Essential Hypertension

Hypertension is the term used to describe high blood pressure.Blood pressure is a measurement of the force against the walls of your arteries as your heart pumps blood through your body. Blood pressure readings are usually given as two numbers -- for example, 120 over 80 (written as 120/80 mmHg). One or both of these numbers can be too high. The top number is called the systolic blood pressure, and the bottom number is called the diastolic blood pressure.. Normal blood pressure is when your blood pressure is lower than 120/80 mmHg most of the time. High blood pressure (hypertension) is when your blood pressure is 140/90 mmHg or above most of the time.

If your blood pressure numbers are 120/80 or higher, but below 140/90, it is called pre-hypertension

Causes:
Many factors can affect blood pressure, including: How much water and salt you have in your body The condition of your kidneys, nervous system, or blood vessels The levels of different body hormones You are more likely to be told your blood pressure is too high as you get older. This is because your blood vessels become stiffer as you age. When that happens, your blood pressure goes up. High blood pressure increases your chance of having a stroke, heart attack, heart failure, kidney disease, and early death. You have a higher risk of high blood pressure if you: Are African American Are obese Are often stressed or anxious Drink too much alcohol (more than one drink per day for women and more than two drinks per day for men) Eat too much salt in your diet Have a family history of high blood pressure Have diabetes Smoke Most of the time, no cause of high blood pressure is found. This is called essential hypertension. High blood pressure that is caused by another medical condition or medication is called secondary hypertension. Secondary hypertension may be due to: Chronic kidney disease Disorders of the adrenal gland (pheochromocytoma or Cushing syndrome) Pregnancy (see: preeclampsia) Medications such as birth control pills , diet pills, some cold medications , and migraine medications Narrowed artery that supplies blood to the kidney (renal artery stenosis) Hyperparathyroidism

Symptoms

Most of the time, there are no symptoms. For most patients, high blood pressure is found when they visit their health care provider or have it checked elsewhere. Because there are no symptoms, people can develop heart disease and kidney problems without knowing they have high blood pressure. If you have a severe headache nausea or vomiting bad headache confusion changes in your vision or nosebleeds you may have a severe and dangerous form of high blood pressure called malignant hypertension.

Exams and Tests

Your health care provider will check your blood pressure several times before diagnosing you with high blood pressure. It is normal for your blood pressure to be different depending on the time of day. Blood pressure readings taken at home may be a better measure of your current blood pressure than those taken at your doctor's office. Make sure you get a good quality, well-fitting home device. It should have the proper sized cuff and a digital readout. Practice with your health care provider or nurse to make sure you are taking your blood pressure correctly. See also: Blood pressure monitors for home Your doctor will perform a physical exam to look for signs of heart disease, damage to the eyes, and other changes in your body. Tests may be done to look for: High cholesterol levels Heart disease, such as an echocardiogram or electrocardiogram Kidney disease, such as a basic metabolic panel and urinalysis or ultrasound of the kidneys

Treatment
The goal of treatment is to reduce blood pressure so that you have a lower risk of complications. You and your health care provider should set a blood pressure goal for you. If you have pre-hypertension, your health care provider will recommend lifestyle changes to bring your blood pressure down to a normal range. Medicines are rarely used for pre-hypertension. Often, a single blood pressure drug may not be enough to control your blood pressure, and you may need to take two or more drugs. It is very important that you take the medications prescribed to you. If you have side effects, your health care provider can substitute a different medication.

cardioselective beta blockers

mechanism of action:

Beta blockers work by changing how certain sensors in the body, called beta receptors, respond to signals from the central nervous system. These medications are used to treat heart and blood pressure problems because both the heart and blood vessels have very high numbers of beta receptors. There are

also high numbers of beta receptors in the lungs, but these receptors are slightly different in structure. Cardioselective beta blockers are able to tell the two apart. The cardioselective beta blockers

