1. Central and peripheral haemodynamics, circulating blood volume and plasma renin activity (PRA) were investigated under resting conditions in 97 patients with chronic nonuraemic renal parenchymatous disease and without anaemia. For comparison a group of 17 healthy subjects was used. 2. An initial abnormality appeared in 12 out of 32 normotensive renal patients. It consisted of a markedly increased circulating blood volume, raised cardiac output, low total peripheral and forearm vascular resistance, hyperfusion of the forearm and increased venous distensibility. PRA was slightly (but insignificantly) higher in these hyperkinetic subjects with relaxed peripheral vessels than in the other 20 normotensive renal patients who did not differ haemodynamically from the control subjects. 3. Fifteen out of 47 renal patients with a mild or moderate hypertension (stage I–II WHO) were hyperkinetic. However, in these there was no compensatory vasodilatation in response to the high cardiac output: forearm blood flow was normal and venous distensibility below that of the control subjects. Blood volume was normal. Plasma renin activity (PRA) was the same as in the normotensive renal patients. 4. The difference between stage I–II and stage III was due entirely to a rise in total peripheral vascular resistance. 5. A re-examination of these patients 2-8 years after they had been first studied revealed that 11 out of the 12 originally hyperkinetic normotensive renal patients were now hypertensive compared with only one-half of the originally normokinetic normotensive renal subjects. 6. It is concluded that an inability of the diseased kidney to control volume homoeostasis leads to hypervolaemia, which raises cardiac output in the renal patients whilst still normotensive. As long as the arterioles adjust to the high output and the capacitance system to the high volume, blood pressure remains normal. When this adaptation of the periphery ceases, blood pressure rises, normalizing (possibly through a pressure diuresis) blood volume. PRA does not correlate with any of these changes and only in advanced renal hypertension may its rise partly contribute to the maintenance of high blood pressure without being its cause.
The aim of this randomized study was to compare the reliability of the treadmill test at constant-load (C-test, 3 km/hr; fixed grade of 12%) recommended in Germany with that of the graded-exercise test (G-test, 3 km/hr; increase in grade of 3.5% every 3 minutes) propagated in the United States. In 50 patients with an absolute claudication distance (ACD) in the C-test of between 50 and 400 m, the two treadmill tests were carried out in randomized order on one and the same day, and repeated on 3 days within 1 week. For the initial claudication distance (ICD), the intraclass correlation was 0.88 in the C-test and 0.87 in the G-test. For the ACD the coefficients were identical at 0.91. The within-subject variation (CVwithin) in the C-test and G-test was 25% and 27% for the ICD and for the ACD 24% and 21%, respectively. The between-subject variation was very similar with 72% and 73% (ICD) and with 78% and 68% (ACD). However, in ACDs below 100 m and between 100 to 150 m, the C-test showed significantly smaller coefficients of variation than the G-test: 13% vs 81% and 14% vs 50%, respectively. In conclusion, the results showed that both C-test and G-test are equally well reproducible.
1 The effect of an intravenous bolus of labetalol (0.6-1.6 mg/kg body weight) on central and peripheral haemodynamics was studied in nine subjects with essential hypertension and in eleven subjects with chronic renal disease and hypertension. 2 The BP reduction amounting to 20/13 mmHg was entirely due to the lowering of the total peripheral vascular resistance. This also included the vascular resistance in the muscles. 3 This peripheral vasodilatation was not counteracted by a reflex increase of the cardiac output. 4 The reflex tachycardia and overshoot of BP in Valsalva's manoeuvre were largely abolished. 5 Central and peripheral venous BPs, vascular volume of the forearm and venous distensibility did not show any significant change after treatment with labetalol. 6 In spite of the lowering of the vascular resistance of the forearm by labetalol, forearm blood flow was not significantly affected due to the parallel decrease in the perfusion pressure. 7 Plasma renin activity fell after labetalol in all instances.
Detailed hemodynamic studies were carried out in 99 subjects with chronic nonuremic renal disease and 17 healthy subjects. The earliest hemodynamic abnormality found in normotensive renal patients was a raised circulating blood volume and an increased cardiac output. The blood pressure remained normal as long as the peripheral vascular bed (arteriolar and venous) adjusted to these conditions. When this adjustment ceased, hypertension developed and the blood volume normalized. It is suggested that a disturbed volume-homeostatic function of the kidney, leading to a rise of the circulating blood volume, is the proper starter of hemodynamic events leading eventually to hypertension in chronic parenchymatous renal disease.
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