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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

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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

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