atenolol

atenolol 50-100mg

ateno50-100mg

atenolol50-100mg

blockium50-100mg

tenormin25-50-100mg

tensolol50-100mg

metoprolol betaloc100mg low press100mg

bisoprolol

bisocard5-10mg

concor2.5-5-10mg

bistol10mg

non cardioselective beta blocker

mechanism of action : Beta-blockers are drugs that bind to beta-adrenoceptors and thereby block the binding of norepinephrine and epinephrine to these receptors. This inhibits normal sympathetic effects that act through these receptors. Therefore, betablockers are sympatholytic drugs. Some beta-blockers, when they bind to the beta-adrenoceptor, partially activate the receptor while preventing norepinephrine from binding to the receptor. These partial agonists therefore provide some "background" of sympathetic activity while preventing normal and enhanced sympathetic activity. These particular beta-blockers (partial agonists) are said to possess intrinsic sympathomimetic activity (ISA). Some beta-blockers also possess what is referred to as membrane stabilizing activity (MSA). This effect is similar to the membrane stabilizing activity of sodium-channels blockers that represent Class I antiarrhythmics. The first generation of beta-blockers were non-selective, meaning that they blocked both beta-1 (1) and beta-1 (2) adrenoceptors. Second generation betablockers are more cardioselective in that they are relatively selective for 1 adrenoceptors. Note that this relative selectivity can be lost at higher drug doses. Finally, the third generation beta-blockers are drugs that also possess vasodilator actions through blockade of vascular alpha-adrenoceptors.

nebivolol

niblet5mg

symbian 5mg

sotolol

betacor

alpha& beta blocker

carvedolol

cardilol 25

dilatrol

carvid 6.25-25mg

carvipress

carvena

carvedolol

calcium channel blocker

mechanism of action:
Currently approved CCBs bind to L-type calcium channels located on the vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue (sinoatrial and atrioventricular nodes). These channels are responsible for regulating the influx of calcium into muscle cells, which in turn stimulates smooth muscle contraction and cardiac myocyte contraction. In cardiac nodal tissue, L-type calcium channels play an important role in pacemaker currents and in phase 0 of the action potentials. Therefore, by blocking calcium entry into the cell, CCBs cause vascular smooth muscle relaxation (vasodilation), decreased myocardial force generation (negative inotropy), decreased heart rate (negative chronotropy), and decreased conduction velocity within the heart (negative dromotropy), particularly at the atrioventricular node.

nicardipine hcl 20-50mg micard pelcard

lacidipine 2-4mg lacipil lodipine lacidac

amlodipine 5_10mg alkapress amilo amlodipine

myodura

norvasc

vasonorm

regcor

cardiovasc

deltiazem 60-90-120-180mg

telzim sr

nimotop

tildiem

slow-zem

peltiam

mono tidiem

dilatcor-xl

delay-tiazem sr

altiazem

nefidipine 10-20mg epilat adalat nifepin

felodipine 2.5-5-10mg

logimax

plentopine

plendil

felocor

nitrate
mechanism of action : General Pharmacology
Nitric oxide (NO), a molecule produced by many cells in the body, and has several important actions (click here for details). In the cardiovascular system, NO is primarily produced by vascular endothelial cells. This endothelial-derived NO has several important functions including relaxing vascular smooth muscle (vasodilation), inhibiting platelet aggregation (anti-thrombotic), and inhibiting leukocyte-endothelial interactions (anti-inflammatory). These actions involve NOstimulated formation of cGMP. Nitrodilators are drugs that mimic the actions of endogenous NO by releasing NO or forming NO within tissues. These drugs act directly on the vascular smooth muscle to cause relaxation and therefore serve as endothelial-independent vasodilators.

There are two basic types of nitrodilators: those that release NO spontaneously (e.g., sodium nitroprusside) and organic nitrates that require an enzymatic process to form NO. Organic nitrates do not directly release NO, however, their nitrate groups interact with enzymes and intracellular sulfhydryl groups that reduce the nitrate groups to NO or to Snitrosothiol, which then is reduced to NO. Nitric oxide activates smooth muscle soluble guanylyl cyclase (GC) to form cGMP. Increased intracellular cGMP inhibits calcium entry into the cell, thereby decreasing intracellular calcium concentrations and causing smooth muscle relaxation (click here for details). NO also activates K+ channels, which leads to hyperpolarization and relaxation. Finally, NO acting through cGMP can stimulate a cGMP-dependent protein kinase that activates myosin light chain phosphatase, the enzyme that dephosphorylates myosin light chains, which leads to relaxation. Tolerance to nitrodilators occurs with frequent dosing, which decreases their efficacy. The problem is partially circumvented by using the smallest effective dose of the compound coupled with infrequent or irregular dosing. The mechanism for tolerance is not fully understood, but it may involve depletion of tissue sulfhydryl groups, or scavenging of NO by superoxide anion and the subsequent production of peroxynitrite that may inhibit guanylyl cyclase.

