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The relationships among blood pressure (BP), blood viscosity and echocardiographic left ventricular (LV) muscle mass were evaluated in 24 patients with essential hypertension and in 13 normotensive control subjects. LV mass was greater in the hypertensive patients than in the control subjects (225 +/- 69 vs 170 +/- 31 g, p less than 0.02) as was blood viscosity at a shear rate of 104 sec-1 (4.7 +/- 0.1 vs 4.3 +/- 0.2 cp, p less than 0.005). Among the hypertensive patients, LV mass was most closely related to viscosity at 104 sec-1 (r = 0.80, p less than 0.001), whereas only weak correlations were found between LV mass and systolic or diastolic BP (r = 0.45, p less than 0.05 for both). The 14 hypertensive patients with normal LV mass had viscosity similar to that in control subjects (4.5 +/- 0.3 vs 4.3 +/- 0.2 cp), whereas viscosity was consistently increased (5.0 +/- 0.4 cp, p less than 0.02) in hypertensive patients with LV hypertrophy. Thus, increased blood viscosity may be a determinant of or a response to hypertensive cardiac hypertrophy.

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In patients with borderline hypertension, total peripheral resistance (TPR) is either elevated or abnormally related to cardiac output. Since blood viscosity is one determinant of TPR, we compared various components of blood viscosity in 25 patients with borderline hypertension and 25 normal subjects. Under all experimental blood flow conditions examined, blood viscosity directly correlated with systolic and diastolic blood pressure (p less than 0.05 or better) and was greater in the hypertensive than in normal subjects. Venous hematocrit and plasma viscosity were higher in the hypertensive patients. These latter rheologic abnormalities accounted for the increased blood viscosity at higher shear rates. At lower shear rates, increased red cell aggregation, primarily mediated by elevated fibrinogen concentration, accounted for the higher blood viscosity in the hypertensive subjects. We conclude that even relatively small elevations in arterial pressure are associated with increased viscous resistance of blood to flow, and that the increased blood viscosity is a consequence of increased hematocrit, plasma viscosity, and red cell aggregation.

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To assess the immediate and long-term effects of exercise on factors regulating blood flow, we measured plasma viscosity (eta p) and plasma renin activity (PRA) in 17 trained runners and 16 sedentary healthy subjects before and 10 min after graded treadmill exercise. Resting eta p was lower in runners primarily because of significantly lower fibrinogen concentration. Compared to nonrunners with similar 24-h urine electrolyte excretion rates, runners were characterized by lower PRA at rest. In view of the overall correlation between heart rate and PRA before exercise, reduced adrenergic tone was probably a major factor contributing to the lower PRA in runners. After exercise, plasma viscosity and PRA exceeded control levels, and were similar in magnitude in runners and sedentary subjects. Changes in plasma viscosity were less than expected from the degree of hemoconcentration, primarily because enhanced fibrinolysis maintained fibrinogen level constant. To the extent that plasma viscosity affects viscous flow resistance, the results suggest that tissue perfusion and oxygen delivery rate at rest are greater in trained runners than in sedentary subjects, but these variables become similar after maximum exertion.

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Blood pressure and components of blood viscosity were measured in 49 normal subjects and in 49 untreated patients with essential hypertension. Blood viscosity values measured at six different shear rates were significantly correlated with blood pressure (r = 0.432 to 0.505, p less than 0.001). Blood viscosity was higher in hypertensive patients. This was due to both higher plasma viscosity (1.29 +/- 0.08 standard deviation versus 1.24 +/- 0.05 centipoise (cPs), p less than 0.001) and increased hematocrit values (44.4 +/- 4 percent versus 41.5 +/- 3 percent, p less than 0.005). When blood viscosity was evaluated in subgroups of normal and hypertensive subjects with matched hematocrit values, it remained higher in the hypertensive patients, and the relationship between blood pressure and viscosity was still significant. Regardless of the hematocrit value, fibrinogen levels were elevated in hypertensive patients (p less than 0.006) and, in association with the increased globulin concentration, fibrinogen was largely responsible for the increased plasma viscosity in hypertensive patients. Since the viscosity of defibrinated blood was similar in normal and hypertensive subjects with matched hematocrit values, the elevated fibrinogen level also affected whole blood viscosity. Defibrinated blood viscosity and arterial pressures were not correlated. These studies demonstrate a direct correlation between blood pressure and blood viscosity among normotensive and hypertensive subjects. This relationship is, in part, due to the rheologic effects of an elevated fibrinogen level and to an increased hematocrit value. The basis for hyperfibrinogenemia in hypertensive patients is unclear.

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Recent research shows that the renin-angiotensin-aldosterone axis either maintains or causes some or all of the high blood pressure of most patients and demonstrates anew that renin-sodium profiling defines this involvement. Performed with a serum potassium measurement, this now reliable test is useful for primary screening and then, in conjunction with renal vein renin studies or an aldosterone profile, for diagnosis or exclusion of surgically curable renovascular or adrenocortical hypertensions. For the remaining majority with essential hypertension, renin profiling exposes the relative participation of either vasoconstriction or volume factors, thereby guiding simpler, more specific, and predictably effective antirenin or antivolume treatments. Renin profiling identifies those in whom treatment should begin with a beta-blocker as opposed to a diuretic while not infrequently also providing baseline information about severity and prognosis in individual patients.

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