Effect of Noradrenaline on Renal Sodium and Water Handling in Euhydrated and Overhydrated Man

1993 ◽  
Vol 85 (4) ◽  
pp. 487-494 ◽  
Author(s):  
Chim C. Lang ◽  
Abdul R. Rahman ◽  
David J. K. Balfour ◽  
Allan D. Struthers
Keyword(s):  
Flow Rate ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Urinary Flow Rate ◽  
Sodium Reabsorption ◽  
Urinary Flow ◽  
Noradrenaline Infusion ◽  
Plasma Vasopressin ◽  
Dose Dependent

1. The renal effects of incremental doses of intravenously infused noradrenaline were evaluated in normal subjects during two different water loads, 5 ml/kg (n = 6) and 20 ml/kg (n = 9), producing conditions of euhydration and overhydration, respectively. 2. Noradrenaline infusion rates ranged from 0.015 to 0.075 μg min−1 kg−1. In the euhydrated subjects, noradrenaline caused a dose-dependent fall in urinary sodium excretion and an increase in urinary flow rate. During overhydration similar doses of noradrenaline caused a fall in urinary sodium excretion but a decrease in urinary flow rate. 3. Although there was no detectable change in glomerular filtration rate, a dose-dependent fall in effective renal plasma flow was observed in both hydration states during noradrenaline infusion. 4. Noradrenaline infusion was associated with a dose-dependent increase in proximal tubular sodium reabsorption as assessed by the lithium clearance method. Fractional reabsorption of sodium by the distal nephron was, however, unchanged by noradrenaline in both hydration states. 5. Plasma vasopressin concentration was unchanged by noradrenaline in euhydrated subjects. The renin-angiotensin-aldosterone axis was stimulated by noradrenaline in both euhydrated and overhydrated subjects. 6. Thus we conclude that plasma circulating noradrenaline has a dose-dependent antinatriuretic effect in man. The antinatriuretic effect of noradrenaline is mediated mainly at the proximal tubule in man. We have also shown that during overhydration, noradrenaline decreased urinary flow rate. In contrast, in euhydrated subjects, noradrenaline increased urinary flow rate with no accompanying changes in plasma vasopressin concentration, which suggests a direct effect of noradrenaline on the renal tubular permeability to water.

Dependence of Urinary Prostaglandin E2 Excretion on Urinary Volume Rather than Solute Handling or Segmental Nephron Function in Man

1984 ◽  
Vol 67 (4) ◽  
pp. 413-420 ◽  
Author(s):  
Sming Kaojarern ◽  
Polavat Chennavasin ◽  
Ann Burdette ◽  
William B. Campbell ◽  
D. Craig Brater
Keyword(s):  
Prostaglandin E2 ◽  
Sodium Excretion ◽  
Fluid Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Urinary Flow ◽  
Urinary Volume ◽  
Water Loading ◽  
Wide Range ◽  
Ad Libitum

1. Eight normal subjects underwent water loading alone and water loading plus 40 mg of frusemide IV, fluid intake ad libitum alone and fluid intake ad libitum plus frusemide, plus each of the preceding after pretreatment with indomethacin. 2. After frusemide administration, increases in urinary sodium excretion paralleled increases in urinary volume, and urinary prostaglandin E2 (PGE2) excretion correlated closely with sodium excretion (y = 1.03x −0.28; r = 0.940; P<.0001). 3. In the absence of the diuretic, urinary volume varied over a wide range with little change in sodium excretion. Again, urinary PGE2 excretion correlated with urinary sodium excretion (y = 0.12x + 0.05; r = 0.789; P<.002). However, the correlation differed markedly from that observed in the studies with frusemide. 4. Expressing urinary PGE2 excretion as a function of urinary volume for all of the studies resulted in a highly significant correlation (y = 10.7x −0.70; r = 0.975; P<.0001). 5. Multiple and stepwise regression analyses assessing the correlation of urinary PGE2 excretion with urinary flow rate and with indices of function of various nephron segments indicate that the correlation with urinary PGE2 could be predominantly accounted for by urinary volume. 6. We conclude that in the condition of this study in man, urinary PGE2 excretion is a correlate of urinary volume.

