My oldest son is in his early 20's and he has type 1 diabetes. But thank God for this piece of article ru-vid.comUgkxVYhghKWmrUgXARZ_ydZTvmmcrw5L0I5i At first he thought he had the flu and was lying down on the bed for three days until his sister took him to the hospital. They took his blood and it was 600. What I do not understand is how he could have gotten it, since no one in the family has it. But he is winning the battle now. This is good stuff.
Hypertension: Blood pressure regulation: Blood pressure = force or tension of blood pressing against artery walls. It depends upon - left ventricle contraction - systemic vascular resistance - elasticity of arterial walls - blood volume Blood Pressure = Cardiac Output * Systemic Vascular Resistance . Arterial BP is regulated by pressure sensitive neurons (Baroreceptors) in Aortic arch and Carotid sinuses If BP drops, Baroreceptors send signals to adrenal medulla => catecholamine release => increased sympathetic activity via alpha and beta receptors. B1 receptor activation => increase heart rate and stroke volume = increased CO and ultimately BP A1 receptor activation on smooth muscle => vasoconstriction= increased vascular resistance = increased BP . RAA axis: Baroreceptors in kidneys respond to BP changes. renin secretion is stimulated by Decreased blood flow, and also by sympathetic B1 receptor activation in kidneys. Renin -> Angiotensin 2 production. AT2 is a potent vasoconstrictor of systemic blood vessels to raise peripheral resistance. It also constricts renal blood vessels. It also stimulates Aldosterone production Aldosterone => Sodium and H20 retention => increased blood volume => increased CO => increased BP . Antihypertensive Drugs: A1 blockers (ZOSINs) Beta blockers (LOLs) Centrally acting adrenergic drugs (clonidine & methyldopa) Calcium channel blockers (dihydropyridines & non-dihydro) Diuretics (loop, thiazide, K+ sparing) RAA axis blockers (Renin inhibitors, ACEi, ARBs) Nitrates Bosentan (Endothelin 1 antagonist) Fenoldopam (Dopamine 1 agonist) Hydralazine Minoxidil ... Alpha 1 blockers (Doxazosin & Prazosin) Block A1 receptors on smooth muscle to decrease systemic vascular resistance => decreased blood pressure Selective beta blockers (atenolol & metoprolol) Selectively block b1 receptors on the heart => decreased CO => decreased BP Non-selective beta blockers (labetalol & carvedilol) Block A1 receptors as well, simultaneously decreasing vascular resistance. Beta blockers block kidney b1, stopping RAA axis resulting in decreased systemic vascular resistance, and a drop in BP . Centrally acting adrenergic drugs Block sympathetic activity in the brain E.g. clonidine and methyldopa Clonidine selectively stimulates presynaptic a2 receptors providing negative feedback => reduced catecholamine prod & release => decreased systemic vascular resistance and CO and BP Methyldopa does the same as clonidine. It isn't an agonist yet. It's a prodrug that must be turned into active metabolite methyl-norepinephrine. . Calcium channel blockers: a. Dihydropyridines and b. non-dihydropyridines a. These selectively inhibit L-type calcium channels in vascular smooth muscle inhibiting contraction and decreasing resistance to blood flow and lowering blood pressure. Drugs are: Amlodipine, Felodipine, Nicardipine, Nifedipine. ADRs: Dizziness, headache, flushing, peripheral edema, gingival hyperplasia (all associated with vasodilation) b. They block calcium channels in vascular smooth muscle and also those on cardiac cells e.g. SA and AV nodes, producing reduced Contractility, slower heart rate, and slower conduction. They produce anti-arrythmic properties. Non-dihydropyridines don't significantly decrease CO as reflex tachycardia sets in due to vasodilation. Drugs are diltiazem and verapamil. ADRs : excessive bradycardia, cardiac conduction abnormalities. Verapamil can exert inhibition of Ça channels of smooth muscle in GI tract causing constipation. . Diuretics: i. Loop diuretics (e.g. furosemide) Reduce Na/Cl reabsorption in kidneys , causing significant diuresis. Decreased CO => decreased BP (especially In chronic kidney disease and volume based hypertension). ii. Thiazides (e.g. hydro-chloro-thiazide) reduce reabs of Na/Cl to a smaller degree than loop diuretics. Long term effects on blood volume are mininal. Sustained Antihypertensive effects are produced by thiazide-induced vasodilation. iii. K+ sparing diuretics (triamterene & Spironolactone) increase diuresis by disturbing Na/K exchange, or by blocking aldosterones actions. They're used in conjunction with the other 2 to reduce K+ loss. ... RAA axis blockers: Renin inhibitors decrease Angiotensin 2 production (aliskiren) ACEi inhibit Angiotensin 2 production and increase Bradykinin release. (PRILs) ARBs inhibit binding of Angiotensin 2 (SARTANs) These drugs decrease