Renal sodium handling in normal humans subjected to low, normal, and extremely high sodium supplies

1985 ◽  
Vol 249 (6) ◽  
pp. F941-F947 ◽  
Author(s):  
J. C. Roos ◽  
H. A. Koomans ◽  
E. J. Dorhout Mees ◽  
I. M. Delawi
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Reabsorption ◽  
Lithium Clearance ◽  
Renal Sodium Handling ◽  
Sodium Handling

We studied renal sodium handling, extracellular fluid volume (ECFV), plasma renin activity, aldosterone and norepinephrine, and blood pressure in eight healthy volunteers after equilibration on intakes of 20, 200, and 1,128 +/- 141 meq sodium, respectively. Renal sodium handling was assessed by means of clearance studies during maximal water diuresis and lithium clearance. Urinary sodium excretions were 22 +/- 4, 202 +/- 19, and 1,052 +/- 86 meq/day. From the lower to the upper sodium intake level, 24-h creatinine clearance rose from 111 +/- 7 to 136 +/- 11 ml/min and inulin clearance from 103 +/- 9 to 129 +/- 9 ml/min, whereas proximal and distal fractional sodium reabsorption (FSRprox and FSRdist, respectively) fell from 86.8 +/- 1.3 to 79.0 +/- 2.7% and from 96.5 +/- 0.5 to 76.0 +/- 1.9%, respectively. During the normal sodium intake (200 meq), intermediate values were recorded. The changes in fractional lithium clearance were less consistent but correlated with FSRprox (r = 0.78, P less than 0.001) and not with FSRdist. Major changes in plasma renin activity, aldosterone, and, to a lesser extent, norepinephrine accompanied these changes in kidney function, displaying inverse and exponential correlations with daily sodium excretion and ECFV. No consistent rise in blood pressure was detected. These observations indicate that in healthy humans renal adaptation to vast variations in sodium intake includes resetting of glomerular filtration rate, FSRprox, and, in particular, FSRdist. Alterations in neurohumoral factors may play a dominant role in this adaptation.

Comparative study on development of corticosterone and DOCA hypertension in rats

1977 ◽  
Vol 233 (5) ◽  
pp. F403-F411 ◽  
Author(s):  
D. Haack ◽  
J. Mohring ◽  
B. Mohring ◽  
M. Petri ◽  
E. Hackenthal
Keyword(s):  
Water Retention ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
The Common ◽  
Renal Sodium Handling ◽  
Plasma Arginine ◽  
Corticosterone Treatment ◽  
Sodium Handling ◽  
Sodium And Water Balance

The administration of corticosterone for 5 consecutive days to normal rats on a standard sodium intake induced negative sodium and water balance. These effects were opposite those observed under DOCA treatment. However, not only under DOCA but also under corticosterone treatment extracellular fluid volume (ECFV) and plasma volume (PV) increased, and blood pressure (BP) rose in parallel. Plasma renin and angiotensin II concentrations declined under the influence of both steroids. Plasma arginine vasopressin concentrations increased under DOCA, whereas they transiently decreased under corticosterone administration. These data suggest that the common mediator for BP elevation due to steroid excess would be an increase in ECFV and PV. The pathways by which this increase is achieved seem to be different. Under DOCA treatment ECFV and PV increased subsequent to renal sodium and water retention. Under corticosterone, however, sodium and water were shifted from intra- to extracellular compartments, and a fraction of this shifted sodium and water was conserved in extracellular space, most likely because corticosterone also affected renal sodium handling.