Plasma Vasopressin Levels and Urinary Sodium Excretion during Cardiopulmonary Bypass with and without Pulsatile Flow

1981 ◽  
Vol 32 (1) ◽  
pp. 63-67 ◽  
Author(s):  
Frederick H. Levine ◽  
Daniel M. Philbin ◽  
Katsuakira Kono ◽  
Cecil H. Coggins ◽  
Clifton W. Emerson ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Pulsatile Flow ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Plasma Vasopressin

The control of sodium excretion

1978 ◽  
Vol 235 (3) ◽  
pp. F163-F173 ◽  
Author(s):  
H. E. de Wardener
Keyword(s):  
Proximal Tubule ◽  
Sodium Excretion ◽  
Collecting Duct ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Sodium Reabsorption ◽  
Loop Of Henle ◽  
Salt Loading ◽  
Large Fluctuations

The kidneys of a normal man filter approximately 24,000 meq sodium/day, reabsorb about 23,900, and yet can make a 1--2 meq change in 24-h urinary sodium excretion. The control of urinary sodium excretion, therefore, depends, first, on ensuring that the bulk of the sodium is reabsorbed, a function which is carried out in the proximal tubule and ascending loop of Henle. Second, it depends on adjusting the reabsorption of the small quantity of sodium which is delivered into the collecting duct so that the amount excreted in the urine is that required to maintain sodium balance. The bulk reabsorptive mechanisms can be considered as buffers to prevent large fluctuations in the amount of sodium delivered to the collecting duct, thus facilitating the fine adjustments of reabsorption which are made at this site. In conditions other than extreme salt loading or deprivation, changes in sodium reabsorption in the proximal tubule and loop of Henle probably have little, if any, effect on urinary sodium excretion. Sodium reabsorption in the proximal tubule and the collecting duct appears to be influenced by unidentified circulating substances.

scholarly journals Plasma vasopressin levels and urinary sodium excretion during cardiopulmonary bypass

1979 ◽  
Vol 77 (4) ◽  
pp. 582-585 ◽  
Author(s):  
Daniel M. Philbin ◽  
Cecil H. Coggins ◽  
Clifton W. Emerson ◽  
Frederick H. Levine ◽  
Mortimer J. Buckley
Keyword(s):  
Cardiopulmonary Bypass ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Plasma Vasopressin

Age-dependent renal effects of intrarenal dopamine infusion

1984 ◽  
Vol 247 (1) ◽  
pp. R212-R216 ◽  
Author(s):  
J. C. Pelayo ◽  
R. D. Fildes ◽  
P. A. Jose
Keyword(s):  
Dopamine Receptors ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Urinary Flow Rate ◽  
Urinary Flow ◽  
Renal Effects ◽  
Dopamine Infusion ◽  
Group Iii ◽  
Group I ◽  
Age Dependent

Three groups of anesthetized puppies 16.4 +/- 1.2 (group I), 29.6 +/- 1.6 (group II), and 49.8 +/- 2.5 (group III) days of age were used to assess the renal response to graded doses of dopamine infusion into the renal artery. Dopamine infusion at 1 microgram X kg-1 X min-1 increased renal blood flow (RBF) from 3.61 +/- 0.31 to 4.22 +/- 0.43 ml X min-1 X g kidney wet wt-1 (P less than 0.05) only in the older puppies (group III). Glomerular filtration rate (GFR) increased in groups II and III from control values of 0.69 +/- 0.14 and 0.61 +/- 0.08 to 1.08 +/- 0.19 and 0.83 +/- 0.05 ml X min-1 X g kidney wet wt-1, respectively (P less than 0.05). However, urinary flow rate and sodium excretion were variably affected. Because dopamine is known to stimulate both alpha- and beta-adrenoceptors in addition to dopamine receptors, two additional groups of puppies 11.2 +/- 1.2 (group IV) and 72.8 +/- 2.4 (group V) days of age were studied to evaluate the renal effects of dopamine during the continuous intrarenal infusion of phentolamine and nadolol (an alpha- and a beta-adrenergic blocker, respectively). Dopamine elicited increases in RBF only in the older puppies (P less than 0.05). GFR, urinary flow rate, and sodium excretion increased in both groups; however, the magnitude of the change was greater for each parameter in the older group (P less than 0.05). These experiments suggest a maturational process for specific dopamine receptors and/or effector response, which may affect the observed age-dependent increases in RBF, GFR, and renal sodium handling.

