scholarly journals Plasma norepinephrine and dietary sodium intake in normal subjects and patients with essential hypertension.

Hypertension ◽  
1983 ◽  
Vol 5 (5) ◽  
pp. 767-771 ◽  
Author(s):  
K Masuo ◽  
T Ogihara ◽  
Y Kumahara ◽  
A Yamatodani ◽  
H Wada
1982 ◽  
Vol 58 (9) ◽  
pp. 1055-1066
Author(s):  
Kazuko MASUO ◽  
Toshio OGIHARA ◽  
Yuichi KUMAHARA ◽  
Atsushi YAMATODANI ◽  
Hiroshi WADA

1989 ◽  
Vol 256 (6) ◽  
pp. R1171-R1175 ◽  
Author(s):  
G. A. Sagnella ◽  
N. D. Markandu ◽  
M. G. Buckley ◽  
M. A. Miller ◽  
D. R. Singer ◽  
...  

The effects of gradual (50 mmol/day) increases in dietary sodium intake from 10 to 350 mmol/day on plasma atrial natriuretic peptide (ANP), aldosterone, and plasma renin activity (PRA) were studied in six normal subjects. With the increases in sodium intake there was a progressive increase in urinary sodium from 12.2 +/- 4.4 to 314.8 +/- 31.4 mmol/24 h; plasma ANP increased gradually from 9.9 +/- 1.1 to 23.3 +/- 2.2 pg/ml, with the increases being closely associated with the changes in cumulative sodium balance. Plasma aldosterone decreased significantly from 2,519.7 +/- 147.4 pmol/l on the 10 mmol/day to 1,393.3 +/- 125.4 pmol/l when the sodium intake was increased to 50 mmol/day and decreased further to 251.6 +/- 78.7 pmol/l by the end of the study. The changes in PRA paralleled those in plasma aldosterone with the exception of no significant change in plasma PRA within 24 h of the initial increase in sodium intake. This marked sensitivity in the responses of both the ANP and the renin-aldosterone system to small increases in sodium intake clearly points to their importance in the renal adaptations to alterations in dietary sodium intake.


BMJ ◽  
1981 ◽  
Vol 283 (6284) ◽  
pp. 94-97 ◽  
Author(s):  
P S Parfrey ◽  
N D Markandu ◽  
J E Roulston ◽  
B E Jones ◽  
J C Jones ◽  
...  

Hypertension ◽  
1980 ◽  
Vol 2 (1) ◽  
pp. 29-32 ◽  
Author(s):  
M G Nicholls ◽  
W Kiowski ◽  
A J Zweifler ◽  
S Julius ◽  
M A Schork ◽  
...  

1983 ◽  
Vol 3 (3_suppl) ◽  
pp. 33-35 ◽  
Author(s):  
Frans H.H. Leenen ◽  
Perween Shah ◽  
Walther H. Boer ◽  
Ramesh Khanna ◽  
Dimitrios G. Oreopoulos

Development of orthostatic hypotension occasionally complicates treatment of end-stage renal failure by continuous ambulatory peritoneal dialysis (CAPD). The cause may be excessive sodium removal via the dialysate relative to the dietary sodium intake, leading to the gradual development of sodium depletion. Therefore, a group of five symptomatic, hypotensive CAPD patients was treated with oral salt-loading without allowing a concomitant increase in body weight. Supine blood pressure increased markedly after salt-loading (from 94/67 mmHg to 121/78 mmHg) and symptomatic orthostatic hypotension disappeared. The mechanisms leading to the improvement after salt-loading were studied in three of these patients. The beneficial effect of salt-loading was related to two mechanisms: 1) an increase in extracellular fluid volume and presumably blood volume; 2) an increase in sympathetic tone, as assessed by plasma norepinephrine levels and the pressor responsiveness to norepinephrine


1976 ◽  
Vol 51 (s3) ◽  
pp. 193s-196s
Author(s):  
G. A. MacGregor ◽  
P. M. Dawes

1. Saralasin (Sar1-Ala8-angiotensin II), a competitive inhibitor of angiotensin II (AII), has been infused into normal subjects and patients with essential hypertension when deprived of sodium by 5 days of a 10 mmol/day sodium diet. 2. When saralasin was given by an incremental rate of infusion starting at 0·25 μg min—1 kg—1, sodium-deprived normal subjects showed a fall in standing blood pressure with no change in lying blood pressure, sodium-deprived normal-renin hypertensive patients showed no change in lying or standing blood pressure and sodium-deprived low-renin patients showed a significant sustained rise in lying and standing blood pressure. 3. These findings suggest that: (a) standing blood pressure in sodium-deprived normal subjects is angiotensin II dependent; (b) normal-renin hypertensive patients when sodium deprived by diet alone do not appear to be angiotensin II dependent (angiotensin II is unlikely therefore to be directly maintaining their blood pressure on their normal sodium intake); (c) the rise in blood pressure seen in low-renin hypertensive patients with saralasin may be a further way of distinguishing this group of patients.


1984 ◽  
Vol 67 (1) ◽  
pp. 83-88 ◽  
Author(s):  
J. N. Harvey ◽  
I. F. Casson ◽  
A. D. Clayden ◽  
G. F. Cope ◽  
C. M. Perkins ◽  
...  

1. The effect of dietary sodium on the urine dopamine excretion of eight hypertensive patients and six matched controls was studied under metabolic balance conditions over a 2 week period during which dietary sodium intake was increased from 20 to 220 mmol/day. 2. The control group showed the expected increase in dopamine excretion in response to sodium but the hypertensive patients showed an initial fall followed by a return to baseline values. 3. Neither group showed a rise in blood pressure but the hypertensive patients showed a greater weight gain on salt loading, although this change was not significant. The cumulative sodium balance was greater and more prolonged in the hypertensive patients, although this difference also did not attain statistical significance. 4. This defect in dopamine mobilization may be important in relation to renal sodium handling by patients with essential hypertension.


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