An Inherited Sodium Ion-Potassium Ion Cotransport Defect in Essential Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 191s-193s ◽  
Author(s):  
R. P. Garay ◽  
G. Dagher ◽  
P. Meyer
Keyword(s):  
Essential Hypertension ◽  
Secondary Hypertension ◽  
Sodium Balance ◽  
Sodium Permeability ◽  
Sodium Potassium ◽  
A Cell ◽  
Cotransport System ◽  
Normotensive Subjects ◽  
Sodium Potassium Pump ◽  
Sodium Extrusion

1. In erythrocytes, the extrusion of a cell sodium load is accomplished by the ouabain-sensitive sodium-potassium pump and by the frusemide-sensitive sodium-potassium cotransport, which operate against the passive sodium permeability. All these three components of the cell sodium balance were studied in essential hypertension (410 subjects were investigated). 2. An abnormally low rate of net sodium extrusion by the sodium-potassium cotransport system was observed in essential hypertensive patients and in a high proportion of their young normotensive offspring. A normal cotransport system found in secondary hypertensive subjects devoid of familial history of hypertension confirmed that the abnormal cotransport system is not the consequence of high blood pressure per se. 3. A 20–40% increase in the rate of net sodium extrusion by the sodium-potassium pump seems to compensate for the abnormal cotransport in erythrocytes from some young normotensive subjects born of essential hypertensive parents and from some benign essential hypertensive subjects. 4. No difference could be detected between the passive sodium permeability of erythrocytes from hypertensive subjects and in those from normotensive controls. 5. In conclusion, essential hypertension seems to be associated with an inherited defect in the sodium-potassium cotransport system. We propose therefore the laboratory study of this system for: (i) the distinction between essential and secondary hypertension and (ii) the preventive investigation of young normotensive subjects in hypertensive families.

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.

Relation of Plasma Noradrenaline to Blood Pressure, Age, Sex and Sodium Balance in Patients with Stable Essential Hypertension and in Normotensive Subjects

1978 ◽  
Vol 55 (s4) ◽  
pp. 81s-83s ◽  
Author(s):  
H. M. Brecht ◽  
W. Schoeppe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Essential Hypertension ◽  
Diastolic Blood Pressure ◽  
Plasma Noradrenaline ◽  
Sodium Balance ◽  
Creatinine Ratio ◽  
Control Subjects ◽  
Normotensive Subjects ◽  
Normotensive Control

1. Plasma noradrenaline was measured in 125 patients with stable essential hypertension (WHO I—II) and in 107 normotensive control subjects lying and standing. 2. In normotensive subjects and in patients with essential hypertension no sex-related differences of plasma noradrenaline were found between age-matched groups. 3. Plasma noradrenaline was not related to sodium balance indexed by urinary sodium/creatinine ratio. 4. In patients with essential hypertension plasma noradrenaline increases with age. 5. Mean plasma noradrenaline concentrations are significantly higher in patients with essential hypertension compared with age-matched normotensive subjects both lying and standing. 6. In patients with essential hypertension diastolic blood pressure and heart rate correlated significantly with supine plasma noradrenaline concentrations.

Evidence for a Plasma Factor Affecting Na+ Cellular Transport in Genetic Normotensive Subjects and in Borderline Hypertensive Subjects

1982 ◽  
Vol 63 (s8) ◽  
pp. 53s-55s ◽  
Author(s):  
F. V. Costa ◽  
L. Montebugnoli ◽  
M. F. Giordani ◽  
L. Vasconi ◽  
E. Ambrosioni
Keyword(s):  
Essential Hypertension ◽  
Sodium Content ◽  
Secondary Hypertension ◽  
Cellular Transport ◽  
Borderline Hypertension ◽  
Dynamic Phase ◽  
Plasma Factor ◽  
History Of ◽  
Family History Of Hypertension ◽  
Normotensive Subjects

1. Lymphocytes from normotensive subjects with normal intralymphocytic sodium content were incubated for 1 h in plasma from subjects with essential hypertension, secondary hypertension or borderline hypertension, and from normotensive subjects with (genetic) and without (non-genetic) family history of hypertension. 2. Lymphocytes from non-genetic normotensive subjects greatly increase their intralymphocytic sodium content after incubation in plasma (diluted 1:4) of patients with essential hypertension (but not with secondary hypertension), of borderline subjects and of genetic normotensive subjects with abnormally high intralymphocytic sodium content (<26 mmol/kg). 3. When plasma is diluted 1:8, an increase in intralymphocytic sodium content is detectable only after incubation in plasma of borderline subjects and of genetic normotensive subjects with high intralymphocytic sodium content. 4. These data suggest that a plasma factor altering Na+ transport is detectable in all the subjects in whom intralymphocytic sodium content is high, independently of their blood pressure values. The concentration (or the activity) of this substance is greater in borderline and genetic normotensive subjects than in patients with sustained essential hypertension. This suggests that these subjects are in a dynamic phase of the development of hypertension.