scholarly journals Vascular Control of Kidney Epithelial Transporters

2021 ◽  
Author(s):  
Matthew A. Sparks ◽  
Emre Dilmen ◽  
Donna L. Ralph ◽  
Fitra Rianto ◽  
Thien A Hoang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Sodium Transporters ◽  
Sodium Transporter ◽  
Transporter Expression ◽  
Specific Deletion

A major pathway in hypertension pathogenesis involves direct activation of Ang II (AT1) receptors in the kidney, stimulating sodium reabsorption. AT1 receptors in tubular epithelia control expression and stimulation of sodium transporters and channels. Recently, we found reduced blood pressure and enhanced natriuresis in mice with cell-specific deletion of AT1 receptors in smooth muscle (SMKOs). While impaired vasoconstriction and preserved renal blood flow might contribute to exaggerated urinary sodium excretion in SMKOs, we considered whether alterations in sodium transporter expression might also play a role and therefore carried out a proteomic analysis of key sodium transporters and associated proteins. Here we show that levels of Na+-K+-2Cl- cotransporter isoform 2 (NKCC2) and Na+/H+ exchanger isoform 3 (NHE3) are reduced at baseline in SMKOs, accompanied by attenuated natriuretic and diuretic responses to furosemide. During Ang II hypertension, we find widespread remodeling of transporter expression in wild-type mice with significant increases in levels of total NCC, phosphorylated-NCCps71, and NKCC2-P, along with the cleaved, activated forms of the a- and g-ENaC. However, the increases in a- and g-ENaC with Ang II were substantially attenuated in SMKOs. This was accompanied by reduced natriuretic response to amiloride. Thus, enhanced urinary sodium excretion observed after cell-specific deletion of AT1 receptors from smooth muscle cells is associated with altered sodium transporter abundance across epithelia in multiple nephron segments. These findings suggest a system of vascular-epithelial cross-talk in the kidney, modulating expression of sodium transporters and contributing to regulation of pressure-natriuresis.

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

1993 ◽  
Vol 85 (2) ◽  
pp. 147-156 ◽  
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.

Proximal tubule response in aldosterone escape

1989 ◽  
Vol 256 (1) ◽  
pp. R86-R90 ◽  
Author(s):  
J. M. Gonzalez-Campoy ◽  
J. Kachelski ◽  
J. C. Burnett ◽  
J. C. Romero ◽  
J. P. Granger ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Reabsorption ◽  
Hormonal Changes ◽  
Proximal Tubular ◽  
Temporal Profiles

The response of the proximal tubule to chronic aldosterone administration (15 micrograms.kg-1.day-1) was evaluated in eight conscious female mongrel dogs. Temporal profiles between hemodynamic and hormonal changes and the fractional excretions of sodium and lithium were established. Aldosterone infusion resulted in a significant decrease in urinary sodium excretion from 9.2 +/- 1.3 to 5.8 +/- 0.9 meq/h after 1 day, returning to normal by the 5th day. These changes in urinary sodium excretion were associated with significant elevations of the mean arterial pressure (MAP) from 105 +/- 5 to 111 +/- 6 mmHg and plasma atrial natriuretic factor concentrations (ANF) from 30 +/- 2 to 57 +/- 7 pg/ml beginning the 1st day of infusion. Plasma renin activity (PRA), on the other hand, was depressed by aldosterone, falling below the level of detectability. The fractional excretion of lithium increased significantly by day 2 of aldosterone infusion (from 29 +/- 3 to 44 +/- 6%), reflecting the proximal tubular response to the above changes. We conclude that the proximal tubule responds to increases in MAP and ANF and decreases in PRA during aldosterone infusion by decreasing sodium reabsorption. Subsequent nephron segments must also respond to the volume expansion produced by aldosterone, since the sustained proximal tubule natriuretic response is insufficient to explain all of escape.

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