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

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.

1982 ◽  
Vol 63 (s8) ◽  
pp. 41s-43s ◽  
Author(s):  
W. Zidek ◽  
H. Vetter ◽  
K.-G. Dorst ◽  
H. Zumkley ◽  
H. Losse

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.


1981 ◽  
Vol 61 (2) ◽  
pp. 181-186 ◽  
Author(s):  
E. Ambrosioni ◽  
F. V. Costa ◽  
L. Montebugnoli ◽  
F. Tartagni ◽  
B. Magnani

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.


1984 ◽  
Vol 66 (4) ◽  
pp. 427-433 ◽  
Author(s):  
Ottar Gudmundsson ◽  
Hans Herlitz ◽  
Olof Jonsson ◽  
Thomas Hedner ◽  
Ove Andersson ◽  
...  

1. During 4 weeks 37 normotensive 50-year-old men identified by screening in a random population sample were given 12 g of NaCl daily, in addition to their usual dietary sodium intake. Blood pressure, heart rate, weight, urinary excretion of sodium, potassium and catecholamines, plasma aldosterone and noradrenaline and intra-erythrocyte sodium content were determined on normal and increased salt intake. The subjects were divided into those with a positive family history of hypertension (n = 11) and those without such a history (n = 26). 2. Systolic blood pressure and weight increased significantly irrespective of a positive family history of hypertension. 3. On normal salt intake intra-erythrocyte sodium content was significantly higher in those with a positive family history of hypertension. During high salt intake intra-erythrocyte sodium content decreased significantly in that group and the difference between the hereditary subgroups was no longer significant. 4. In the whole group urinary excretion of noradrenaline, adrenaline and dopamine increased whereas plasma aldosterone decreased during the increased salt intake. 5. Thus, in contrast to some earlier studies performed in young subjects, our results indicate that moderately increased sodium intake acts as a pressor agent in normotensive middle-aged men whether there was a positive family history of hypertension or not. We confirm that men with positive family history of hypertension have an increased intra-erythrocyte sodium content, and that an increase in salt intake seems to increase overall sympathetic activity.


1981 ◽  
Vol 61 (s7) ◽  
pp. 367s-368s ◽  
Author(s):  
A. Fernandez-Cruz ◽  
M. Luque Otero ◽  
L. Llorente Perez ◽  
C. Fernandez Pinilla ◽  
N. Martell Claros

1. Human leucocyte AB antigens were determined by means of a lymphocyte toxicity test in 84 patients with essential hypertension and in 1000 blood donors. 2. The prevalence of HLA B8 was 16.4% in hypertensive patients and 8.9% in controls (P = 0.07). 3. The prevalence of HLA B12 was 34.5% in hypertensive patients and 26.9% in the control group (N.S.). In WHO stage III hypertension HLA B12 was found in six out of 10 patients. 4. The prevalence of HLA B15 was 1.2% in hypertensive patients and 6.4% in controls (P &lt; 0.05). 5. In view of a previous report of HLA antigens in a Spanish diabetic population, this study does not support the suggestion of a genetic and possibly HLA-linked connection between essential hypertension and diabetes mellitus among the Spanish population. 6. A positive family history of hypertension tended to be more common in those patients with essential hypertension associated with HLA B8.


1989 ◽  
Vol 7 (7) ◽  
pp. 912-915 ◽  
Author(s):  
A F Kantor ◽  
F P Li ◽  
A J Janov ◽  
N J Tarbell ◽  
S E Sallan

The prevalence of hypertension was investigated in 119 adults who have survived for up to 53 years following the diagnosis of renal cancer in childhood (Wilms' tumor, 116 patients; renal carcinoma, three patients). Twenty-four (20%) have developed definite or borderline hypertension, as compared with 18.1 cases expected based on US population rates (relative risk [RR], 1.3; 95% confidence interval [CI], 0.9 to 2.0; P = .20). This nonsignificant excess is due to the heightened prevalence of definite hypertension among one subgroup of male patients. The findings are not explained by cigarette smoking, obesity, age, and stage at diagnosis of Wilms' tumor, or family history of hypertension. A case-comparison analysis within the cohort showed no consistent hypertensive effect associated with radiation therapy dose, radiotherapy concurrent with dactinomycin chemotherapy, or extent of renal surgery. Hypertension is not a common late complication of Wilms' tumor in our patients.


2005 ◽  
Vol 109 (3) ◽  
pp. 311-317 ◽  
Author(s):  
Hans Herlitz ◽  
Eva Palmgren ◽  
Bengt Widgren ◽  
Mattias Aurell

The renin–angiotensin system is implicated in the pathophysiology of hypertension. Renin release is regulated by a number of factors, including circulating Ang II (angiotensin II), the so-called short feedback loop. The aim of the present study was to investigate the responsiveness of circulating Ang II on PRA (plasma renin activity) in normotensive subjects with a PFH or NFH (positive or negative family history of hypertension respectively). PRA, renal haemodynamics and urinary sodium excretion were measured during infusion of Ang II without and with pretreatment with the AT1 (Ang II type 1) receptor blocker irbesartan. Normotensive men with a PFH (n=13) and NFH (n=10), with a mean age of 38 years, were given on different occasions intravenous Ang II infusions of 0.1, 0.5 and 1.0 ng·kg−1 of body weight·min−1 before and after pretreatment with 150 mg of irbesartan once a day for 5 consecutive days. RPF (renal plasma flow) and GFR (glomerular filtration rate) were also measured. Before Ang II infusion, the PFH and NFH groups did not differ with respect to BP (blood pressure), body mass index, PRA, RBF (renal blood flow) or urinary sodium. There was no difference in BP or renal haemodynamic response to the highest Ang II dose between the groups. PRA declined with the highest Ang II dose (P<0.01) in subjects with a NFH, but not in subjects with a PFH. After treatment with irbesartan when Ang II had no effect on BP in either group, Ang II also suppressed PRA in subjects with a PFH (P<0.01), and the difference between the groups at baseline was thus eliminated. In conclusion, these findings indicate that subjects with a PFH have a defective Ang II suppression of PRA, which is corrected by AT1 receptor blockade.


1988 ◽  
Vol 6 (4) ◽  
pp. S568-571 ◽  
Author(s):  
Satoshi Umemura ◽  
Kazuaki Uchino ◽  
Gen Yasuda ◽  
Yoshihiro Ishikawa ◽  
Yutaka Hatori ◽  
...  

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