The Relationship between Sodium Excretion and Renin Secretion by the Perfused Kidney

1975 ◽  
Vol 150 (3) ◽  
pp. 728-734 ◽  
Author(s):  
M. H. Humphreys ◽  
I. A. Reid ◽  
R. C. Ufferman ◽  
R. A. Lieberman ◽  
L. E. Earley
Keyword(s):  
Sodium Excretion ◽  
Renin Secretion ◽  
The Relationship ◽  
Perfused Kidney

Normotensive sodium loading in normal man: regulation of renin secretion during β-receptor blockade

2009 ◽  
Vol 296 (2) ◽  
pp. R436-R445 ◽  
Author(s):  
Simon Mølstrøm ◽  
Nils H. Larsen ◽  
Jane A. Simonsen ◽  
Remon Washington ◽  
Peter Bie
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Venous Pressure ◽  
Macula Densa ◽  
Renin Secretion ◽  
Sodium Reabsorption ◽  
Plasma Sodium ◽  
Adrenergic Blockade ◽  
Saline Loading

Saline administration may change renin-angiotensin-aldosterone system (RAAS) activity and sodium excretion at constant mean arterial pressure (MAP). We hypothesized that such responses are elicited mainly by renal sympathetic nerve activity by β1-receptors (β1-RSNA), and tested the hypothesis by studying RAAS and renal excretion during slow saline loading at constant plasma sodium concentration (Na+ loading; 12 μmol Na+·kg−1·min−1 for 4 h). Normal subjects were studied on low-sodium intake with and without β1-adrenergic blockade by metoprolol. Metoprolol per se reduced RAAS activity as expected. Na+ loading decreased plasma renin concentration (PRC) by one-third, plasma ANG II by one-half, and plasma aldosterone by two-thirds (all P < 0.05); surprisingly, these changes were found without, as well as during, acute metoprolol administration. Concomitantly, sodium excretion increased indistinguishably with and without metoprolol (16 ± 2 to 71 ± 14 μmol/min; 13 ± 2 to 55 ± 13 μmol/min, respectively). Na+ loading did not increase plasma atrial natriuretic peptide, glomerular filtration rate (GFR by 51Cr-EDTA), MAP, or cardiac output (CO by impedance cardiography), but increased central venous pressure (CVP) by ∼2.0 mmHg ( P < 0.05). During Na+ loading, sodium excretion increased with CVP at an average slope of 7 μmol·min−1·mmHg−1. Concomitantly, plasma vasopressin decreased by 30–40% ( P < 0.05). In conclusion, β1-adrenoceptor blockade affects neither the acute saline-mediated deactivation of RAAS nor the associated natriuretic response, and the RAAS response to modest saline loading seems independent of changes in MAP, CO, GFR, β1-mediated effects of norepinephrine, and ANP. Unexpectedly, the results do not allow assessment of the relative importance of RAAS-dependent and -independent regulation of renal sodium excretion. The results are compatible with the notion that at constant arterial pressure, a volume receptor elicited reduction in RSNA via receptors other than β1-adrenoceptors, decreases renal tubular sodium reabsorption proximal to the macula densa leading to increased NaCl concentration at the macula densa, and subsequent inhibition of renin secretion.

Ion association. VII. Dependence of calciuresis on natriuresis during sulfate infusion

1961 ◽  
Vol 201 (5) ◽  
pp. 769-773 ◽  
Author(s):  
Mackenzie Walser
Keyword(s):  
Calcium Ion ◽  
Sodium Excretion ◽  
Ion Association ◽  
Free Calcium ◽  
Calcium Excretion ◽  
Sodium Potassium ◽  
Sulfate Ions ◽  
The Relationship ◽  
Complexing Anions ◽  
Sodium Clearance

Sulfate was infused intravenously into dogs as the salt of sodium, potassium, or the organic amine, "tris." Calcium clearance was more closely correlated with sodium clearance than with sulfate excretion. When sodium excretion was low, little calciuresis occurred. The clearance of free calcium ions was calculated, making allowance for the electrostatic association between calcium and sulfate ions in the urine. The relationship between free calcium ion clearance and sodium clearance closely resembled that previously observed during saline or mannitol diuresis. Thus, in the absence of hypercalcemia, calcium excretion in the dog, in these experiments, is dependent primarily on the simultaneous sodium excretion, which determines free calcium ion excretion, and secondarily on the concentration of complexing anions in the urine, which determines how much additional calcium is excreted in bound form.

