Elevated total body noradrenaline spillover in normotensive members of hypertensive families

1993 ◽  
Vol 84 (2) ◽  
pp. 225-230 ◽  
Author(s):  
Claudia Ferrier ◽  
Helen Cox ◽  
Murray Esler
Keyword(s):  
Essential Hypertension ◽  
Family History ◽  
Positive Family History ◽  
Sympathetic Nervous System Activity ◽  
Nervous System Activity ◽  
History Of ◽  
Normotensive Subjects ◽  
Sympathetic Nervous ◽  
Arterial Plasma ◽  
Total Body

1. In prehypertension, abnormalities in cardiovascular control mechanisms have been described. It has been postulated that this may involve hereditary disturbances in the sympathetic regulation of blood pressure. Since the neurochemical methods used to test sympathetic nervous system activity have been rather imprecise, in the present study we have applied noradrenaline plasma kinetic methodology to evaluate sympathetic activity in normotensive subjects with a familial predisposition to essential hypertension. 2. Total body noradrenaline spillover to plasma, an index of integrated sympathetic nerve firing rates, was calculated during infusion of l-[7-3H] noradrenaline in 11 normotensive offspring of essential hypertensive parents and 11 age-, height- and weight-matched normotensive offspring of normotensive parents. 3. The resting arterial plasma noradrenaline concentration was higher in healthy subjects with a family history of essential hypertension (1.41 ± 0.15 nmol/l, mean ± SEM, P < 0.002) than in normotensive subjects with no family history of essential hypertension (0.82 ± 0.07 nmol/l). The overall rate of spillover of noradrenaline to plasma was also elevated in the normotensive offspring of hypertensive parents (4.34 ± 0.54 nmol/min) compared with subjects with a negative family history of essential hypertension (2.02 ± 0.20 nmol/min). Similarly, the arterial plasma concentration of the noradrenaline precursor 3,4-dihydroxyphenylalanine was higher in subjects with a positive family history of essential hypertension (7.55 ± 0.24 nmol/l) than in normotensive control subjects (5.97 ± 0.30 nmol/l, P < 0.001). Despite this apparent evidence of relative sympathetic nervous activation in the subjects with a positive family history of hypertension, their blood pressure and heart rate were only marginally, and non-significantly, higher. 4. Biochemical indices of sympathetic function in normotensive offspring of hypertensive parents suggest a familial disturbance in sympathetic nervous system activity, which may be a predictor for the development of hypertension in adult life.

Kinetics of Ca2(+)-ATPase activation in platelet membranes of essential hypertensives and normotensives

1990 ◽  
Vol 258 (6) ◽  
pp. C988-C994 ◽  
Author(s):  
J. Takaya ◽  
N. Lasker ◽  
R. Bamforth ◽  
M. Gutkin ◽  
L. H. Byrd ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Family History ◽  
Positive Family History ◽  
Plasma Renin ◽  
Initial Reaction ◽  
Activation Kinetics ◽  
Negative Family History ◽  
History Of ◽  
Blacks And Whites ◽  
Kinetics Of

To explore the etiology of altered Ca metabolism in essential hypertension, we studied parameters, i.e., maximal initial reaction velocity (Vmax) and Michaelis constant (Km), of Ca activation kinetics of Ca2(+)-ATPase in membrane fractions (isolated by a sucrose gradient) from platelets of blacks and whites, 27 of whom were essential hypertensives, 17 of whom were normotensives with a family history of essential hypertension, and 10 of whom were normotensives without a family history of the disease. The Vmax of hypertensives was significantly lower than in normotensives without a family history of essential hypertension (hypertensives, 14.99 +/- 1.71 nmol Pi.mg protein-1.min-1; normotensives, positive family history, 22.67 +/- 3.17 nmol Pi.mg protein-1.min-1; normotensives, negative family history, 27.54 +/- 4.37 nmol Pi.mg protein-1.min-1; overall, P = 0.0078). The Km was lower in both hypertensives and normotensives with a positive family history of essential hypertension as compared with normotensives with a negative family history of the disease (hypertensives, 1.70 +/- 0.23 microM; normotensives, positive family history, 1.38 +/- 0.2 microM; normotensives, negative family history, 2.79 +/- 0.58 microM; overall, P = 0.0251). Furthermore, the Km in whites was inversely related to plasma renin activity (r = 0.50; P less than 0.005). We propose that a lower Vmax for Ca2(+)-ATPase may play a role in the higher level of free Ca in platelets of essential hypertensives and that a higher affinity of the enzyme to Ca may reflect a process compensating for the lower Vmax. We also suggest that a higher Km for Ca2(+)-ATPase in juxtaglomerular cells of whites would result in blunting the release of renin.

