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Figure 4 Interaction between the various parameters that control blood pressure, showing how they set up a positive feedback leading to worsening blood pressure. BP, blood pressure; CO, cardiac output; TPR, total peripheral resistance.

Figure 4 Interaction between the various parameters that control blood pressure, showing how they set up a positive feedback leading to worsening blood pressure. BP, blood pressure; CO, cardiac output; TPR, total peripheral resistance.

Early in the hypertensive process there is an increase in the thickness of the arteriolar muscle wall. This is probably a compensatory process which returns the wall tension to normal. Contrary to expectations, compliance of larger arteries is normal or increased in young hypertensive patients. However, the thickening of the resistance vessels, depending on the way it takes place, has certain consequences, and for a similar degree of muscle contraction there is a greater increase in vascular tone and thus peripheral resistance rises more, leading to a higher blood pressure, greater wall tension, and a further increase in vessel thickness. This is a positive feedback response and a vicious cycle may result (Figure 4). In the early hypertensive process the systolic and diastolic blood pressures rise more or less in parallel. However, in the older hypertensive patient the pulse pressure widens, due probably to increased stiffness of the arteries. This increased stiffness, which is associated with a loss of elastin and an increase in collagen, has important effects on the heart.

The endothelium of blood vessels is a major regulator of vascular tone and an important mechanism is the production of nitric oxide. If nitric oxide is removed, peripheral resistance rises and hypertension results. However, it is unlikely that defects in nitric oxide production are the cause of high blood pressure. In fact in early hypertension the nitric oxide production may be increased as a compensatory event modulating the rise in pressure, and this may explain why dynamic compliance is normal (Figure 5). However, when hypertension is established and there is vessel disease the nitric oxide response and endothelial control become impaired. This is probably an important factor leading to stiffness of the arteries and atherosclerosis.

► Increased vasoconstriction

Increased blood pressure

Increased shear stress ^ Vessel hypertrophy

Increased NO

Increased vascular compliance-------► Reduced compliance

Figure 5 An outline indicating how the initial response of the endothelium is to prevent the rise of blood pressure by releasing nitric oxide (NO). This increases vessel compliance, reducing the adverse effects. If this system's capacity is exceeded the arterial damage process is accelerated. The dotted lines represent negative feedback attempting to restore the status quo.

Table 2 Factors determining extent of reflection and site where the reflected wave meets the flow wave

Poor arterial compliance

Arterial branch points Peripheral resistance

Increased pulse wave velocity Reflected wave closer to heart Reflective site Increased reflection

The stiffness of blood vessels in older hypertensive patients has a number of important consequences. The pulse wave velocity is increased and thus reflected waves arrive back at the heart while the ventricle is still contracting, thereby augmenting the central systolic pressure (Table 2). In normotensive people the place at which the reflected wave and the oncoming flow meet is near the brachial artery, and thus central systolic pressure is lower than brachial artery systolic pressure (Figure 6). This increased central systolic blood pressure means that the heart contracts against a greater load and thus performs more work, leading to hypertrophy greater than might be predicted from the brachial artery pressure. The extent of the augmentation due to the pressure wave depends upon the degree of reflection, which is controlled in part by the peripheral resistance. The site at which augmentation

Figure 6 The central aortic and brachial artery pulse wave forms in normotensive (A) and hypertensive (B) subjects. In (B) the heart pumps blood out against a higher pressure leading to cardiac hypertrophy. See O'Rourke (1995) for discussion of how central aortic pressure is higher than brachial artery pressure due to reflected waves.

Figure 6 The central aortic and brachial artery pulse wave forms in normotensive (A) and hypertensive (B) subjects. In (B) the heart pumps blood out against a higher pressure leading to cardiac hypertrophy. See O'Rourke (1995) for discussion of how central aortic pressure is higher than brachial artery pressure due to reflected waves.

is highest depends on the pulse wave velocity. The deterioration in the elastic properties of the large blood vessels with loss of elastin and more collagen leads to increased pulse pressure, increased augmentation of central systolic pressure and a decrease in the peripheral diastolic pressure, all of which are common in the elderly hypertensive patient.

The Heart

In hypertensive patients the left ventricle is frequently enlarged and this is associated with an increased risk of cardiovascular death. When assessed by electro-cardiography left ventricular hypertrophy (LVH) is relatively uncommon, but if assessed by echocardio-graphy LVH is present in up to 50% of mild hypertensive patients and in adolescents not classified as hypertensive, but in the upper 10 percentile of blood pressure there is a 10-15% prevalence of LVH (Table 3). The cause of the LVH is not certain (Table 4). There is a better correlation with 24 h blood pressure than with clinic values, but the r value is about 0.14 indicating considerable variability. It is possible that acute elevations of blood pressure sustained for 1-2 h may have a potent effect by increasing wall stress and activating the processes that lead to myocyte hypertrophy. This may be of particular importance if it occurs at a time when plasma levels of potential growth factors such as angiotensin II and growth hormone are elevated. These hormones are elevated during sleep and thus blood pressure elevation at that time may be particularly detrimental. This is supported by observations that people who do not have the usual night-time (sleep) fall in blood pressure are more likely to have cardiac and renal complications. There is a significant genetic influence on cardiac hypertrophy and it has been proposed that cardiac enlargement may be antecedent to and the cause of hypertension. High blood pressure can undoubtedly cause cardiac enlargement, but independent of blood pressure elevation angio-tensin II and salt can probably enlarge the heart.

The strongest predictor in some studies of cardiac size was the salt intake. In animals a high salt intake

Table 3 Prevalence of left ventricular hypertrophy

Subjects

Prevalence (%)

Normotensive

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