Adenovirus-mediated human prostasin gene delivery is linked to increased aldosterone production and hypertension in rats

2003 ◽  
Vol 284 (4) ◽  
pp. R1031-R1036 ◽  
Author(s):  
Cindy Wang ◽  
Julie Chao ◽  
Lee Chao
Keyword(s):  
Blood Pressure ◽  
Gene Transfer ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Sodium Reabsorption ◽  
Elevated Plasma ◽  
Aldosterone Production ◽  
Renal Kallikrein

Prostasin has been demonstrated to be an activator of epithelial sodium channels in cultured renal and bronchial epithelial cells. In this study, we evaluated the effects of adenovirus-mediated gene transfer of human prostasin on blood pressure regulation and sodium reabsorption in Wistar rats. Expression of human prostasin mRNA was identified in rat adrenal gland, liver, kidney, heart, lung, and aorta, and immunoreactive human prostasin was detected in the circulation and urine of rats receiving prostasin gene transfer. A single injection of adenovirus carrying the prostasin gene caused prolonged increases in blood pressure for 3–4 wk. Blood pressure increase was accompanied by elevated plasma aldosterone levels and reduced plasma renin activity. The increase in blood pressure and plasma aldosterone levels as well as the reduction of plasma renin activity correlated with the expression of human prostasin transgene. Elevated plasma aldosterone levels were detected at 3 days after gene transfer before the development of hypertension, indicating that stimulation of mineralocorticoid production is the primary target of prostasin. Prostasin gene transfer significantly reduced urinary K+ excretion but increased urinary Na+ and kallikrein excretion. Elevated renal kallikrein levels promote natriuresis, which may lead to sodium escape and prevent further increases of blood pressure after prostasin gene transfer. In summary, these results suggest that prostasin participates in blood pressure and electrolyte homeostasis by regulating the renin-angiotensin-aldosterone and kallikrein-kinin systems.

Angiotensin II Blockade before and after Marked Sodium Depletion in Patients with Hypertension

1978 ◽  
Vol 54 (1) ◽  
pp. 75-83 ◽  
Author(s):  
P. Van Hoogdalem ◽  
A. J. M. Donker ◽  
F. H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Renin Activity ◽  
Mean Blood Pressure ◽  
Sodium Depletion ◽  
Before And After

1. Angiotensin II blockade before and after marked sodium depletion in patients with hypertension [unilateral renovascular (eight), bilateral renovascular (four) and essential (four)] was performed by intravenous administration of the angiotensin II antagonist Sar1-Ala8-angiotensin II (saralasin). 2. On normal sodium intake, saralasin decreased mean blood pressure by 8 mmHg in the unilateral renovascular group, by 6 mmHg in the bilateral renovascular group and increased it by 3 mmHg in the essential hypertensive group. After sodium depletion saralasin decreased mean blood pressure by 33 mmHg, 35 mmHg and 18 mmHg respectively. The saralasin-induced decrease in blood pressure significantly correlated with the log of the initial plasma renin activity. 3. Saralasin infusion decreased effective renal plasma flow (ERPF) in all three hypertension subgroups, both on normal sodium intake and after sodium depletion. Glomerular filtration rate decreased in direct relation to the hypotensive effect of saralasin but ERPF showed this relationship only after sodium depletion. On normal sodium intake saralasin increased filtration fraction by 17%, but decreased it by 7% after sodium depletion. 4. It is concluded that the hypotensive action of saralasin closely correlates with the value of circulating plasma renin activity, apparently independent of the aetiology of the hypertension. The decrease in ERPF during saralasin infusion in the patients on normal sodium intake seems mainly related to the agonistic activity of saralasin, but that after sodium depletion to the hypotensive effect of saralasin.

Effect of Volume Depletion and Subsequent Propranolol Treatment on Blood Pressure and Plasma Renin Activity in Patients with Essential and with Renovascular Hypertension

1974 ◽  
Vol 48 (s2) ◽  
pp. 69s-71s
Author(s):  
G. G. Geyskes ◽  
P. Boer ◽  
F. H. H. Leenen ◽  
E. J. Dorhout Mees
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Plasma Volume ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Extracellular Fluid Volume ◽  
Renin Activity

