Hypertension (HTN) is the most common condition man¬aged in primary care and a major risk factor for cardio-vascular disease. Numerous randomized controlled trials have demonstrated that the use of antihypertensives to manage blood pressure (BP) helps reduce cardiovascular disease risk. Prevalence of HTN increases with age so that around 33% of men and 25% of women aged 45– 54 years have a clinical diagnosis. It is generally defined as a raised blood pressure exceeding 140/ 90 mmHg, divided into two types: ● Essential (or primary) hypertension: accounts for 95% of cases and is where no secondary cause is identified. ● Secondary hypertension: the result of an underlying disease (e.g. renal, pulmonary, endocrine, or drug/ toxin). Pre- HTN is defined as systolic BP (SBP) 120– 139 mmHg and diastolic BP (DBP) 80– 89 mmHg. BP is the product of cardiac output (heart stroke volume and heart rate) and the total peripheral resistance of vessels supplied by the heart. Thus, three main systems are responsible for generating BP: the heart (pumping pressure), vessel tone (being the systemic resistance), and the kidney (regulating intravascular volume). Three main physiological systems regulate heart, vessels, and kidney with respect to blood pressure: 1. The sympathetic nervous system: changes in BP are sensed by a feedback mechanism mediated by baroreceptors in the walls of the aortic arch and carotid sinuses. Increasing BP causes firing of glossopharyngeal and vagus nerves, inhibiting sympathetic outflow via the medulla (tractus solitarius). This, in turn, leads to parasympathetic dominance and a reduction in peripheral resistance (vasodilation through β1- adrenoceptors) and cardiac output (by reduced heart rate and reduced contractility through α1- adrenoceptors). Centrally acting antihypertensive drugs act at the nucleus tractus solitarius (e.g. clonidine/ methyldopa) or ventrolateral medulla (e.g. moxonidine). 2. The renin- angiotensin- aldosterone system: this system regulates blood volume and systemic vascular resistance, thus influencing cardiac output and arterial pressure. This feedback mechanism starts in the kidney with the release of renin into the peripheral circulation. Renin release, from juxtaglomerular cells (JC), is stimulated by sympathetic mechanisms (involving α1- receptors on JC themselves), decreased afferent arteriole pressure (from systemic hypotension or renal artery stenosis) or declining Na<sup>+</sup> levels in the distal tubules of the kidney. Prostaglandins, such as PGE2 and PGI2 (prostacyclin), also cause release of renin secondary to reduced NaCl transport in the macular densa (see Topic 5.2 ‘Acute kidney injury’).
Evaluation of exercise hypertension in healthy young adults: an observational study