Page 261 - Concise Pathology for Exam Preparation ( PDFDrive )

246 SECTION II Diseases of Organ Systems

Essential (Primary) Hypertension
• Genetic and environmental factors are both thought to play a role in its development.
• Genetic factors: Familial clustering and prevalence in twins has been observed,
indicating a role of genetic factors.
• Racial and environmental factors: Essential hypertension has been found to be more
prevalent amongst blacks than in whites. Environmental factors like high salt intake,
obesity, occupation (skilled population is more affected than unskilled), higher living
standards and high levels of stress are also implicated.
• There are some risk factors which modify the course of essential hypertension. These
include:
• Age: Younger the age at which hypertension is seen, lower the life expectancy,
particularly if it is left untreated.
• Sex: Females with hypertension appear to do better than males.
• Atherosclerosis: Hypertension increases the incidence of atherosclerosis-related
complications.
• Other risk factors include excess of alcohol intake and diabetes mellitus.
Secondary Hypertension
Secondary hypertension can result from conditions affecting different organs:
• Renal causes: Acute glomerulonephritis, chronic renal failure, polycystic disease,
pyelonephritis, interstitial nephritis, amyloidosis, diabetic nephropathy and renin-
producing tumours.
• Endocrine causes: Cushing syndrome, hyperaldosteronism, oral contraceptives, oes-
trogens, pregnancy induced, pheochromocytoma, acromegaly, primary hypothyroidism,
thyrotoxicosis and hyperparathyroidism
• Cardiovascular causes: Coarctation of aorta (causes systolic hypertension in the upper
part of the body) and polyarteritis nodosa
• Neurological causes: Acute stress, increased intracranial pressure and psychogenic
• Miscellaneous causes: Alcohol, obesity and pregnancy (preeclampsia)

Renal Regulation of Blood Pressure
The kidneys and heart interact to regulate the vascular tone and blood volume by altering
sodium balance. The various regulatory mechanisms involved are the following:
1. Activation of renin–angiotensin system: Renin is an enzyme that is produced by renal
juxtaglomerular cells that are present in the proximity of afferent glomerular arterioles.
It is released in response to decreased blood pressure in the afferent arterioles, increased
levels of circulating catecholamines or low sodium levels. Renin cleaves angiotensino-
gen to angiotensin I, which undergoes peripheral catabolism to produce angiotensin II.
Angiotensin II regulates blood pressure by:
• Increasing vascular smooth muscle tone
• Stimulating secretion of aldosterone
• Regulating renal sodium and water resorption (reduction in GFR due to reduced
blood flow results in increase in proximal tubular reabsorption of sodium)
2. Release of vasodepressor material: A number of vasodepressor materials and antihy-
pertensives, eg, prostaglandins and nitrous oxide counter balance the vasopressor effect
of angiotensin II.
3. Natriuretic factors: Atrial and ventricular myocardium secretes natriuretic peptides
which inhibit the renin–angiotensin system thereby causing sodium excretion, diuresis
and vasodilatation. Increased stretching of atria and ventricles of the heart due to in-
creased BP induces release of natriuretic factors.

Role of Cardiac Output and Peripheral Resistance in Regulation
of Blood Pressure

Role of cardiac output and peripheral resistance in regulation of blood pressure is depicted
in Flowchart 10.5.

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