1. In nineteen patients, five with unilateral renal artery stenosis and fourteen with essential hypertension (WHO grades I–II), blood pressure, plasma and extracellular fluid volumes and plasma renin activity were studied at the end of three sequential periods: (a) after at least 3 days on a 60 mmol Na+ diet; (b) after 3 days of salt depletion induced with a diuretic and sustained on a 20 mmol Na+ diet; (c) after 3 days during which the 20 mmol Na+ diet was continued and beta-receptor blockade was induced by increasing dosages of propranolol up to 320 mg daily. 2. After sodium depletion extracellular fluid volume and plasma volume decreased and plasma renin activity increased; blood pressure did not change significantly. 3. After adding propranolol, plasma volume and extracellular fluid volume remained low, and there was a significant decrease in plasma renin activity and blood pressure. 4. No correlation could be demonstrated between changes of blood pressure and plasma renin activity. 5. When the responses of the five patients with renal artery stenosis were compared with those of the fourteen patients with essential hypertension, no significant differences were found. 6. Propranolol has a strong anti-hypertensive effect after Na+ depletion, irrespective of the absolute activities of plasma renin.

Biochemical Correlates of the Increase in Blood Pressure with Age

1978 ◽  
Vol 55 (s4) ◽  
pp. 377s-379s ◽  
Author(s):  
C. E. Grim ◽  
M. H. Weinberger ◽  
D. P. Henry ◽  
F. C. Luft ◽  
N. S. Fineberg
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Multiple Correlation Analysis ◽  
Normotensive Subjects ◽  
Relationship Of ◽  
The Relationship

1. Blood pressure, plasma renin activity, plasma aldosterone, urinary noradrenaline during sleep (UNA-S) and several estimates of sodium intake were determined in 379 normotensive subjects (age 13–70) to investigate the relationship of these variables to blood pressure. 2. Blood pressure was correlated with age, weight, plasma renin activity UNA-S, and estimates of sodium intake. These variables were frequently intercorrelated. 3. Multiple-correlation analysis revealed that after removal of the effects of age, blood pressure was related to weight, plasma renin activity, UNA-S and estimates of sodium intake. 4. However, multiple-regression analysis failed to demonstrate an effect of plasma renin activity, UNA-S, or estimates of sodium intake on blood pressure when the effects of age, weight, race and sex were removed. 5. Careful matching of subjects by age, weight, race and sex in studies of blood pressure and biochemical factors in normal subjects is crucial to proper interpretation of such data.

Does the Renin—Angiotensin System Maintain Blood Pressure in Both Hypertensive and Normotensive Subjects? a Comparison of Propranolol, Saralasin and Captopril

1979 ◽  
Vol 57 (s5) ◽  
pp. 145s-148s ◽  
Author(s):  
G. A. MacGregor ◽  
N. D. Markandu ◽  
J. E. Roulston
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Normotensive Subjects

1. Propranolol, saralasin and captopril changed blood pressure in normotensive as well as hypertensive subjects. 2. The percentage change in blood pressure with these three drugs for a given plasma renin activity was similar in normotensive and hypertensive subjects. 3. This suggests that when the renin-angiotensin system is maintaining blood pressure, it maintains the blood pressure to the same extent in percentage terms in normotensive and hypertensive subjects for a given plasma renin activity. 4. Saralasin has marked agonist activity, and probably underestimates the participation of the renin—angiotensin—aldosterone system in the maintenance of blood pressure. The fall in blood pressure that occurred with captopril in normal subjects on their normal sodium intake suggests that the renin—angiotensin—aldosterone system may have an important role in the control of blood pressure in normal subjects on their normal sodium intake. If it does, our results suggest that the renin—angiotensin—aldosterone system plays no greater role in maintaining blood pressure in patients with essential hypertension than normotensive subjects for a given plasma renin activity.

Effect of Progesterone on Renal Sodium Handling in Man: Relation to Aldosterone Excretion and Plasma Renin Activity

1975 ◽  
Vol 49 (2) ◽  
pp. 139-147 ◽  
Author(s):  
Suzanne Oparil ◽  
E. N. Ehrlich ◽  
M. D. Lindheimer
Keyword(s):  
Plasma Renin Activity ◽  
Sodium Excretion ◽  
Renal Plasma Flow ◽  
Free Water ◽  
Plasma Renin ◽  
Urinary Sodium ◽  
Renin Activity ◽  
Sodium Reabsorption ◽  
Renin Substrate ◽  
Sodium Handling

