” and “biometric” risk factors. Among the death-discordant pairs, the cause of death was IHD in 57 pairs and other than IHD in 148 pairs. Analyses revealed that the prevalence rate of myocardial infarction, angina pectoris, pathologic Q-wave, and ST depressions in connection with exercise, were significantly higher among the surviving cotwins whose partners had died from IHD than those whose partners had died from other causes. The same trends were seen for most of the risk factors measured both singly and in combination, although not very pronounced. The results indicate a substantial genetic influence in the development of IHD. The genetic influence is possibly transmitted not only through some of the risk factors measured, but also through other factors, still unknown.


1998 ◽  
Vol 274 (1) ◽  
pp. H375-H381 ◽  
Author(s):  
Phillip F. Pratt ◽  
Cecilia J. Hillard ◽  
William S. Edgemond ◽  
William B. Campbell

It has been reported that the endogenous cannabinoid N-arachidonylethanolamide (AEA), commonly referred to as anandamide, has the characteristics of an endothelium-derived hyperpolarizing factor in rat mesenteric artery. We have carried out studies to determine whether AEA affects coronary vascular tone. The vasorelaxant effects of AEA were determined in isolated bovine coronary artery rings precontracted with U-46619 (3 × 10−9 M). AEA decreased isometric tension, producing a maximal relaxation of 51 ± 9% at a concentration of 10−5 M. Endothelium-denuded coronary arteries were not significantly affected by AEA. The CB1 receptor antagonist SR-141716A (10−6 M) failed to reduce the vasodilatory effects of AEA, suggesting that the CB1 receptor is not involved in this action of AEA. Because AEA is rapidly converted to arachidonic acid and ethanolamine in brain and liver by a fatty acid amide hydrolase (FAAH), we hypothesized that the vasodilatory effect of AEA results from its hydrolysis to arachidonic acid followed by enzymatic conversion to vasodilatory eicosanoids. In support of this hypothesis, bovine coronary arteries incubated with [3H]AEA for 30 min hydrolyzed 15% of added substrate; ∼9% of the radiolabeled product was free arachidonic acid, and 6% comigrated with the prostaglandins (PGs) and epoxyeicosatrienoic acids (EETs). A similar result was obtained in cultured bovine coronary endothelial cells. Inhibition of the FAAH with diazomethylarachidonyl ketone blocked both the metabolism of [3H]AEA and the relaxations to AEA. Whole vessel and cultured endothelial cells prelabeled with [3H]arachidonic acid synthesized [3H]PGs and [3H]EETs, but not [3H]AEA, in response to A-23187. Furthermore, SR-141716A attenuated A-23187-stimulated release of [3H]arachidonic acid, suggesting that it may have actions other than inhibition of CB1 receptor. These experiments suggest that AEA produces endothelium-dependent vasorelaxation as a result of its catabolism to arachidonic acid followed by conversion to vasodilatory eicosanoids such as prostacyclin or the EETs.


2015 ◽  
Vol 115 (7) ◽  
pp. 48B-58B ◽  
Author(s):  
A. Mark Richards ◽  
Salvatore Di Somma ◽  
Thomas Mueller

2001 ◽  
Vol 280 (1) ◽  
pp. H76-H82 ◽  
Author(s):  
Qiong Yang ◽  
Elizabeth Scalbert ◽  
Philippe Delagrange ◽  
Paul M. Vanhoutte ◽  
Stephen T. O'Rourke

The present study was designed to determine the effects of melatonin on coronary vasomotor tone. Porcine coronary arteries were suspended in organ chambers for isometric tension recording. Melatonin (10−10-10−5 M) itself caused neither contraction nor relaxation of the tissues. Serotonin (10−9-10−5 M) caused concentration-dependent contractions of coronary arteries, and in the presence of melatonin (10−7 M) the maximal response to serotonin was increased in rings with but not without endothelium. In contrast, melatonin had no effect on contractions produced by the thromboxane A2 analog U-46619 (10−10-10−7 M). The melatonin-receptor antagonist S-20928 (10−6 M) abolished the potentiating effect of melatonin on serotonin-induced contractions in endothelium-intact coronary arteries, as did treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (10−5 M), methylene blue (10−5 M), or NG -nitro-l-arginine (3 × 10−5 M). In tissues contracted with U-46619, serotonin caused endothelium-dependent relaxations that were inhibited by melatonin (10−7 M). Melatonin also inhibited coronary artery relaxation induced by sodium nitroprusside (10−9-10−5 M) but not by isoproterenol (10−9-10−5 M). These results support the hypothesis that melatonin, by inhibiting the action of nitric oxide on coronary vascular smooth muscle, selectively potentiates the vasoconstrictor response to serotonin in coronary arteries with endothelium.


2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Lili Wang ◽  
Qianhui Zhang ◽  
Kexin Yuan ◽  
Jing Yuan

The incidence rate of cardiovascular disease (CVD) has been increasing year by year and has become the main cause for the increase of mortality. Mitochondrial DNA (mtDNA) plays a crucial role in the pathogenesis of CVD, especially in heart failure and ischemic heart diseases. With the deepening of research, more and more evidence showed that mtDNA is related to the occurrence and development of CVD. Current studies mainly focus on how mtDNA copy number, an indirect biomarker of mitochondrial function, contributes to CVD and its underlying mechanisms including mtDNA autophagy, the effect of mtDNA on cardiac inflammation, and related metabolic functions. However, no relevant studies have been conducted yet. In this paper, we combed the current research status of the mechanism related to the influence of mtDNA on the occurrence, development, and prognosis of CVD, so as to find whether these mechanisms have something in common, or is there a correlation between each mechanism for the development of CVD?


2015 ◽  
Vol 1 (2) ◽  
pp. 3-9
Author(s):  
Riaz Gul ◽  
Sumaira Naz

Objectives:To determine different risk factors associated with ischemic heart diseases in different age group patients of tertiary care hospitals of Peshawar.Methodology:A cross sectional study conducted on 350 patients of different age groups presented with ischemic heart diseases in tertiary care hospitals of Peshawar. Study was conducted for duration of 3 months from December 2013 to February 2014. Non probability convenient sampling technique was used. Sample size was calculated using standard sample size calculator. Semi structured questionnaire was used as data collection tool. Patient’s record and investigations were used as adding tools. Standard definition was made for ischemic heart disease. Different modifiable and non-modifiable factors were assessed and were analyzed using SPSS version 16.Results:This study contains 350 patients in which female patients were 133(38%) and male were 217(62%).The mean age was 57.23±11.36 years. The age of the patients ranges from 22 to 80 years. The frequencies of risk factors were stress (73.1%) followed by hypertension (65.7%), sedentary life style (59.4%), family history (57.1%), smoking (50.6%), over weight and obese (39.1%), below normal HDL (30.3%), high LDL (29.1%), hypertriglyceridemia (28%), hypercholesterolemia (23.7%). 64.3% patients were presenting with acute IHD and 35.7% were with chronic IHD. Stress, HTN, DM and sedentary life style were found to be significantly associated with male gender (p- value <0.05). Age was divided into two groups, <45 years and >45 years. Stress, HTN, DM and hypercholesterolemia had a significant association with >45 years of age group. (P-value <0.05).Conclusion:Stress, HTN, DM, sedentary life styles were the major risk factors. And they were found to be more in male gender and in equal to more than 45 years of age group.


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