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Physiology and Pharmacological Treatment of Hypertension

Introduction:

Hypertension refers to arterial blood pressure of above 120/80 mmHg took in the relaxed sitting position, 120 mmHg being the systolic pressure and 80 mmHg the diastolic pressure. Normal systolic blood pressure range is 90-119 mmHg while normal diastolic pressure range is 60-79 mmHg. Elevated systolic blood pressure is associated with coronary artery disease and stroke whereas elevated diastolic pressure is more emphasized in assessing high blood pressure. Hypertension can be classified as primary and secondary hypertension. Primary hypertension is also referred to as essential hypertension and occurs when the cause is unknown. Essential hypertension is the most common and occurs in about 90-95% of patients. Secondary hypertension occurs as a result of other conditions such as renal and endocrine disorders. Secondary hypertension occurs in about 10-15% of patients. Further classification is according to the following factors; type of blood pressure elevation- systolic hypertension, diastolic hypertension, or mixed. It can also be classified according to the severity of the condition- mild hypertension, moderate hypertension, and severe hypertension. According to etiology, there is renal, adrenal and cardiovascular hypertension. Hypertension is a chronic condition that requires active management to maintain the patient’s blood pressure within normal range.

Physiology of hypertension:

Hypertension results from changes in cardiac output and systemic vascular resistance. Factors that affect cardiac output include renal failure. Arteriosclerosis increases systemic vascular resistance thus increases the blood pressure. Primary causes of hypertension include damage to arteries and reduction of arterial luminal diameter. Damage to arteries increases vascular resistance therefore straining the heart and the kidney. Reduced luminal diameter increases peripheral vascular resistance. Renal failure causes reduced blood flow in the renal arteries thus causing ischemia in the kidneys. As a result, kidney produces more renin that increases systemic vascular resistance and blood pressure. Neurological mechanisms such as defective baroreceptor autoregulation also play a role in causing hypertension (Mancia, Grassi, Giannattasio, & Seravalle, 1999). Defective baroreceptor activation leads to activation of the sympathetic nervous system therefore initiating essential hypertension.

According to Sarkis and Roman (2004), systemic factors such as inappropriate activation of renin-angiotensin-aldosterone system (RAAS) plays a key role in causing hypertension. Inadequate renal blood flow stimulates production of renin. Factors that lead to decreased renal blood flow include obstruction of renal arteries and excessive hemorrhage. Renin flows in the blood stream and stimulates the production of angiotensin in the tissues and in the blood. As the angiotensin produced flows through the blood stream, it gets to the adrenal cortex and stimulates production of aldosterone. Aldosterone facilitates reabsorption of sodium ions thus increasing the reabsorption of water (Weber, 2000). As a result, blood volume increases therefore increasing the blood pressure.

Nitric oxide is produced by the endothelium for the purpose of vasodilation. When the endothelium is injured, release of nitric oxide is impaired resulting in decreasing vasodilation (Hermann, Flammer, Luscher, 2006). Inadequate vasodilation causes increased intravascular resistance and hence hypertension.

 

Treatment of hypertension:

Hypertension mainly results from increased cardiac output as a result of elevated blood volume and increased vascular resistance. Therefore, treatment for hypertension mainly comprises diuretics, beta-blockers, calcium-channel blockers, and vasodilators.

Diuretics are classified based on their primary site of action. Diuretics act on the nephron that is proximal convoluted tubule, loop of Henle, distal convoluted tubule and collecting duct. Classes of diuretics include carbonic anhydrase inhibitors, thiazide diuretics, loop diuretics, potassium-sparing diuretics and sodium channel blockers. Diuretics increase excretion of excess water through the kidney thus reducing the blood volume. Diuretics also have natriuretic effect thus decreasing sodium levels in the body.