1. The effect of progesterone on renal haemodynamics and intrarenal sodium handling was evaluated in thirteen normal men on a constant diet. Clearances were measured during maximal water diuresis and again 4–7 days later, this time 3 h after progesterone was given intramuscularly. Seven additional studies were performed 3 days after progesterone administration. Another four tests were performed on volunteers who had manifested renal ‘escape’ from the sodium-retaining effect of deoxycorticosterone acetate. 2. In acute progesterone studies glomerular filtration rate was unchanged, whereas effective renal plasma flow increased, so that filtration fraction decreased significantly. A similar increase in urinary sodium occurred whether subjects received a low or high sodium diet. Indices which related to the distal delivery of filtrate (fractional urine flow and the sum of fractional free water and sodium clearances) increased significantly in both groups. The progesterone-induced increase in sodium excretion was not related to changes in plasma renin activity, renin substrate or urinary aldosterone. After 3 days of progesterone, the increase of sodium excretion was less than in the acute studies and urinary aldosterone increased two- to four-fold. Progesterone failed to produce an acute increase in urinary sodium in subjects hyperexpanded by administration of exogenous mineralocorticoids. 3. Results suggest that the acute natriuretic action of progesterone is in part independent of aldosterone inhibition and that progesterone may inhibit sodium reabsorption at proximal as well as distal sites in the nephron.

Effects of Salt and Water Depletion on the Early Phase of Hypertension in Goldblatt two-Kidney Hypertensive Dogs

1981 ◽  
Vol 60 (6) ◽  
pp. 625-631
Author(s):  
M. L. Watson ◽  
J. McCormick ◽  
A. Thom ◽  
P. Whelpdale ◽  
A. Ungar
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Sodium Restriction ◽  
Arterial Plasma ◽  
Venous Plasma

1. Hypertension was induced in dogs by partial occulsion of one renal artery, the opposite kidney remaining intact, and the changes in blood pressure, plasma renin activity, aldosterone and prostaglandin E (PGE) were monitored. 2. Two days after induction of hypertension, the retained sodium and water were removed by haemodialysis and the animals were then maintained on a low dietary intake of sodium for the following 7 days. 3. Removal of the accumulated sodium and water had no immediate effect on blood pressure, but during the ensuing 7 days there was a small decrease in blood pressure, which again increased after re-institution of a normal sodium intake. 4. Plasma renin activity and aldosterone increased during development of hypertension and remained elevated during the period of sodium restriction. 5. Sodium and water retained during the development of hypertension was not responsible for the elevated blood pressure. 6. The concentration of PGE in arterial plasma and renal venous plasma from the undamped kidney were unchanged during the study, although we have previously shown that in the absence of sodium depletion, PGE rises. 7. PGE released from the kidney may be important in mediating the excretion of sodium and water that is retained during the development of renal hypertension.

Influence of right atrial stretch on plasma renin activity in the conscious rat

1987 ◽  
Vol 65 (2) ◽  
pp. 257-259 ◽  
Author(s):  
Susan Kaufman
Keyword(s):  
Plasma Renin Activity ◽  
Superior Vena ◽  
Vena Cava ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Renin Activity ◽  
Right Atrial ◽  
Balloon Inflation ◽  
Conscious Rat ◽  
Basal Plasma

Rats were prepared with inflatable balloons at the superior vena cava – right atrium junction. After recovery 1 week later, when blood was taken from conscious, normovolaemic animals plasma renin activity was found not to be influenced by right atrial stretch. Plasma renin activity was then measured in rats in which an extracellular fluid deficit had been produced by peritoneal dialysis against a hyperoncotic, isotonic solution. Although basal plasma renin activity was elevated (6.8 ± 0.9 from 1.5 ± 0.2 ng∙mL∙h, n = 19), no depression was observed in the experimental group after 15 or 90 min of balloon inflation. In rats pretreated with isoprenaline (10 μg/kg body wt.) plasma renin activity was also increased over basal levels, but again balloon inflation caused no reduction in plasma renin activity. It would appear that right atrial stretch has little, if any, influence on renin release in the conscious rat.

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