Intrarenal Pressure and Exaggerated Natriuresis in Essential Hypertension

1970 ◽  
Vol 38 (3) ◽  
pp. 359-374 ◽  
Author(s):  
J. Lowenstein ◽  
E. R. Beranbaum ◽  
H. Chasis ◽  
D. S. Baldwin
Keyword(s):  
Essential Hypertension ◽  
Hypertonic Saline ◽  
Sodium Excretion ◽  
Renal Vein ◽  
Sodium Balance ◽  
Prolonged Infusion ◽  
Saline Loading ◽  
Arteriolar Resistance ◽  
Normotensive Subjects ◽  
Intrarenal Pressure

1. Intrarenal pressure, estimated by measurement of wedged renal vein pressure, was elevated in patients with essential hypertension. Despite increased afferent arteriolar resistance, glomerular pressure was elevated indicating that the higher systemic pressure in essential hypertension is transmitted beyond the arterioles and accounts for elevation of intrarenal pressure. 2. During hypertonic saline loading in hypertensives, renal arteriolar resistance falls, resulting in further increase in intrarenal pressure. Increments in intrarenal pressure paralleled increases in sodium excretion in patients with essential hypertension during the exaggerated natriuresis and in normotensive subjects after the prolonged infusion of hypertonic saline. 3. The marked increase in intrarenal pressure which appears to be responsible for exaggerated natriuresis in essential hypertension is attributable to an altered (exaggerated) response of the renal arterioles. The data suggest that elevated intrarenal pressure may play a role in the regulation of sodium balance in patients with essential hypertension.

Effect of Captopril on the Blood Pressure and Renal Responses to Acute Saline Loading in Normal and Essential Hypertensive Subjects

1982 ◽  
Vol 63 (s8) ◽  
pp. 223s-225s ◽  
Author(s):  
A. Mimran ◽  
J. Ribstein
Keyword(s):  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Normal Subjects ◽  
Sodium Balance ◽  
Saline Loading ◽  
Diuretic Response ◽  
Normotensive Subjects ◽  
Renal Responses

1. Systemic, humoral and renal responses to isotonic volume expansion (1800 ml in 3 h) were assessed in normal subjects and patients with normal renin essential hypertension before and during captopril administration. 2. Essential hypertensive subjects had a greater natriuretic and diuretic response to volume expansion than had normotensive subjects. 3. Captopril induced a fall in pre-saline mean arterial pressure more marked in hypertensive (20 ± 3 mmHg) than in normotensive subjects (9 ± 2 mmHg) and did not produce any change in sodium balance. 4. Captopril exaggerated the response of arterial pressure to volume expansion since mean arterial pressure increased more markedly after than before captopril in both normotensive (18.7 ± 3.8%) and hypertensive subjects (16.9 ± 3.7%). 5. Captopril blunted the exaggerated natriuretic response to volume expansion observed in patients with essential hypertension, whereas the renal response was unchanged in normotensive subjects.

Captopril Enhances Vascular and Adrenal Responsiveness to Angiotensin II in Essential Hypertension

1984 ◽  
Vol 66 (3) ◽  
pp. 299-305 ◽  
Author(s):  
Richard J. Koletsky ◽  
Murray B. Gordon ◽  
Meryl S. Leboff ◽  
Thomas J. Moore ◽  
Robert G. Dluhy ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Blood Pressure Response ◽  
Sodium Balance ◽  
Ang Ii ◽  
Before And After ◽  
Pah Clearance ◽  
Normotensive Subjects ◽  
Renal Vascular

1. The converting-enzyme inhibitor captopril (25–50 mg orally every 6 h for 66 h) was used to dissociate the circulating levels of angiotensin II (ANG II) from changes in sodium balance in 11 patients with normal renin essential hypertension on 10 mmol of sodium/day intake. Pressor, renal vascular and adrenal responses to graded infusions of ANG II (0.3, 1 and 3 pmol kg−1 min−1) were measured before and after captopril administration. Systemic vascular responses were assessed by measuring diastolic blood presusre (DBP), renovascular responses by measuring p-aminohippurate (PAH) clearance and adrenal responses by measuring plasma aldosterone. 2. After receiving captopril for 66 h the hypertensive subjects showed a significantly (P<0.004) enhanced blood pressure response to the infused ANG II but not to noradrenaline when compared with the response before captopril. ANG II (3 pmol kg−1 min−1) also produced a significantly (P<0.03) greater reduction in PAH clearance after (−194 ± 40 ml/min) compared with before (−104 ± 15 ml/min) captopril. These results suggest that the responsiveness to ANG II in these two target tissues is determined by the circulating ANG II level. 3. In the adrenal gland the aldosterone responses to ANG II also were significantly greater after (P < 0.01) than before captopril (increment at 3 pmol kg−1 min−1: 660 ± 88 vs 381 ± 94 pmol/l). These results are in distinct contrast with the responses previously reported for normotensive subjects and support the hypothesis that the regulation of aldosterone secretion is altered in subjects with essential hypertension.

