AcLlon AngloLensln ll ls a very poLenL chemlcal LhaL causes vasoconsLlcLlon 1he narrowlng of Lhe vessels lncreases Lhe pressure wlLhln Lhe vessels and cause hyperLenslon AngloLensln ll ls formed from angloLensln l by Lhe enzyme angloLensln converLlng enzyme (ACL) 1he use of ACL lnhlblLors lnhlblL Lhe acLlvlLy of Lhe enzyme ACL whlch decreases Lhe producLlon of angloLensln ll hereby relaxlng Lhe blood vessel and lower down blood pressure
pharmacologIcal aspects of care A persIstent dry cough Is a common adverse effect belIeved to be assocIated wIth the Increases In bradykInIn levels produced by ACE InhIbItors. PatIents who experIence thIs cough are often swItched to angIotensIn receptor antagonIsts.
Ang|otens|n II receptor b|ockers
Lxamples of AngloLensln ll recepLor blockers AngloLensln ll recepLor blockers (A88s) are medlcaLlons LhaL block Lhe acLlon of angloLensln ll by prevenLlng angloLensln ll from blndlng Lo Lhe angloLensln ll recepLors As a resulL Lhe blood vessels dllaLed and blood pressure ls reduced 1he effecLs of A88s are slmllar Lo ACL lnhlblLors buL ACL lnhlblLors acL by prevenLlng Lhe formaLlon of angloLensln ll raLher Lhan by blocklng Lhe blndlng of angloLensln ll Lo Lhe blood vessels
Calclum channel blockers Calclum channel blockers prevenL calclum from enLerlng Lhe cardlac muscle and arLerles 1he enLry of calclum lnLo Lhese cells causes Lhe hearL Lo conLracL and arLerles Lo narrowCalclum channel blockers also called calclum anLagonlsLs decrease Lhe conLracLlon of Lhe hearL and dllaLe blood vessels maklng Lhe hearL Lo pump easler Some calclum channel blockers have Lhe added beneflL of slowlng Lhe hearL raLe whlch can furLher reduce blood pressure relleve anglna (as Lhe hearL needs less oxygen) and conLrol an lrregular hearLbeaL (LreaLlng cerLaln abnormal hearL rhyLhms such as arLerlal flbrlllaLlon)
ulrecL acLlng vasodllaLors vasodllaLors are medlcaLlons LhaL dllaLe Lhe blood vessels 1hey work dlrecLly on Lhe walls of arLerles prevenLlng Lhe muscles from LlghLenlng and Lhe walls from narrowlng As a resulL blood flows more easlly Lhrough Lhe arLerles pumplng of Lhe hearL ls easler and blood pressure ls reduced
CardloLonlc/lnoLroplc
Cardlac glycosldes
-ames uegoxln Cardlac glycoslde has poslLlve lnoLroplc acLlvlLy characLerlzed by an lncrease ln Lhe force of myocardlal conLracLlon lL also reduces Lhe conducLlvlLy of Lhe hearL Lhrough Lhe aLrlovenLrlcular (Av) node lL works by affecLlng cerLaln mlnerals (sodlum and poLasslum) lnslde Lhe cardlac cell 1hls reduces sLraln on Lhe hearL and helps lL malnLaln a normal sLeady and sLrong hearLbeaL
8eLa blockers also known as beLaadrenerglc blocklng agenLs are drugs LhaL block noreplnephrlne and eplnephrlne (adrenallne) from blndlng Lo beLa recepLors on nerves8y blocklng Lhe effecL of noreplnephrlne and eplnephrlne beLa blockers reduce hearL raLe reduce blood pressure by dllaLlng blood vessels and may consLrlcL alr passages by sLlmulaLlng Lhe muscles LhaL surround Lhe alr passages Lo conLracL
Class lll anLlarrhyLhmlcs oLasslum channel blocker
8lle acld sequesLranLs are medlcaLlons for lowerlng LuL cholesLerol 8lle acld sequesLranLs blnd blle aclds ln Lhe lnLesLlne and cause more of Lhe blle aclds Lo be excreLed ln Lhe sLool 1hls reduces Lhe amounL of blle aclds reLurnlng Lo Lhe llver and forces Lhe llver Lo produce more blle aclds Lo replace Lhe blle aclds losL ln Lhe sLool ln order Lo produce more blle aclds Lhe llver converLs more cholesLerol lnLo blle aclds whlch lowers Lhe level of cholesLerol ln Lhe blood
8lle acld sequesLranLs are noL absorbed lnLo Lhe body and Lherefore Lhey do noL have sysLemlc slde effecLs 1herefore Lhelr mosL common slde effecLs are gasLrolnLesLlnal such as consLlpaLlon dlarrhea vomlLLlng and bloaLlng Lncourage fluld lnLake and lv lnfuslon ls essenLlal Lo resLore fluld and elecLrolyLes ln Lhe body
SLaLlns are a class of drugs LhaL lower Lhe level of cholesLerol ln Lhe blood by reduclng Lhe producLlon of cholesLerol by Lhe llver SLaLlns block Lhe enzyme ln Lhe llver LhaL ls responslble for maklng cholesLerol 1hls enzyme ls called hydroxymeLhylgluLarylcoenzyme A reducLase (PMCCoA reducLase) CholesLerol conLrlbuLes Lo Lhe developmenL of aLherosclerosls1hese cholesLerolconLalnlng plaques block Lhe arLerles and reduce blood flow Lo Lhe Llssues LhaL arLerles supply When plaques rupLure a blood cloL forms and Lhereby furLher blocklng Lhe arLery and reduclng Lhe flow of blood When blood flow ls reduced sufflclenLly ln Lhe arLerles LhaL supply blood Lo Lhe hearL Lhe resulL ls anglna or a hearL aLLack 8y reduclng Lhe producLlon of cholesLerol sLaLlns are able Lo slow Lhe formaLlon of new plaques and occaslonally can reduce Lhe slze of plaques LhaL already exlsL
llbraLes -ame gemflbrozll (Lopld) and fenoflbraLe (1rlcor)
llbrlc acld derlvaLlves (flbraLes) are a class of medlcaLlons LhaL lower blood Lrlglycerlde levels llbraLes lower blood Lrlglycerlde levels by reduclng Lhe llver s producLlon of vLuL and by speedlng up Lhe removal of Lrlglycerldes from Lhe blood llbraLes are also modesLly effecLlve ln lncreaslng blood PuL cholesLerol levels however flbraLes are noL effecLlve ln lowerlng LuL cholesLerol llbraLes have also been used alone Lo prevenL hearL aLLacks especlally ln paLlenLs wlLh elevaLed blood Lrlglycerldes and low PuL cholesLerol levels llbraLes can lncrease Lhe effecLlveness of blood Lhlnners such as warfarln (Coumadln) when boLh medlcaLlons are used LogeLher 1hus Lhe dose ofwarfarln should be ad[usLed Lo avold overLhlnnlng of Lhe blood whlch can lead Lo excesslve bleedlng