The Meaning of Dopamine β-Hydroxylase in Essential Hypertension

1975 ◽  
Vol 49 (6) ◽  
pp. 573-579
Author(s):  
J. M. Alexandre ◽  
G. M. London ◽  
C. Chevillard ◽  
P. Lemaire ◽  
M. E. Safar ◽  
...  

1. Resting plasma dopamine β-hydroxylase (DBH) activity and haemodynamic parameters were studied in untreated borderline (twenty-nine) and permanent (twenty-seven) essential hypertensive patients. DBH was also measured in sixty-three apparently healthy subjects. 2. Mean DBH values were not significantly different between the groups. 3. Cardiac output, cardiopulmonary blood volume and the cardiopulmonary blood volume/total blood volume ratio (CPBV/TBV) were significantly higher in borderline than in permanent hypertensive patients. 4. In borderline hypertensive patients, plasma DBH activity was directly correlated with diastolic arterial pressure and with values of cardiac output, cardiopulmonary blood volume and CPBV/TBV ratio. No such correlations could be observed in the permanent hypertensive group. 5. These results suggest that plasma DBH activities in borderline hypertension mainly depend on the sympathetic activity responsible for the haemodynamic variations. Contrariwise, plasma DBH activities in permanent essential hypertensive patients appear to reflect other factors.

1974 ◽  
Vol 47 (2) ◽  
pp. 153-164 ◽  
Author(s):  
M. E. Safar ◽  
Y. A. Weiss ◽  
G. M. London ◽  
R. F. Frackowiak ◽  
P. L. Milliez

1. A haemodynamic study which included estimation of cardiopulmonary blood volume (CPBV), total blood volume (TBV) and vascular reactivity to noradrenaline was performed in seventeen borderline and sixteen permanent hypertensive patients. 2. Borderline hypertensive patients had higher values of cardiac index, stroke index and heart rate when compared with the permanent hypertensive patients, and lower values of blood pressure and total peripheral resistance. 3. The CPBV/TBV ratio was significantly higher in borderline hypertensive patients. In that group, this ratio was directly correlated with cardiac index, stroke index and the pressor dose of noradrenaline (P < 0.01). 4. In permanent hypertensive patients, none of these correlations was observed. Only the total blood volume was correlated directly with cardiac index and inversely with total peripheral resistance. 5. The study suggests that a redistribution of intravascular volume from peripheral veins to the cardiopulmonary capacitance bed occurs in borderline hypertension when compared with permanent hypertension and that hypertension is related to a neural mechanism in the borderline state and to a volume mechanism in the permanent state.


1961 ◽  
Vol 1 (04) ◽  
pp. 353-379
Author(s):  
Jacques Lammerant ◽  
Norman Veall ◽  
Michel De Visscher

Summary1. The technique for the measurement of cardiac output by external recording of the intracardiac flow of 131I labelled human serum albumin has been extended to provide a measure of the mean circulation time from right to left heart and hence a new approach to the estimation of the pulmonary blood volume.2. Values for the basal cardiac output in normal subjects and its variations with age are in good agreement with the previously published data of other workers.3. The pulmonary blood volume in normal man in the basal state was found to be 28.2 ± 0.6% of the total blood volume.4. There was no correlation between cardiac output and pulmonary blood volume in a series of normal subjects in the basal state.5. The increase in cardiac output during digestion was associated with a decrease in pulmonary blood volume equal to 6.3 ± 1.2% of the total blood volume, that is, about 280 ml.6. The increase in cardiac output during exercise was associated with a decrease in pulmonary blood volume equal to 4.5 ± 1.0% of the total blood volume, that is, about 200 ml.7. The increase in cardiac output attributed to alarm is not associated with a decrease in pulmonary blood volume, the latter may in fact be increased.8. The total blood volume is advocated as a standard of reference for studies of this type in normal subjects in preference to body weight or surface area.9. The significance of these results and the validity of the method are discussed.


1989 ◽  
Vol 256 (3) ◽  
pp. H760-H765 ◽  
Author(s):  
R. W. Lee ◽  
S. Goldman

To examine the mechanism by which atrial natriuretic peptide (ANP) decreases cardiac output, we studied changes in the heart, peripheral circulation, and blood flow distribution in eight dogs. ANP was given as a bolus (3.0 micrograms/kg) followed by an infusion of 0.3 microgram.kg-1.min-1. ANP did not change heart rate, total peripheral vascular resistance, and the first derivative of left ventricular pressure but decreased mean aortic pressure from 91 +/- 4 to 76 +/- 3 mmHg (P less than 0.001) and cardiac output from 153 +/- 15 to 130 +/- 9 ml.kg-1.min-1 (P less than 0.02). Right atrial pressure and left ventricular end-diastolic pressure also decreased. Mean circulatory filling pressure decreased from 7.1 +/- 0.3 to 6.0 +/- 0.3 mmHg (P less than 0.001), but venous compliance and unstressed vascular volume did not change. Resistance to venous return increased from 0.056 +/- 0.008 to 0.063 +/- 0.010 mmHg.ml-1.kg.min (P less than 0.05). Arterial compliance increased from 0.060 +/- 0.003 to 0.072 +/- 0.004 ml.mmHg-1.kg-1 (P less than 0.02). Total blood volume and central blood volume decreased from 82.2 +/- 3.1 to 76.2 +/- 4.6 and from 19.8 +/- 0.8 to 17.6 +/- 0.6 ml/kg (P less than 0.02), respectively. Blood flow increased to the kidneys. We conclude that ANP decreases cardiac output by decreasing total blood volume. This results in a lower operating pressure and volume in the venous capacitance system with no significant venodilating effects. Cardiac factors and a redistribution of flow to the splanchnic organs are not important mechanisms to explain the decrease in cardiac output with ANP.