Primary Cardiovascular Actions of Nitrodilators Systemic vasculature

vasodilation (venous dilation > arterial dilation) decreased venous pressure decreased arterial pressure (small effect)

Cardiac
reduced preload and afterload (decreased wall stress) decreased oxygen demand

Coronary

 prevents/reverses vasospasm vasodilation (primarily epicardial vessels) improves subendocardial perfusion increased oxygen delivery Although nitrodilators can dilate both arteries and veins, venous dilation predominates when these drugs are given at normal therapeutic doses. Venous dilation reduces venous pressure and decreases ventricular preload. This reduces ventricular wall stress and oxygen demand by the heart, thereby enhancing the oxygen supply/demand ratio. A reduction in preload (reduced diastolic wall stress) also helps to improve subendocardial blood flow, which is often compromised in coronary artery disease. Mild coronary dilation or reversal of coronary vasospasm will further enhance the oxygen supply/demand ratio and diminish the anginal pain. Coronary dilation occurs primarily in the large epicardial vessels, which diminishes the likelihood of coronary vascular steal. Systemic arterial dilation reduces afterload, which can enhance cardiac output while at the same time reducing ventricular wall stress and oxygen demand. At high concentrations, excessive systemic vasodilation may lead to hypotension and a baroreceptor reflex that produces tachycardia. When this occurs, the beneficial effects on the oxygen supply/demand ratio are partially offset. Furthermore, tachycardia, by reducing the duration of diastole, decreases the time available for coronary perfusion, most of which occurs during diastole (click here for more details).

isosorbide mononitrate 20-25-40-50-100mg monomack monocard cardioguard m

effox

ismo

imdur

nicorandil 20mg randil

isosorbide dinitrate 1.25-2-5-10-20-40mg

cardiket

coronit

dinitra

isomack

isordil

nitroglycerin

angised

nitromack retard

nitroderm tts

nitroguard

nitronal

nitrostat

nitrotard

deponitnt5

nitrocare SR

tridil

Angiotensin II Receptorantagonist
valsartan

disartan

tareg

valsar

idisartan

losartan potasium

losartan

remtozar

lozapress

lozar

kanzar

cozaar

amozar

losarmepha

irbesartan

aprovel

eprosartan

teveten

telmisartan

micardis

candisartan

atacand

atacand plus

candesar

Angiotensin II Receptor inhibitors

mechanism of action:
These drugs have very similar effects to angiotensin converting enzyme (ACE) inhibitors and are used for the same indications (hypertension, heart failure, postmyocardial infarction). Their mechanism of action, however, is very different from ACE inhibitors, which inhibit the formation of angiotensin II. ARBs are receptor antagonists that block type 1 angiotensin II (AT1) receptors on bloods vessels and other tissues such as the heart. These receptors are coupled to the Gqprotein and IP3 signal transduction pathway that stimulates vascular smooth muscle contraction. Because ARBs do not inhibit ACE, they do not cause an increase in bradykinin, which contributes to the vasodilation produced by ACE

inhibitors and also some of the side effects of ACE inhibitors (cough and angioedema). ARBs have the following actions, which are very similar to ACE inhibitors: Dilate arteries and veins and thereby reduce arterial pressure and preload and afterload on the heart. Down regulate sympathetic adrenergic activity by blocking the effects of angiotensin II on sympathetic nerve release and reuptake of norepinephrine. Promote renal excretion of sodium and water (natriuretic and diuretic effects) by blocking the effects of angiotensin II in the kidney and by blocking angiotensin II stimulation of aldosterone secretion. Inhibit cardiac and vascular remodeling associated with chronic hypertension, heart failure, and myocardial infarction.