Thiazide diuretics are most common antihypertensive medication used. Examples of thiazide diuretics include hydrochlorothiazide and Chlorthalidone. Thiazide diuretics are used as the first line treatment of hypertension. According to Kaplan (2000), thiazide diuretics have maximum effects when administered in small doses. Thiazide diuretics are usually combined with other antihypertensive medications, most commonly beta-blockers. Thiazides inhibit Na+/Cl- transporter in the distal convoluted tubule. Loop diuretics have a slightly higher efficacy than thiazide diuretics. The primary site of action of loop diuretics is the thick ascending loop of Henle. Thiazide diuretics can result in adverse effects such as dizziness, headache, weakness and itching. In the cause of treatment, the patient may complain of stomach upset and increased sensitivity to sunlight. Hypo kalemia and hypo magnesium also tend to occur during treatment with thiazide diuretics.

Potassium-sparing diuretics include Amiloride, Eplerenone, Spironolactone, and Triamterene. Potassium-sparing diuretics are weak antihypertensive and, therefore, are rarely used alone. Potassium-sparing diuretics primary site of action is on the distal part of the distal convoluted tubule. Potassium-sparing diuretics also act in the collecting tubules. The mechanism of action of potassium-sparing diuretics involves inhibiting sodium/potassium exchange. The side effects of potassium-sparing diuretics include electrolyte imbalance, increased frequency of urination and muscle cramps. Like any other diuretic, the more common side effects are fatigue, dizziness, and dehydration. Potassium-sparing diuretics can also cause blurred vision, skin rash, headache, nausea, and vomiting. Rarely can the patient taking potassium-sparing diuretics experience irregular menstrual cycles, decreased growth of hair and breast tenderness in both men and women.

Beta blockers include Labetalol, metoprolol, carvedilol, atenolol and many others. Beta blockers are most commonly used first-line therapy of hypertension (Lindholm, Carlberg, & Samuelsson, 2005; Bradley, Wiysonge, Volmink, Mayosi, & Opie, 2006). Beta blockers inhibit the action of the sympathetic nervous system. Beta 1 receptors are found in the heart and kidneys while beta 2 receptors are found the lungs and peripheral vessels. Beta 1 blockers inhibit the release of renin thus increasing loss of sodium from the renal tubules. As a result, cardiac output is decreased thus controlling the blood pressure. The likely adverse effects of beta blockers include dizziness, bradycardia, edema, and difficulty in breathing. Cold hands and feet may also develop.

Vasodilators include hydralazine and minoxidil. Vasodilators are second-line therapy in treatment of hypertension and are therefore used to treat persistent hypertension. Vasodilators act by dilating blood vessels. Vasodilation occurs when the action of the medication opens adenosine triphosphate-sensitive potassium channels in the vascular endothelium. Vasodilators are more preferred because they do not cause hypotension by dilating the veins. When the vessels are dilated, systemic and peripheral vascular resistance decreases and hence lowers the blood pressure. When vasodilators are administered alone, they tend to cause fluid overload and tachycardia. Vasodilators should, therefore, be administered in combination to increase the efficacy in the treatment of hypertension.

Carbonic anhydrase inhibitors include acetazolamide, chlorphenamide and methazolamide. Carbonic anhydrase inhibitors act by inhibiting carbonic anhydrase enzyme in the renal tubules. The drug primarily acts in the proximal convoluted tubules. Mechanism of action of carbonic anhydrase inhibitors involves inhibiting reabsorption of bicarbonates back into the blood stream. As a result, the bicarbonate in the tubular lumen inhibits reabsorption of sodium ions. More water is thus secreted leading to decreased blood volume and hence decreases blood pressure. Carbonic anhydrase inhibitors have minimal action in controlling blood pressure. Toxic effects due to carbonic anhydrase inhibitors include electrolyte imbalance, formation of renal stones and hypersensitivity reactions due to sulfonamide compounds in the medication.

