Sodium appetite elicited by intracerebroventricular infusion of angiotensin II in the rat: I. Relation to urinary sodium excretion.

1. The effects of intravenous injection of Fab fragments of anti-digoxin IgG (Digibind) on the changes in blood pressure, urine volume and urinary sodium excretion after intracerebroventricular infusion of artificial cerebrospinal fluid with normal or high sodium concentration were examined in anaesthetized rats. 2. The biological efficacy of Digibind was confirmed by experiments in vitro and in vivo, which showed that pre-treatment with Digibind completely abolished or significantly attenuated the aortic contractile response or pressor response to digoxin in guinea-pigs. 3. Infusion of high-sodium cerebrospinal fluid, but not normal-sodium cerebrospinal fluid, into the lateral brain ventricle of rats caused marked increases in blood pressure, urine volume and urinary sodium excretion. 4. Digibind did not significantly affect the increases in blood pressure, urine volume and urinary sodium excretion caused by intracerebroventricular infusion of high-sodium cerebrospinal fluid. 5. Digoxin-like immunoreactive factor may play a minor role, if any, in central nervous system-induced natriuresis in rats.

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Long-term exercise attenuates blood pressure responsiveness and modulates kidney angiotensin II signalling and urinary sodium excretion in SHR

Journal of the Renin-Angiotensin-Aldosterone System ◽

10.1177/1470320311408750 ◽

2011 ◽

Vol 12 (4) ◽

pp. 394-403 ◽

Cited By ~ 22

Author(s):

Silmara Ciampone ◽

Rafael Borges ◽

Ize P de Lima ◽

Flávia F Mesquita ◽

Elizabeth C Cambiucci ◽

...

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Exercise Training ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Urinary Sodium ◽

Receptor Expression ◽

Spontaneously Hypertensive ◽

Wistar Kyoto

Observations have been made regarding the effects of long-term exercise training on blood pressure, renal sodium handling and renal renin–angiotensin–aldosterone (RAS) intracellular pathways in conscious, trained Okamoto–Aoki spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKy) normotensive rats, compared with appropriate age-matched sedentary SHR and WKy. To evaluate the influence of exercise training on renal function and RAS, receptors and intracellular angiotensin II (AngII) pathway compounds were used respectively, and lithium clearance and western blot methods were utilised. The current study demonstrated that increased blood pressure in SHR was blunted and significantly reduced by long-term swim training between the ages of 6 and 16 weeks. Additionally, the investigators observed an increased fractional urinary sodium excretion in trained SHR (SHRT) rats, compared with sedentary SHR (SHRS), despite a significantly decreased creatinine clearance (CCr). Furthermore, immunoblotting analysis demonstrated a decreased expression of AT1R in the entire kidney of TSHR rats, compared with SSHR. Conversely, the expression of the AT2R, in both sedentary and trained SHR, was unchanged. The present study may indicate that, in the kidney, long-term exercise exerts a modulating effect on AngII receptor expression. In fact, the present study indicates an association of increasing natriuresis, reciprocal changes in renal AngII receptors and intracellular pathway proteins with the fall in blood pressure levels observed in TSHR rats compared with age-matched SSHR rats.

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Verapamil prevents insulin antinatriuresis in euglycemic rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1992.262.6.r1145 ◽

1992 ◽

Vol 262 (6) ◽

pp. R1145-R1148 ◽

Cited By ~ 2

Author(s):

A. K. Gupta ◽

R. Clark ◽

K. A. Kirchner

Keyword(s):

Angiotensin Ii ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Calcium Entry ◽

Urinary Sodium ◽

Inulin Clearance ◽

Insulin Administration ◽

Lower Baseline

To determine whether calcium entry is necessary for insulin antinatriuresis, urinary sodium excretion was determined before and during euglycemic insulin administration in rats receiving verapamil (10 micrograms.kg-1.min-1) or vehicle. In vehicle rats, insulin reduced sodium excretion from 2.7 +/- 0.5 to 0.98 +/- 0.2 mu eq/min (P less than 0.05) without altering arterial pressure or inulin clearance. Insulin did not reduce sodium excretion in rats receiving verapamil. Baseline mean arterial pressure was lower in verapamil rats than in vehicle rats. To exclude the possibility that lower baseline arterial pressures prevented insulin antinatriuresis, insulin's effect on sodium excretion was determined in rats receiving captopril at a dose that reduced arterial pressure to the level observed in verapamil rats, and in verapamil rats with angiotensin II levels fixed to maintain arterial pressure equivalent to vehicle rats. In captopril rats, insulin reduced (P less than 0.05) sodium excretion from 1.07 +/- 0.3 to 0.3 +/- 0.01 mu eq/min, even though arterial pressure was not different from that in verapamil rats. Insulin failed to reduce sodium excretion in verapamil rats receiving angiotensin II. Thus verapamil prevents insulin antinatriuresis by renal mechanisms related to inhibition of calcium entry. Additionally, insulin antinatriuresis is independent of angiotensin II.