systemic vascular resistance without affecting cardiac output greatly. They reduce efferent arteriole vasoconstriction, so they improve renal blood flow, reducing risk of renal injury. ADRs: use can cause hyperkalemia (they inhibit aldosterone prod) ACEi can cause dry cough and angioedema (due to Bradykinin and substance P) ... Bosentan, competitive endothelin 1 antagonist. Acts on endothelin a and b receptors on pulmonary vascular cells. By blocking these it causes vasodilation, decreasing pulmonary vascular resistance. Indication: pulmonary hypertension. . Fenoldopam is a dopamine 1 receptor agonist on smooth muscle cells of peripheral vasculature, and renal, coronary, cerebral and mesenteric arteries. It produces generalised arterial vasodilation => decreased peripheral resistance => lower BP It inhibits tubular Na reabsorption => natriuresis & diuresis. Indication: short term management of severe hypertension (due to rapid Onset of action and short Duration of action). . Sodium nitroprusside and Nitroglycerin (sources of NO -> activates Guanyl cyclase=> increased cGMP => decreased Ca2+ => vasodilation) . Direct Acting smooth muscle relaxants: hydralazine and minoxidil. They produce compensatory reflex tachycardia, and Renin release, so are typically used with a diuretic and beta blocker
This is one of the greatest blood pressure solution I`ve read BloodHeart.xyz Simple language is used to write it, meaning it is easy to understand and do. I strongly recommend this book for anyone wanting to lower her or his blood pressure. My blood returned to the normal 120/80 right after pursuing the suggestions on the program.
In times of Corona, when a subject already difficult enough is made even more incomprehensible because its being taught online I'm thankful for youtube and pages like this!
hi everyone ,if anyone else trying to find out how to treat blood pressure try Nevolly Overcome BP Nerd ( search on google ) ? Ive heard some great things about it and my colleague got excellent success with it.
Great video. I just wanna make one small correction in the begging you say that renin is stimulating the convertion of angiotensin 1 -> angiotensin 2, this job is done by ACE(lungs). What renin does is to cleave Angiotensinogen made from the liver to Angiotensin 1
Here we have the smartest guy/girl of the class . He actually said Renin is necessary for the production of Angiotensin II . Then , later in the video he actually explains correctly the mechanism again . Be sure of double check something before you make a correction !
This is a very useful refresher presentation for me, since I have been taking combinations of these medications for a number of years. Understanding their mechanisms of action often allows me to identify causation of changes in my conditions. I can then communicate more intelligently with my physicians.
Western medication forever can't effectively treat and revese hypertension. Forget those bullshit hypertensive drugs because they're of no use. How to reverse calcified and hardened internal elastic lamina? Western medication can't clear up AGEs (advanced glycation endproducts) so that vessels can restore their elasticity, flexibility and plasticity. God's mercy nano-medication is the last-ditch treatment for hypertension. Is it so amazing that to lower sys.pressure from 220 mm Hg to 110 mm Hg by nano-medication. Nano-medication is based on: God created humans out of extract of clay from ground During past five decades, USA, Russia, France and Germany have made great efforts to unravel nano-medication unsuccessfully. Nanoparticles of nano-medication are AGE-breakers and so-called Universal Ligand (Antibody) All glory belongs to God !
I wish I had found these videos while I was taking pharmacology. You just put 4wks of frustration and confusion into a nice bubble for me as I am currently studying CV diseases, diagnoses and treatments. Thank you so much. I have already bookmarked the diabetes information for next month.
Western medication forever can't effectively treat and revese hypertension. Forget those bullshit hypertensive drugs because they're of no use. How to reverse calcified and hardened internal elastic lamina? Western medication can't clear up AGEs (advanced glycation endproducts) so that vessels can restore their elasticity, flexibility and plasticity. God's mercy nano-medication is the last-ditch treatment for hypertension. Is it so amazing that to lower sys.pressure from 220 mm Hg to 110 mm Hg by nano-medication. Nano-medication is based on: God created humans out of extract of clay from ground During past five decades, USA, Russia, France and Germany have made great efforts to unravel nano-medication unsuccessfully. Nanoparticles of nano-medication are AGE-breakers and so-called Universal Ligand (Antibody) All glory belongs to God !