lisinopril

lisopril

lisinopril

sinopril

zestril

maxitrel

perindopril

coversyl

adwipril

enalpril

acapril

enalapril

lotrial

ezalapril

renitic

press light

benzapril

cibacen

ramipril

ramitac

tritace

tritace protect

ramipril

corpril

moexipril

primox

captopril

capoten

captopril

lotensine

hypopress

fosinopril

monopril

centrally acting anti hypertensive

clonidine

catapress

phentolamine

rogitine

prazocin

minipress

methyl dopa

methyldopa

aldomet

adamat

kadomet

farcodopa

epidopa

vasodilator antihypertensive
sodium nitroprusside

niprid

nipruss

sodium nitroprusside

adenergic and dopamenergic agent

dobutamine

dobutrix

dobutamine

adrenaline

adrenaline

dopamine

dopamine

intropin

isoprenaline

isupril

natural product
hybisc master-hibiscus royatens

multiingredient
atenolol+chlorthalidone 50-100+12.5-25mg tenoret tenoretic

blockium diu

tenedone

capotril+indapamide 33+3mg

normaten

verpamil+trandolapril 180+2mg

tarka

atenolol+amiloride 50-100 +2.5-5mg

teklo

hipress D

atenoretic

atenolol+nefidipine

tenolat SR

amlodipine +valsartan

exforge 5_10+160mg

resperine+clopramide+dihydroergocristine 1+5+0.1mg

brinerdin

hypoten

perindopril+indapamide 2+0.625mg preterex bipreterex

bisoprolol+hydrochlorthalidone 2.5-5-10+6.25-12.5-25mg

lodoz

concor plus 5

concor plus 10

bisocard plus

bistol plus

cardivo care

telmisartan+hydrochlorthalidone 80-12.5mg micardis plus

captopril+hydrochlorthalidone 50+25mg

capozide

farcopril plus

capojed H

hypopress D

ramipril+hydrochlorthalidone 2.5-5+12.5-25mg

tritace comp

tritace comp l s

fosinopril+hydrochlorthalidone 10-20+12.5mg

monozide

valsartan+hydrochlorthalidone 80-160+12.5mg

disartan co

co tareg

co diovan

benzapril+hydrochlorthalidone

cibradex 10-12.5mg

enalapril maleate+hydrochlorthalidone

co renitic 20+12.5mg

enalazide 10+1.5mg

thiazopril 20+12.5mg

ezapril co 20+12.5mg

lisinopril+hydrochlorthalidone

zestoretec 20+12.5mg

sinopril co 20+12.5mg

lisitens20+12.5mg

losartan k+hydrochlorthalidone

losartan comp50+12.5mg

losazide50+12.5mg

remtozar d 100+12.5mg

kanazar h 100+12.5mg

modazar 100+25mg

losarmephaplus50+12.5mg

fortzaar 100+25mg

hyzaar 50+12.5mg

hysartan 50+12.5mg

lora-z 50+12.5mg

irbesartan +hydrochlorthalidone

coaprovel 300mg+12.5mg

coaprovel fort 300mg+25mg

xtension 150+12.5mg

xtension plus 300+12.5mg

felodipine+metoprolol

logimax 5+50mg

minoxidil 2.5+5+10mg

loniten

minoxidil

imidazoline receptor antagonist

mechanism of action:

There are three classes of imidazoline receptors:[1] I1 receptor mediates the sympatho-inhibitory actions of imidazolines to lower blood pressure, (NISCH or IRAS, imidazoline receptor antisera selected) I2 receptor an allosteric binding site of monoamine oxidase and is involved in pain modulation and neuroprotection. I3 receptor regulates insulin secretion from pancreatic beta cells Activated I1-imidazoline receptors trigger the hydrolysis of phosphatidylcholine into DAG. Elevated DAG levels in turn trigger the synthesis of second messengers arachidonic acid and downstream eicosanoids.[2] In addition, the sodium-hydrogen antiporter is inhibited, and enzymes of catecholamine synthesis is induced. The I1-imidazoline receptor may belong to the neurocytokine receptor family, since its signaling pathways are similar to those of interleukins.[2]

moxonidine

cynt 0.2-0.3mg

relminidine

hyperium0.4-1mg

Advices to The Patients:

You can do many things to help control your blood pressure, including: Eat a heart-healthy diet, including potassium and fiber, and drink plenty of water. See: High blood pressure and diet Exercise regularly -- at least 30 minutes of aerobic exercise a day. 30

 If you smoke, quit -- find a program that will help you stop. Limit how much alcohol you drink -- one drink a day for women, two a day for men. Limit the amount of sodium (salt) you eat -- aim for less than 1,500 mg per day. Reduce stress -- try to avoid things that cause you stress. You can also try meditation or yoga. Stay at a healthy body weight -- find a weight-loss program to help you, if you need it

Possible Complications
When blood pressure is not well controlled, you are at risk for: Bleeding from the aorta, the large blood vessel that supplies blood to the abdomen, pelvis, and legs Chronic kidney disease Heart attack and heart failure Poor blood supply to the legs Stroke Problems with your vision

References:
http://www.nlm.nih.gov/medlineplus/ency/article/000468.htm http://www.medicinenet.com/high_blood_pressure/article.htm http://www.cvpharmacology.com/cardioinhibitory/beta-blockers.htm