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Angiotensin II and Not Sodium Status is the Major Determinant of the Agonistic/Antagonistic Balance of Saralasin's Actions

Clinical Science ◽

10.1042/cs059075s ◽

1980 ◽

Vol 59 (s6) ◽

pp. 75s-78s ◽

Cited By ~ 3

Author(s):

R. Fagard ◽

A. Amery ◽

P. Lijnen

Keyword(s):

Angiotensin Ii ◽

Sodium Excretion ◽

Sodium Intake ◽

Plasma Renin ◽

Urinary Sodium Excretion ◽

Urinary Sodium ◽

Plasma Angiotensin ◽

Group 3 ◽

Group 2 ◽

Group 1

1. To study which factors determine the balance between the antagonistic and agonistic effects of the angiotensin II analogue [Sar1,Ala8]-angiotensin II (saralasin) in man, saralasin was infused in subjects on a ‘normal’ sodium intake (group 1) during sodium restriction with appropriately elevated plasma angiotensin II levels (group 2) and in sodium-restricted subjects in whom plasma angiotensin II was suppressed by converting enzyme inhibition with captopril (group 3). 2. The action of saralasin was agonistic in group 3, antagonistic in group 2 and variable in group 1. 3. For groups 1 and 2 together the saralasin-induced changes of arterial pressure, of plasma aldosterone and of plasma renin were significantly related to control plasma angiotensin II but also to the 24 h urinary sodium excretion. When group 3 was included the changes remained significantly related to plasma angiotensin II but not to the urinary sodium excretion. 4. The results indicate that angiotensin II and not sodium status determines the agonistic/antagonistic balance of saralasin's actions.

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Effect of Angiotensin II on Urinary Sodium Excretion in Normal Subjects and in Cirrhotic Patients

The American Journal of the Medical Sciences ◽

10.1097/00000441-196812000-00007 ◽

1968 ◽

Vol 256 (6) ◽

pp. 373-379 ◽

Cited By ~ 4

Author(s):

H. Ajzen ◽

U. Andrade ◽

J. P. Cipullo ◽

D. R. Sustovich ◽

O. L. Ramos

Keyword(s):

Angiotensin Ii ◽

Sodium Excretion ◽

Normal Subjects ◽

Urinary Sodium Excretion ◽

Urinary Sodium ◽

Cirrhotic Patients

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Circulating Angiotensin II and Renal Sodium Handling in Man: A Dose-Response Study

Clinical Science ◽

10.1042/cs0850147 ◽

1993 ◽

Vol 85 (2) ◽

pp. 147-156 ◽

Cited By ~ 5

Author(s):

A. R. A. Rahman ◽

J. G. Motwani ◽

C. C. Lang ◽

A. D. Struthers

Keyword(s):

Angiotensin Ii ◽

Dose Response ◽

Sodium Excretion ◽

Response Curve ◽

Statistical Significance ◽

Urinary Sodium Excretion ◽

Urinary Sodium ◽

Dose Response Curve ◽

Sodium Reabsorption ◽

Flat Dose

1. Animal studies have shown that angiotensin II has a biphasic effect on urinary sodium excretion. To examine whether this is also true in man, we studied seven salt-replete male subjects in a single-blind placebo-controlled manner. 2. While undergoing maximum diuresis, subjects were infused with 0, 1, 2, 5 or 10 ng of angiotensin II min−1 kg−1 over 80 min. Subjects were studied while seated, and stood every 20 min for urine collection. 3. Angiotensin II produced a dose-dependent antidiuretic effect. The urine flow rate, in ml/min expressed as the change from baseline with increasing dose of angiotensin, was: + 3.4 ±1.77, −1.26 ±0.49 (P <0.05), −2.75±1.23 (P <0.05), −4.21 ± 0.82 (P <0.05) and −6.51 ±1.07 (P <0.01). 4. In contrast, the effect of angiotensin II on sodium excretion showed a flat dose-response curve beyond 5 ng min−1 kg−1. The urinary sodium excretion, in μmol/min expressed as the change from baseline with increasing dose of angiotensin, was: 9.5 ±21.2, −18.9± 29.6, −37.0±11.6 (P <0.05), −67.7 ± 19.6 (P <0.01) and −63.8±14.3 (P <0.01). 5. The fractional distal reabsorption of sodium, determined by using the lithium clearance technique, showed a rise with all doses of angiotensin II used and reached statistical significance with the top two doses. 6. Unlike antidiuresis, antinatriuresis after graded doses of angiotensin II in human subjects showed a flat dose-response curve beyond 5 ng min−1 kg−1. Pressor doses of angiotensin II also have a significant effect on the distal tubule in promoting sodium reabsorption.

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