After getting this t.co/GsO1JmyXtf for keeping blood pressure and looking it a week ago, I noticed the difference in my blood pressure levels. It definitely is stabilizing!!! After Twenty days of everyday use my blood pressure is down! Right after 25 days my pressure is normal (for me) 120/55.?
Awesome video :) I have a question about methyldopa and clonide though. I understand that clonidine serves as an alfa-2 agonist in presynaptic neurons in the brain (however there is a dilemma as some sources it works on postsynaptic neurons? and other sources say it works not only in the brain- plz clarify) which therefore causes less release of NE,E-> less stimultion of alfa and beta = decreased blood pressure through a decrease in cardiac output + total peripheral resistance. However since normally we have compensatory mechanisms that prevent a decrease in blood pressure (baroreceptors) we would have reflex tachycardia but because clonidine works on receptors in nucleus solitarius and imidazole receptors (as an agonist?) these prevent the reflex from activating???? is this correct? How come clonidine is used in ADHD- apparently it raises norepinephrine levels in the prefrontal cortex (it doesnt make any sense since its an alfa-2 agonist so it should inhibit norepinephrine) and when it comes to methyldopa, i read that it is a L-dopa analogue. You say it is converted to an active metabolite which then works on alfa-2 receptors in presynaptic neurons = less NE+E (basically like clonidine). however since it is an analogue, it surely competes with L-dopa for the enzyme dopa decarboxylase, meaning less dopamine + noradrenaline is made-> this should be the main mechanism of action? or is it both???? HELP.
For the first question I was confuse too about the contradictory action of clonidine but then I did a little research and found that clonidine is indeed an alpha 2 adrenoreceptor agonist, but since alpha 2 receptors are autoregulators for NE release, the overall activity of sympathetic activity decreases because of less NE production. So it's a sort of agonist that works like an antagonist for the whole system. The same effect it has on central nervous system, decreasing the overall sympathetic outflow.
Alpha 2 receptors are inhibitory I.e they keep an inhibitory check , when the levels of NE increases in the synapse alpha 2 agonist will bind to the receptors and decrease the release of NE
This video is amazing. It discussed the major actions of the drugs at cellular level. Which is exactly what Im looking for!! ❤ Thank you so muchh! Please do more videos like this. Its easy to understand :)
Look I have been on beta blockers for two years and this is the first time I’m understanding… I am pregnant and just got swapped from the Toprol to obey the law… Also swapped from the certain to hydralazine… They are trying to prevent pre-clamp Sia since I already had a high pressure… Anyway just wanted to say please do more videos your descriptions plus pictures make it very easy for nonmedical people LOL
If we stop the production of any enzyme through a drug, how does the body react? Will it end up producing some other material? Alternatively what happens to the materials involved in the synthesis of the enzyme?
Man 50yo. I have high blood pressure build up about 3 hours after sex. It stays high 170/105 for about one day (without tablets reach 205/115) then normalize 130/90. I have seen many doctors. I take LOSARTAN 50mg. If you know why or know someone with the same symptoms please let mi know. Thanks
Good videos! As a pharmacology teacher, I often use it to help my students. Of commonly used drugs, there are no moxonidine. Is it not so common in your country?
Western medication forever can't effectively treat and revese hypertension. Forget those bullshit hypertensive drugs because they're of no use. How to reverse calcified and hardened internal elastic lamina? Western medication can't clear up AGEs (advanced glycation endproducts) so that vessels can restore their elasticity, flexibility and plasticity. God's mercy nano-medication is the last-ditch treatment for hypertension. Is it so amazing that to lower sys.pressure from 220 mm Hg to 110 mm Hg by nano-medication. Nano-medication is based on: God created humans out of extract of clay from ground During past five decades, USA, Russia, France and Germany have made great efforts to unravel nano-medication unsuccessfully. Nanoparticles of nano-medication are AGE-breakers and so-called Universal Ligand (Antibody) All glory belongs to God !
I have CKD and my blood pressure goes up up to 180/100. I take Telizartan 80mg, metropolol 100mg and amlodipine 10mg. All I do all day is to take anti-hypertensive meds. arrrrggggghhh... I'm gonna die soon.
I spent only 1 month and a half following the recommendations in solving blood pressure level issues t.co/GsO1JmyXtf . I have stage II diabetes, high BP and over weight. I needed to pass the exam for D.O.T. Physical. I dropped Thirteen lbs, my Blood pressure went from average of 1.55 to 136. My everyday blood sugars went from 160`s down to 125 - 130.?
I am confused for the activity of Bradykinin. If Bradykinin leads to vasodilatation, how its breakdown again leads to bradykinin induced vasodilatation? Thank you.