1965 ◽  
Vol 208 (4) ◽  
pp. 790-794
Author(s):  
Shu Chien ◽  
Shunichi Usami

In sympathectomized-splenectomized dogs under pentobarbital anesthesia, the total blood volume averaged 78 ml/kg, with 20% in the splanchnic circulation and 28% in the central blood volume. These values are almost the same as those found in the splenectomized (control) dogs with the sympathetic system intact. The over-all and the splanchnic Fcells factors are also not significantly different between these two groups. The sympathectomized animals had lower arterial pressure, cardiac output, and splanchnic blood flow, but the resistances calculated for the total and the splanchnic circulations were not significantly different from those of the control dogs. The mean circulation times for the total, the central, and the splanchnic circulations were all longer in the sympathectomized dogs. The data indicate that, under pentobarbital anesthesia, sympathectomized dogs are characterized by slower blood flows without any significant changes in either the blood volume or vascular resistance.


1980 ◽  
Vol 59 (s6) ◽  
pp. 393s-395s ◽  
Author(s):  
M. P. Lynn ◽  
F. Fouad ◽  
S. A. Cook ◽  
Carmen A. Napoli ◽  
C. M. Ferrario

1. Chronic sodium depletion in dogs is associated with a blunting of the pressor response to carotid occlusion. After section of the vagus nerves this pressor response reverts to normal although atropine is without effect, suggesting a possible role for increased activity of cardiopulmonary vagal afferents in suppressing sympathetic outflow. Since increases in central blood volume stimulate vagal afferents, cardiopulmonary haemodynamics were studied by radioisotope dilution before and after 3 and 4 weeks of dietary sodium restriction together with frusemide. 2. Sodium depletion was associated with significant decreases in cardiac output, ejection fraction and total blood volume; the cardiopulmonary blood volume increased but the change was not statistically significant (P&lt;0.2). These changes were accompanied by a significant increase in the ratio cardiopulmonary blood volume/total blood volume and a decrease in the ratio cardiac output/cardiopulmonary blood volume. 3. Results indicate that sodium depletion may be accompanied by a paradoxical translocation of blood to the cardiopulmonary region in part due to depressed ventricular performance.


1997 ◽  
Vol 87 (Supplement) ◽  
pp. 588A
Author(s):  
Gotz Wietasch ◽  
Thomas Scheeren ◽  
Andreas Hoeft ◽  
Joachim O. Arndt

1986 ◽  
Vol 64 (4) ◽  
pp. 383-387 ◽  
Author(s):  
Clive V. Greenway ◽  
W. Wayne Lautt

Cardiac output is determined by heart rate, by contractility (maximum systolic elastance, Emax) and afterload, and by diastolic ventricular compliance and preload. These relationships are illustrated using the pressure–volume loop. Diastolic compliance and Emax place limits determined by the heart within which the pressure–volume loop must lie. End-diastolic and end-systolic pressures and hence the exact position of the loop within these limits are determined by the peripheral circulation. In the presence of minimal sympathetic tone, some 60% of total blood volume is hemodynamically inactive and constitutes a blood volume reserve (the unstressed volume). The remainder of the blood volume (the stressed volume) and the compliance of the venous system determine the venous pressure. This venous pressure together with venous resistance determines venous return, right atrial pressure, cardiac preload, and hence cardiac output. Venoconstriction causes conversion of unstressed volume to the stressed volume, the blood volume reserve is converted into hemodynamically active blood volume. After hemorrhage this replaces the lost stressed volume, while in other situations where total blood volume is not reduced, it allows a sustained increase in cardiac output. The major blood volume reserve is in the splanchnic bed: the liver and intestine, and in animals but not man, the spleen. A major unsolved problem is how the conversion of unstressed volume to stressed volume by venoconstriction is reflexly controlled.


1984 ◽  
Vol 67 (3) ◽  
pp. 313-319 ◽  
Author(s):  
G. M. London ◽  
M. E. Safar ◽  
J. L. Bouthier ◽  
R. M. Gitelman

1. Cardiac output, oxygen consumption, total blood volume and mean circulatory transit time were investigated at rest in men with sustained essential hypertension in comparison with normal subjects of the same age and sex. 2. In normal subjects and in patients with hypertension, oxygen consumption was positively correlated to cardiac output. In hypertensives, the slope of the curve was significantly shallower with an increase in arteriovenous oxygen difference. 3. Oxygen consumption in both populations was negatively correlated with mean circulatory transit time but not with total blood volume. 4. In normal subjects, mean circulatory transit time and arteriovenous oxygen difference were positively correlated. The correlation was not significant in hypertensive patients. 5. The study suggests important abnormalities in the transport and cost of energy in erythrocytes of patients with sustained essential hypertension.


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