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EnneaActivists

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William Thomas
William Thomas

Blockers


Other names: calcium antagonists, calcium channel antagonists, calcium channel blockers, CCBWhat are Calcium channel blocking agents?Calcium channel blocking agents restrict the amount of calcium entering cardiac and smooth muscle cells by blocking voltage-gated calcium channels. This causes blood vessels to relax and widen (vasodilate), improves oxygen supply to the heart, and lowers blood pressure. Some calcium channel blockers also slow the heart rate.




Blockers


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The use of ad blockers is more prevalent among men than women. Men are the bigger users of ad blockers across every age group. Ad blockers are most popular among men aged 16-24, 49.2% of whom use ad blocking software (compared to 43.2% of women).


Globally, the most commonly reported reasons for using ad blockers include excessive amounts of ads (22.3%), the irrelevance of ad messages (22.3%), and the intrusion factor (19.9%).


In fact, per eMarketer figures, the share of American internet users blocking ads has increased by 71.97% since 2014. Seven years ago, only 15.7% of US users utilized ad blockers.


Ad blocking is detected in 18% of web sessions on computers among American users. The detected usage of ad blockers has declined slightly since 2016 when the use of blocking technology was tracked in 23% of sessions.


Meanwhile, the detected rate of ad blocking on mobile devices is lower than desktop. However, unlike on desktop, the percentage of mobile sessions demonstrably using ad blockers is on the rise. 7% of mobile sessions involve detectable ad blocking, an increase from 2% in 2016.


Based on data from AudienceProject, ad blockers in the US are predominantly used by men. 49% of male respondents in the US reported the use of ad blockers. Interestingly, the disparity between male and female users is far more pronounced in the US than it is globally. Just 33% of US women use ad blockers.


By age group, ad blockers in the US are most popular with internet users aged 15-25. Meanwhile, the lowest usage of ad blockers is seen among the 36-45 age group, with 38% of respondents in this demographic using blocking software.


Another data source (eMarketer) provides a significantly different outlook. According to the eMarketer figures, US men and women use ad blockers equally, with 27.2% of each group using blocking software.


Usage in the 18-24 age group is the most common, with 41% of US internet users utilizing ad blockers. Usage of ad blockers in the US is least common for people older than 65: 15.6% of those in the oldest age bracket use ad blocking tools.


36% of internet users in the UK use ad blockers. The share of UK users utilizing ad blockers has been on a steady decline since 2016 when almost half (47%) of those surveyed admitted to blocking ads.


As in the US, viewing websites without banners is the primary stated reason for using ad blockers in the UK. Avoiding irrelevant or offensive images and/or messages is the second most popular reason provided.


Beta blockers are a group of drugs that inhibit the sympathetic activation of β-adrenergic receptors. Cardioselective blockers (e.g., atenolol, bisoprolol) primarily block β1 receptors in the heart, causing decreased heart rate, cardiac contractility, cardiac workload, and AVN conduction. Nonselective beta blockers (e.g., pindolol, propranolol) inhibit all β receptors and may cause bronchoconstriction, peripheral vasoconstriction, and metabolic imbalances (e.g., hypoglycemia and hyperglycemia, hypertriglyceridemia) in addition to cardiac effects. Cardioselective beta blockers have a lower side-effect profile and are preferred in the management of coronary heart disease, compensated heart failure, acute coronary syndrome, and certain types of arrhythmias. Propranolol, a nonselective beta blocker, is the first-line drug in the management of essential tremor, portal hypertension, migraine prophylaxis, and thyroid storm. Beta blockers are contraindicated in patients with symptomatic bradycardia, AV block, decompensated heart failure, and asthma. Initiation and cessation of beta-blocker therapy should always be gradual to avoid side effects or symptoms of withdrawal (e.g., rebound tachycardia, hypertension, acute cardiac death).


With the exception of nebivolol, all cardioselective beta blockers begin with the letters A to M (B1 = first half of the alphabet). Except for beta blockers with alpha-blocking action (labetalol, bucindolol, carvedilol), all noncardioselective beta blockers begin with the letters N to Z (B2 = second half of the alphabet).


Beta blockers competitively inhibit adrenergic substances (e.g., adrenaline, noradrenaline) at β receptors. A rule to remember the main effector organs for β receptors: There is 1 heart (β1 blockers act on the heart) and 2 lungs (β2 blockers affect bronchial smooth muscles).