Increased Intralymphocytic Sodium Content in Essential Hypertension: An Index of Impaired Na+ Cellular Metabolism

1981 ◽  
Vol 61 (2) ◽  
pp. 181-186 ◽  
Author(s):  
E. Ambrosioni ◽  
F. V. Costa ◽  
L. Montebugnoli ◽  
F. Tartagni ◽  
B. Magnani
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Sodium Concentration ◽  
Sodium Content ◽  
Secondary Hypertension ◽  
Mean Value ◽  
History Of ◽  
Wet Weight ◽  
Normotensive Subjects ◽  
The Mean

1. The sodium concentration in lymphocytes was measured in a group of 66 normotensive subjects (40 without familial hypertension and 26 with familial hypertension), in a group of 81 patients with essential hypertension and in a group of 14 patients with secondary hypertension. 2. The mean value (±sd) in normotensive subjects with no history of familial hypertension was 21.9 ± 3.1 mmol/kg wet weight, which was significantly lower (P < 0.005) than that of normotensive subjects with familial hypertension (mean value 27.9 ± 4.2 mmol/kg). Lymphocyte sodium concentration was significantly higher in patients with essential hypertension (33.2 ± 3.3 mmol/kg; P < 0.001) than in the subjects with normal blood pressure without familial hypertension. 3. In the patients with essential hypertension there was a significant correlation between lymphocyte sodium concentration and systolic (P < 0.005), diastolic (P < 0.001) and mean (P < 0.001) blood pressure. In the normotensive subjects there was no correlation between the lymphocyte sodium concentration and the blood pressure. 4. The patients with secondary forms of hypertension had normal lymphocyte sodium concentration, except in the case of Conn's disease. 5. Incubation with ouabain increased lymphocyte sodium concentration in the normotensive subjects and patients with essential hypertension; the final sodium concentration was similar in the two groups. 6. When lymphocytes from normotensive subjects without familial hypertension were incubated in plasma of patients with essential hypertension there was an increase in their sodium content.

scholarly journals Urinary Kallikrein in Normotensive Subjects and in Patients with Essential Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 247s-250s ◽  
Author(s):  
H. Zschiedrich ◽  
P. Fleckenstein ◽  
R. Geiger ◽  
E. Fink ◽  
K. Sinterhauf ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Primary Role ◽  
Urinary Kallikrein ◽  
Sodium Potassium ◽  
Urinary Kallikrein Excretion ◽  
Normotensive Subjects

1. Excretion of urinary kallikrein was normal in 13 out of 15 patients with uncomplicated essential hypertension. 2. Frusemide increased urinary kallikrein excretion in normotensive subjects and in patients with essential hypertension. The stimulating effect of frusemide on urinary kallikrein was significantly diminished in patients with essential hypertension. 3. No correlations of urinary kallikrein with sodium, potassium, and aldosterone excretion were found. 4. The results do not support the idea that urinary kallikrein plays a primary role in the pathogenesis of essential hypertension.

Renal effects of hyperinsulinaemia in subjects with two hypertensive parents

1999 ◽  
Vol 97 (6) ◽  
pp. 681-687
Author(s):  
Ulrik B. ANDERSEN ◽  
Peter SKØTT ◽  
Niels E. BRUUN ◽  
Harriet DIGE-PETERSEN ◽  
Hans IBSEN
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Genetic Predisposition ◽  
Sensitivity Index ◽  
Renal Metabolism ◽  
Sodium Potassium ◽  
The Family ◽  
Normotensive Subjects ◽  
Sodium Clearance ◽  
Sodium And Potassium

The aim of this investigation was to study the effects of isoglycaemic hyperinsulinaemia on the renal metabolism of electrolytes and water in subjects with a strong genetic predisposition to essential hypertension, compared with that in non-predisposed subjects. We studied 25 normotensive subjects aged 18–35 years whose parents both had essential hypertension, and 22 age- and sex-matched subjects whose parents were both normotensive. Diabetes or morbid obesity in any subject or parent excluded the family. The 24-h blood pressure was measured. The subjects received an isocaloric diet with a fixed content of sodium and potassium for 4 days before the study. An isoglycaemic, hyperinsulinaemic clamp with infusion of insulin (40 munits·min-1·m-2) was performed. We measured the renal clearance of diethylenetriaminepenta-acetic acid, sodium, potassium and lithium both under basal conditions and during hyperinsulinaemia. In response to hyperinsulinaemia, renal sodium clearance decreased to a significantly greater extent in the hypertension-prone subjects [0.57 (0.74, 0.36) ml·min-1·1.73 m2 (median and quartiles)] than in the controls [0.34 (0.56, 0.18) ml·min-1·1.73 m2] (P = 0.04). Compared with the controls, the subjects predisposed to hypertension had a higher 24-h diastolic blood pressure [78 (70, 82) mmHg, compared with 73 (68, 77) mmHg], but a similar insulin sensitivity index {107×[313 (225, 427)] compared with 107×[354 (218, 435)] l2·min-1·pmol-1·kg-1}. Thus the sodium-retaining effect of insulin was more pronounced in subjects with a strong genetic predisposition to essential hypertension than in subjects with normotensive parents. This effect may contribute to the development of hypertension in subjects with a genetic predisposition to hypertension.

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