Interaction of renal beta 1-adrenoceptors and prostaglandins in reflex renin release

1983 ◽  
Vol 244 (4) ◽  
pp. F418-F424 ◽  
Author(s):  
U. Kopp ◽  
G. F. DiBona
Keyword(s):  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Prostaglandin Synthesis ◽  
Urinary Sodium ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Renal Perfusion Pressure

Anesthetized dogs with isolated carotid sinus preparation were used to examine the mechanisms involved in the increase in renin secretion rate produced by carotid baroreceptor reflex renal nerve stimulation (RNS) at constant renal perfusion pressure. Lowering carotid sinus pressure by 41 +/- 5 mmHg for 10 min increased mean arterial pressure and heart rate, caused no or minimal renal hemodynamic changes, decreased urinary sodium excretion, and increased renin secretion rate. Metoprolol, a beta 1-adrenoceptor antagonist, given in the renal artery, did not affect the decrease in urinary sodium excretion but attenuated the increase in renin secretion rate, from 1,764 +/- 525 to 412 +/- 126 ng/min (70 +/- 8%). Indomethacin or meclofenamate, prostaglandin synthesis inhibitors, did not affect the decrease in urinary sodium excretion but attenuated the increase in renin secretion rate, from 1,523 +/- 416 to 866 +/- 413 ng/min (51 +/- 18%). Addition of metoprolol to indomethacin-pretreated dogs attenuated the increase in renin secretion rate from 833 +/- 327 to 94 +/- 60 ng/min (86 +/- 10%). These results indicate that reflex RNS at constant renal perfusion pressure results in an increase in renin secretion rate that is largely mediated by renal beta 1-adrenoceptors and is partly dependent on intact renal prostaglandin synthesis. The beta 1-adrenoceptor-mediated increase in renin secretion rate is independent of and not in series with renal prostaglandins.

Dissociation of urinary kallikrein activity and salt and water excretion in the rat

1986 ◽  
Vol 250 (6) ◽  
pp. F1082-F1089 ◽  
Author(s):  
D. M. Pollock ◽  
M. I. Butterfield ◽  
J. L. Ader ◽  
W. J. Arendshorst
Keyword(s):  
Sodium Excretion ◽  
Linear Regression Analysis ◽  
Urine Flow ◽  
Urinary Kallikrein ◽  
Water Excretion ◽  
Time Control ◽  
Dose Dependent Decrease ◽  
State Group ◽  
Kallikrein Activity ◽  
The Relationship

Experiments were designed to examine the relationship, if any, between urinary kallikrein activity (amidolytic assay) and sodium and water excretion in 12-wk-old Munich-Wistar rats. Five groups of animals were studied: euvolemic, saline-expanded and water-loaded anesthetized rats, and euvolemic and saline-expanded conscious restrained rats. Following surgery, animals were allowed to stabilize (60-180 min) and reach a steady-state urine flow. By design, basal sodium and/or water excretion varied markedly among groups as a function of hydration state. Group means for sodium excretion and urine flow ranged from 0.8 to 12.4 mu eq/min and 6 to 112 microliter/min, respectively. In contrast, neither active nor total urinary kallikrein activity differed significantly among the five groups. In anesthetized euvolemic rats, intravenous administration of aprotinin produced a dose-dependent decrease in urinary kallikrein activity. The greatest inhibition of 93 +/- 3% (active) and 72 +/- 10% (total) was observed with a dose of 5,000 kallikrein inhibiting units (KIU)/kg and 1,000 KIU X kg-1 X min-1. This dose produced a significant decrease in active and total kallikrein activity in each group (P less than 0.001). However, sodium and water excretion were unchanged in aprotinin-treated rats and similar to values in vehicle-treated time-control groups. Linear regression analysis revealed no significant correlations between urinary kallikrein activity and sodium excretion or urine flow either among or within groups. These results indicate that urinary kallikrein activity is not related to acute sodium and water homeostasis in anesthetized or conscious rats.

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