Beta blockers are a group of drugs that inhibit the sympathetic activation of \u03B2-adrenergic receptors. Cardioselective blockers (e.g., atenolol, bisoprolol) primarily block \u03B21 receptors in the heart, causing decreased heart rate, cardiac contractility, cardiac workload, and AVN conduction. Nonselective beta blockers (e.g., pindolol, propranolol) inhibit all \u03B2 receptors and may cause bronchoconstriction, peripheral vasoconstriction, and metabolic imbalances (e.g., hypoglycemia and hyperglycemia, hypertriglyceridemia) in addition to cardiac effects. Cardioselective beta blockers have a lower side-effect profile and are preferred in the management of coronary heart disease, compensated heart failure, acute coronary syndrome, and certain types of arrhythmias. Propranolol, a nonselective beta blocker, is the first-line drug in the management of essential tremor, portal hypertension, migraine prophylaxis, and thyroid storm. Beta blockers are contraindicated in patients with symptomatic bradycardia, AV block, decompensated heart failure, and asthma. Initiation and cessation of beta-blocker therapy should always be gradual to avoid side effects or symptoms of withdrawal (e.g., rebound tachycardia, hypertension, acute cardiac death).


Beta blockers competitively inhibit adrenergic substances (e.g., adrenaline, noradrenaline) at \u03B2 receptors. A rule to remember the main effector organs for \u03B2 receptors: There is 1 heart (\u03B21 blockers act on the heart) and 2 lungs (\u03B22 blockers affect bronchial smooth muscles).


Beta-blockers are drugs that bind to beta-adrenoceptors and block the binding of norepinephrine and epinephrine to these receptors. This inhibits normal sympathetic effects that act through these receptors. Therefore, beta-blockers are sympatholytic drugs. Some beta-blockers, when they bind to the beta-adrenoceptor, partially activate the receptor while preventing norepinephrine from binding to the receptor. These partial agonists therefore provide some "background" of sympathetic activity while preventing normal and enhanced sympathetic activity. Partial agonist beta-blockers possess intrinsic sympathomimetic activity (ISA). Some beta-blockers also possess membrane stabilizing activity (MSA), which is similar to the membrane stabilizing activity of sodium-channels blockers (Class I antiarrhythmics).


First generation of beta-blockers are non-selective, meaning that they block both beta-1 (β1) and beta-2 (β2) adrenoceptors. Second generation beta-blockers are more cardioselective in that they are relatively selective for β1 adrenoceptors. Note that this relative selectivity can be lost at higher drug doses. Finally, third generation beta-blockers are drugs that also possess vasodilator actions by blocking vascular alpha-adrenoceptors.


Beta-blockers bind to beta-adrenoceptors in cardiac nodal tissue, the conducting system, and contracting myocytes. The heart has both β1 and β2 adrenoceptors, although the predominant receptor type in number and function is β1. These receptors primarily bind norepinephrine that is released from sympathetic adrenergic nerves. Additionally, they bind norepinephrine and epinephrine that circulate in the blood. Beta-blockers prevent the normal ligand (norepinephrine or epinephrine) from binding to the beta-adrenoceptor by competing for the binding site.


Because there is some level of sympathetic tone on the heart, beta-blockers can reduce sympathetic influences that normally stimulate chronotropy (heart rate), inotropy (contractility), dromotropy (electrical conduction) and lusitropy (relaxation). Therefore, beta-blockers cause decreases in heart rate, contractility, conduction velocity, and relaxation rate. These drugs have an even greater effect when there is elevated sympathetic activity.


Compared to their effects in the heart, beta-blockers have relatively little direct vascular effect because β2-adrenoceptors have only a small modulatory role on basal vascular tone. Blockade of β2-adrenoceptors is associated with a small amount of vasoconstriction in many vascular beds. This occurs because beta-blockers remove a small β2-adrenoceptor vasodilator influence (e.g., originating from circulating epinephrine) that is normally opposing the more dominant alpha-adrenoceptor mediated vasoconstrictor influence originating from sympathetic tone.


Beta-blockers decrease arterial blood pressure by reducing cardiac output. Many causes of hypertension are associated with an increase in blood volume and cardiac output. Therefore, reducing cardiac output by beta-blockade can be an effective treatment for hypertension, especially when used with a diuretic. Acute treatment with a beta-blocker is not very effective in reducing arterial pressure because of a compensatory increase in systemic vascular resistance produced by baroreceptor reflexes. Chronic treatment with beta-blockers lowers arterial pressure more than acute treatment, possibly because of reduced release of renin by the kidneys (the release of which is partly regulated by β1-adrenoceptors in the kidney). Decreasing circulating plasma renin leads to a decrease in angiotensin II and aldosterone, which enhances renal loss of sodium and water and further diminishes arterial pressure. Hypertension in some patients is caused by emotional stress, which causes enhanced sympathetic activity. Beta-blockers can be very effective in these patients. 041b061a72


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