👉📝WANT STUDY NOTES FOR THIS PRESENTATION? 👉Join Patreon at
So let’s get right into it hypertension or high blood pressure is a any symptoms now in order to gain a better understanding of pharmacology of pressure regulation so when we talk about blood pressure we are generally now this pressure in the arteries is maintained by among other things of the arterial walls as well blood volume in other words blood pressure is couple of major
Systems involved in blood pressure regulation first arterial located in the aortic arch and carotid sinuses so for example if blood pressure causing release of catecholamines and activation of alpha and beta receptors so activation of beta-1 receptors causes leads to increase in blood pressure on the other hand activation of alpha-1 vascular resistance which again leads to
Increase in blood pressure now another renin-angiotensin-aldosterone system so we also have baroreceptors in the releasing enzyme called renin additionally renin secretion is also in the kidneys now renin is necessary for the production of angiotensin ii angiotensin ii is a very potent vasoconstrictor which constricts systemic constricts renal blood vessels and stimulates
Aldosterone secretion which output and ultimately increased blood pressure now let’s switch gears and classes of antihypertensive drugs which work by interrupting different parts of doxazosin and prazosin which block alpha-1 receptors on the smooth muscle decrease in blood pressure next we have selective beta blockers such as atenolol causing decrease in cardiac output and
Thereby decrease in blood pressure as labetalol and carvedilol that can additionally block alpha-1 receptors and inhibit beta-1 receptors present on the kidneys and thus suppress release of effects result in decrease in systemic vascular resistance and again fall in out my video about adrenergic antagonists now the next major class of blocking sympathetic activity within
The brain example of drugs that belong to presynaptic alpha-2 receptors thus providing negative feedback to reduce in systemic vascular resistance and cardiac output and ultimately decreased blood pressure methyldopa on the other hand also lowers blood pressure through the agonist itself so first it must be converted to its active metabolite antihypertensive agents that is
Calcium channel blockers so calcium channel nondihydropyridines now dihydropyridines selectively inhibit l-type calcium enters the smooth muscle cell it causes it to contract which leads to increased blocks the entry of calcium into the vascular smooth muscle cell the thus lowering of blood pressure example of drugs that belong to this group are effects of dihydropyridines
They’re related to systemic vasodilation so you that may occur with this class is swelling of gums also known as gingival hyperplasia now let’s move on to nondihydropyridines which are non selective blocking calcium channels on vascular smooth muscle but also calcium channels myocardial contractility slower heart agents exhibit significant antiarrhythmic properties for
More now it’s important to remember that even though decreased heart contractions most likely because of the reflex tachycardia that occurs as a result of namely diltiazem and verapamil now when can cause excessive bradycardia and cardiac conduction abnormalities blocker can exert significant inhibition that lines the gi tract which can lead to constipation now the next
Major class of antihypertensive agents are diuretics there hypertension first we have loop diuretics such as furosemide which significant diuresis with less volume in the heart so cardiac output decreases this in turn leads to decrease in blood kidney disease secondly we have thiazide diuretics such as hydrochlorothiazide smaller degree than loop diuretics this leads to
Initial decrease in pressure however the long term effects on blood volume are minimal and vasodilation lastly we have potassium-sparing diuretics such as triamterene sodium potassium exchange in the kidneys or by blocking the actions of aldosterone potassium-sparing diuretics are often used in combination sure you check out my video about diuretics now let’s move on to
Another renin-angiotensin-aldosterone system so here we have three pharmacological ultimately responsible for causing blood the enzyme responsible for conversion of angiotensinogen to precursor of which selectively inhibit this enzyme thus decreasing production of secondly we have angiotensin-converting enzyme that is responsible of ace inhibitors so just like inhibition
Of renin inhibition of however what makes ace inhibitors different is that in addition to bradykinin is a peptide that causes blood vessels to dilate by stimulating inhibition leads to bradykinin induced vasodilation the example of drugs that belong to this class are benazepril captopril enalapril of angiotensin ii to these receptors is actually responsible for most of
The aldosterone release these receptors are the target of angiotensin ii receptor this renin-angiotensin-aldosterone system either block the production of decreased systemic vascular resistance but without significant changes in renal hemodynamics specifically angiotensin ii constricts the efferent lead to injury so by reducing activity of angiotensin ii these agents also
It comes to side effects because these agents suppress aldosterone release ace inhibitors in particular may cause dry cough or in rare cases angioedema levels of bradykinin and substance p now before we end this lecture i wanted to briefly discuss few other antihypertensive agents that do not fall which is a competitive antagonist of a which acts on the endothelin-a and
Endothelin-b receptors located these receptors bosentan leads to vasodilation which decreases pulmonary vascular resistance for that reason bosentan is often a drug of choice for dopamine-1 receptor agonist the dopamine-1 receptors are located on the dopamine-1 receptors fenoldopam produces generalized arterial vasodilation additionally fenoldopam inhibits tubular sodium
Reabsorption which short duration of action fenoldopam is often used in the agents that are also used for hypertensive emergency are sodium nitroprusside and nitroglycerin which simply serve as a source of nitric oxide relaxants namely hydralazine with mechanism of action that has not been atp-activated potassium channels in the smooth muscle which leads to membrane
Significantly decrease peripheral resistance they also produce significant drugs are typically administered in combination with a diuretic and a beta growth which is why this drug is used more often for treatment of baldness you enjoyed this video and as always stay tuned for more
Transcribed from video
Pharmacology – HYPERTENSION & ANTIHYPERTENSIVES (MADE EASY) By Speed Pharmacology
