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Pharm Ch 25

Drugs for Hypertension Key Terms

TermDefinition
aldosterone hormone secreted by the adrenal cortex that increase sodium reabsorption in the distal tubule of the kidney
angiotensin II chemical released in response to falling blood pressure that causes vasoconstriction and release of aldosterone
angiotensin-converting enzyme (ACE) enzyme responsible for converting angiotensin I to angiotensin II
antidiuretic hormone (ADH) potent vasoconstrictor that can also increase blood pressure by raising blood volume
baroreceptors nerves located in the walls of the atria, aortic arch, vena cava, and carotid sinus that sense changes in blood pressure
calcium channel blockers (CCBs) drug that blocks the flow of calcium ions into myocardial cells
cardiac output the volume of blood pumped per minute
chemoreceptors nerves located in the aortic arch and carotid sinus that sense changes in oxygen content, pH, or carbon dioxide levels in the blood
diuretics substance that increases urine output
hypertension (HTN) the consistent elevation of systemic arterial blood pressure
peripheral resistance amount of friction encountered by blood as it travels through the vessels
primary hypertension HTN having no identifiable cause
reflex tachycardia temporary increase in heart rate that occurs when blood pressure falls
renin-angiotensin-aldosterone system (RAAS) body mechanism for raising blood pressure initiated by the release of renin by the kidney
secondary hypertension HTN that has a specific cause
stroke volume amount of blood pumped out by a ventricle in a single beat
vasomotor center area of the medulla that controls baseline blood pressure
alpha 2 agonists decrease sympathetic impulses from the CNS to the heart and arterioles, causing vasodilation
alpha1 blockers inhibit sympathetic activation in arterioles, causing vasodilation
direct vasodilators act on the smooth muscle of arterioles, causing vasodilation
beta blockers decrease the heart rate and myocardial contractility, reducing cardiac output
calcium channel blockers block calcium ion channels in arterial smooth muscle, causing vasodilation
angiotensin receptor blockers prevent angiotensin II from reaching its receptors, causing vasodilation
diuretics increase urine output and decrease fluid volume
ACE inhibitors block formation of angiotensin II, causing vasodilation, and block aldosterone secretion, decreasing fluid volume
 

 



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