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Figure 11 1 The 2005 Canadian Hypertension Education Program recommendations for the assessment and diagnosis of hypertension Patients with an elevated blood pressure measured during visits 4 5 may still have white-coat (office-induced) hypertension (Applying the 2005 Canadian Hypertension Education Program recommendations: 1 Diagnosis of hypertension Reprinted, with permission from CMAJ 30-Aug-05; 173(5), Page(s) 480 483 2005 CMA Media Inc)

1 Sympathetic nervous system hyperactivity This is most apparent in younger persons with hypertension, who may exhibit tachycardia and an elevated cardiac output However, correlations between plasma catecholamines and blood pressure are poor Insensitivity of the baroreflexes may play a role in the genesis of adrenergic hyperactivity 2 Abnormal cardiovascular or renal development The normal cardiovascular system develops so that elasticity of the great arteries is matched to the resistance in the periphery to optimize large vessel pressure waves In this way, myocardial oxygen consumption is minimized and coronary flow maximized Elevated blood pressure

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later in life could arise from abnormal development of aortic elasticity or reduced development of the microvascular network This has been postulated as the sequence of events in low birth weight infants, who have an increased risk of hypertension developing in adulthood Another hypothesis proposes that the association between low birth weight and hypertension arises from reduced nephron number 3 Renin angiotensin system activity Renin, a proteolytic enzyme, is secreted by cells surrounding glomerular afferent arterioles in response to a number of stimuli, including reduced renal perfusion pressure, diminished intravascular volume, circulating catecholamines, increased sympathetic

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nervous system activity, increased arteriolar stretch, and hypokalemia Plasma renin levels are classified in relation to dietary sodium intake or urinary sodium excretion Renin acts on angiotensinogen to cleave off the ten-amino-acid peptide angiotensin I This peptide is then acted upon by angiotensinconverting enzyme (ACE) to create the eight-amino-acid peptide angiotensin II, a potent vasoconstrictor and a major stimulant of aldosterone release from the adrenal glands The incidence of hypertension and its complications may be increased in individuals with the DD genotype of the allele coding for ACE Despite the role of this system in the regulation of blood pressure, it probably does not play a central role in the pathogenesis of most primary (essential) hypertension; although approximately 10% of patients have high levels, 60% have normal levels, and 30% have low levels Black persons with hypertension and older patients tend to have lower plasma renin activity, which may be associated with expanded intravascular volume 4 Defect in natriuresis Normal individuals increase their renal sodium excretion in response to elevations in arterial pressure In hypertensive patients, this pressurenatriuresis relationship is reset so that maintenance of sodium homeostasis requires increased extracellular fluid volume and higher arterial pressure 5 Intracellular sodium and calcium Intracellular Na+ is elevated in blood cells and other tissues in primary (essential) hypertension This may result from abnormalities in Na+ K+ exchange and other Na+ transport mechanisms An increase in intracellular Na+ may lead to increased intracellular Ca2+ concentration as a result of facilitated exchange and might explain the increase in vascular smooth muscle tone that is characteristic of established hypertension 6 Exacerbating factors A number of conditions elevate blood pressure, especially in predisposed individuals Obesity is associated with an increase in intravascular volume, elevated cardiac output, activation of the renin-angiotensin system and, probably, increased sympathetic outflow Weight reduction lowers blood pressure modestly The relationship between sodium intake and hypertension remains controversial, and some not all persons with hypertension respond to high salt intake with substantial increases in blood pressure Patients with high normal or elevated blood pressures should consume no more than 100 mmol/d of salt (24 g of sodium, 6 g of sodium chloride daily) Excessive use of alcohol also raises blood pressure, perhaps by increasing plasma catecholamines Hypertension can be difficult to control in patients who consume more than 40 g of ethanol (two drinks) daily or drink in binges Cigarette smoking raises blood pressure, again by increasing plasma norepinephrine Although the long-term effect of smoking on blood pressure is less clear, the synergistic effects of smoking and high blood pressure on cardiovascular risk are well documented The relationship of exercise to hypertension is variable Aerobic exercise lowers blood pressure in previously sedentary individuals, but increasingly strenuous exercise in already active subjects has less effect The relationship between stress and hypertension is not established Polycythemia, whether primary or due to.

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