Angiotensin Converting Enzyme (ACE) inhibitors include enalapril, lisinopril, and many others. Angiotensin enzyme converts angiotensin I to angiotensin II. ACE inhibitors block the action of angiotensin enzyme. Angiotensin II dilates the efferent arteriole of the kidneys thus decreasing glomerular pressure. ACE inhibitors are more commonly used in patients with cardiac failure. Side effects if ACE inhibitors are angioedema and hyperkalemia. ACE inhibitors should not be given to pregnant mothers as it causes congenital malformations of the cardiovascular system and central nervous system (Cooper, Hernandez-Diaz, Arbogast, Dudley, Dyer, Gideon, Hall, Ray, & Arbogast, 2006). Potential side effects of ACE inhibitors include cough, drowsiness, abnormal metallic taste, hyperkalemia and sexual dysfunction. Diarrhea and hypotension may also occur.

Calcium channel blockers are more preferred in treating hypertensive patients with comorbid angina. Some of the examples of calcium channel blockers include amlodipine, nifedipine, and verapamil. Calcium channel blockers inhibit calcium influx into the smooth muscles of the blood vessels thus leading to vasodilation. Epstein, Vogel, & Palmer (2007) found out that calcium channel blockers are safer to use in patients who are at higher risk of getting stroke. Verapamil and diltiazem are more suitable for hypertensive patients with co-existing arrhythmias. Side effects of calcium channel blockers include headache, swelling of ankles and bradycardia. Verapamil causes constipation in patients.

Conclusion:

In conclusion, hypertension is not a disease but a symptom of other conditions. Hypertension results from the defect of arterial blood vessels and also increase in the blood volume. Diseases affecting other systems such as renal system, endocrine system, and neurological system also lead to the occurrence of hypertension. Different types of medication can be used in the management of hypertension. These include diuretics, calcium channel blockers, beta-blockers, ACE inhibitors, and vasodilators. These medications can be used singly or in combination. Many combination therapies have been developed to increase efficacy of the drugs. Despite the positive effects of the medication in the management of hypertension, the drugs have many adverse effects on the patients. Health care workers should, therefore, be very careful while administering the antihypertensive medication to ensure maximum efficacy of the medication and safety of the patient is maintained.

References

Bradley, H. A., Wiysonge, C. S., Volmink, J. A., Mayosi, B. M., & Opie, L. H. (2006). How strong is the evidence for use of beta-blockers as first-line therapy for hypertension? Systematic review and meta-analysis. Journal of Hypertension, 24, 2131-2141.

Cooper, W. O., Hernandez-Diaz, S., Arbogast, P. G., Dudley, J. A., Dyer, S., Gideon, P. S., Hall, K., & Ray, W. A,. & Arbogast, P. G. (2006). Major congenital malformations after first-trimester exposure to ACE inhibitors. The New England Journal of Medicine, 354 (23), 2443–51

Epstein, B., Vogel, K., & Palmer, B. (2007). Dihydropyridine Calcium Channel Antagonist in Management of Hypertension. Drugs Textbook, 67(9), 1309-1327.

Hermann, M., Flammer, A., & Luscher, T. F. (2006). Nitric oxide in hypertension. Journal of Clinical Hypertension, 8, 17–29

Kaplan, N. M. (2000). Diuretics as a basis for antihypertensive therapy: an overview. Drugs Textbook, 59, 21–5.

Lindholm, L. H., Carlberg, B., & Samuelsson, O. (2005). Should beta blockers remain the first choice in the treatment of primary hypertension? A meta-analysis. Lancet Research Report, 366, 1545-1553.

Mancia, G., Grassi, G., Giannattasio, C., & Seravalle, G. (1999). Sympathetic activation in the pathogenesis of hypertension and progression of organ damage. Journal of Hypertension. 34, 724–728.

Sarkis, A., & Roman, R. J. (2004). Role of cytochrome P450 metabolites of arachidonic acid in hypertension. Current Drug Metabolism, 5, 245–256.

Weber, K. T. (2000). Heart-hitting tales of salt and destruction. Journal of Laboratory and Clinical Medicine, 136, 7–13.

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