Intracellular Na+ and Ca2+ Activities in Essential Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 41s-43s ◽  
Author(s):  
W. Zidek ◽  
H. Vetter ◽  
K.-G. Dorst ◽  
H. Zumkley ◽  
H. Losse
Keyword(s):  
Essential Hypertension ◽  
Family History ◽  
Secondary Hypertension ◽  
Genetic Trait ◽  
Hypertensive Patients ◽  
Intracellular Na Activity ◽  
History Of ◽  
Family History Of Hypertension ◽  
Normotensive Subjects

1. The intracellular Na+ and Ca2+ activity and Na+ concentration were measured in erythrocytes of normotensive subjects, with and without a familial disposition to hypertension, in essential hypertensive patients with and without a family history of hypertension, and in patients with secondary hypertension. 2. In normotensive subjects without a genetic trait of hypertension intracellular Na+ activity and concentration were 7.00 ± 1.38 mmol/l and 5.67 ± 0.95 mmol/l respectively. The intracellular Ca2+ activity was 4.82 ± 4.49 μmol/l. In normotensive subjects with a familial hypertensive disposition intracellular Na+ activity and concentration were 9.74 ± 1.43 mmol/l (P < 0.01) and 6.63 ± 0.88 mmol/l (P < 0.05). Intracellular Ca2+ was 9.59 ± 9.71 μmol/l (P < 0.05). 3. Essential hypertensive patients without a familial genetic trait had an elevated intracellular Na+ activity (8.35 ± 2.08 mmol/l, P < 0.05). Intracellular Na+ concentration was 6.64 ± 0.79 mmol/l (P < 0.05). The intracellular Ca2+ activity was markedly elevated to 25.33 ± 19.03 μmol/l (P < 0.01). The essential hypertensive patients with a familial disposition had an elevated intracellular Na+ activity (17.19 ± 4.37 mmol/l, P < 0.001) and Ca2+ activity (32.8 ± 32.51 μmol/l, P < 0.01). The intracellular Na+ concentration was 6.25 ± 1.23 mmol/l. 4. The results indicate that in essential hypertension intracellular Na+ activity is increased, particularly in patients with a familial disposition for hypertension. Intracellular Ca2+ is increased in essential hypertension whether or not there was a family disposition to hypertension.

Increased Erythrocyte Sodium-Lithium Countertransport Activity in essential Hypertension is Due to an Increased Affinity for Extracellular Sodium

1990 ◽  
Vol 79 (4) ◽  
pp. 365-369 ◽  
Author(s):  
P. A. Rutherford ◽  
T. H. Thomas ◽  
R. Wilkinson
Keyword(s):  
Essential Hypertension ◽  
Family History ◽  
Positive Family History ◽  
Maximum Velocity ◽  
Normal Subjects ◽  
Sodium Concentration ◽  
Affinity Constant ◽  
Low Sodium ◽  
Standard Assay ◽  
History Of

1. Sodium-lithium countertransport activity in a standard assay, its sodium affinity constant and maximum velocity were measured in erythrocytes from normal subjects and from essential hypertensive patients with and without a family history of hypertension. 2. In normal subjects the sodium concentration used in the standard assay was similar to the sodium affinity constant so that the activity measured in this assay was less than the maximum velocity. 3. In patients with essential hypertension and a positive family history, 33% had a sodium-lithium countertransport activity greater than the upper limit of the normal control range (0.4 mmol of Li+ h−1 l−1 of cells). 4. The reason for the raised sodium-lithium countertransport activity was an increased sodium affinity (lower sodium affinity constant) at the outside ion-binding site. 5. Of the patients with essential hypertension and a positive family history but sodium-lithium countertransport activity within the normal range in the standard assay, 30% also had a low sodium affinity constant. 6. A low sodium affinity constant at the outside site of the sodium-lithium countertransporter may be a more specific indicator for a group of patients with inherited hypertension than the standard sodium-lithium countertransport activity assay.

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