Normotensive sodium loading in conscious dogs: regulation of renin secretion during β-receptor blockade

2009 ◽  
Vol 296 (2) ◽  
pp. R428-R435 ◽  
Author(s):  
Peter Bie ◽  
Simon Mølstrøm ◽  
Søren Wamberg
Keyword(s):  
Sodium Excretion ◽  
Renin Secretion ◽  
Conscious Dogs ◽  
Renal Nerves ◽  
Receptor Blockade ◽  
Juxtaglomerular Cells ◽  
Ang Ii ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Per Se

Renin secretion is regulated in part by renal nerves operating through β1-receptors of the renal juxtaglomerular cells. Slow sodium loading may decrease plasma renin concentration (PRC) and cause natriuresis at constant mean arterial blood pressure (MAP) and glomerular filtration rate (GFR). We hypothesized that in this setting, renin secretion and renin-dependent sodium excretion are controlled by via the renal nerves and therefore are eliminated or reduced by blocking the action of norepinephrine on the juxtaglomerular cells with the β1-receptor antagonist metoprolol. This was tested in conscious dogs by infusion of NaCl (20 μmol·kg−1·min−1 for 180 min, NaLoad) during regular or low-sodium diet (0.03 mmol·kg−1·day−1, LowNa) with and without metoprolol (2 mg/kg plus 0.9 mg·kg−1·h−1). Vasopressin V2 receptors were blocked by Otsuka compound OPC31260 to facilitate clearance measurements. Body fluid volume was maintained by servocontrolled fluid infusion. Metoprolol per se did not affect MAP, heart rate, or sodium excretion significantly, but reduced PRC and ANG II by 30–40%, increased plasma atrial natriuretic peptide (ANP), and tripled potassium excretion. LowNa per se increased PRC (+53%), ANG II (+93%), and aldosterone (+660%), and shifted the vasopressin function curve to the left. NaLoad elevated plasma [Na+] by 4.5% and vasopressin by threefold, but MAP and plasma ANP remained unchanged. NaLoad decreased PRC by ∼30%, ANG II by ∼40%, and aldosterone by ∼60%, regardless of diet and metoprolol. The natriuretic response to NaLoad was augmented during metoprolol regardless of diet. In conclusion, PRC depended on dietary sodium and β1-adrenergic control as expected; however, the acute sodium-driven decrease in PRC at constant MAP and GFR was unaffected by β1-receptor blockade demonstrating that renin may be regulated without changes in MAP, GFR, or β1-mediated effects of norepinephrine. Low-sodium diet augments vasopressin secretion, whereas ANP secretion is reduced.

Effect of renal denervation on the suppression of renin secretion by vasopressin in conscious dogs

1984 ◽  
Vol 247 (6) ◽  
pp. F881-F887 ◽  
Author(s):  
L. C. Gregory ◽  
I. A. Reid
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Conscious Dogs ◽  
Reflex Response ◽  
Renal Nerves ◽  
Ang Ii ◽  
Before And After

Previous studies have shown that the inhibition of renin secretion by vasopressin (AVP) in conscious dogs is related to vasoconstrictor activity and may be a reflex response mediated by the renal nerves. The aim of the present experiments was to determine whether the suppression of plasma renin activity (PRA) by AVP is blocked by renal denervation. AVP and, for comparison, angiotensin II (ANG II) were infused intravenously for 45 min in seven conscious dogs before and after bilateral renal denervation. Before denervation, AVP infusion at 0.2 and 1.0 ng X kg-1 X min-1 suppressed PRA from 7.4 +/- 1.1 to 4.7 +/- 1.0 (P less than 0.01) and from 7.9 +/- 1.8 to 3.8 +/- 0.8 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. ANG II infusion at 5.0 and 10.0 ng X kg-1 X min-1 decreased PRA from 7.5 +/- 2.3 to 2.5 +/- 0.7 (P less than 0.01) and from 6.0 +/- 1.1 to 1.8 +/- 0.4 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. One to three weeks following renal denervation, PRA had decreased from 6.7 +/- 1.3 to 2.9 +/- 0.5 ng X ml-1 X 3 h-1 (P less than 0.01), and renal norepinephrine was undetectable. After denervation, neither AVP infusion at 0.2 (3.0 +/- 0.5 to 2.4 +/- 0.4 ng X ml-1 X 3 h-1) nor 1.0 ng X kg-1 X min-1 (3.1 +/- 0.8 to 2.8 +/- 1.0 ng X ml-1 X 3 h-1) suppressed PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

Interactions between angiotensin II and renal nerves during chronic sodium deprivation

1988 ◽  
Vol 255 (5) ◽  
pp. F823-F827 ◽  
Author(s):  
H. L. Mizelle ◽  
J. E. Hall ◽  
L. L. Woods
Keyword(s):  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Left Kidney ◽  
Control Period ◽  
Urine Volume ◽  
Renal Nerves ◽  
Ang Ii ◽  
Sodium Potassium ◽  
Low Sodium Diet ◽  
Low Sodium

The aim of this study was to examine the importance of the renal nerves in mediating the sodium-retaining actions of angiotensin II (ANG II) during chronic sodium deprivation. In seven female dogs the left kidney was denervated and the urinary bladder was split, allowing continuous urine collection from separate innervated and denervated kidneys in the same dog. The dogs were maintained on a low-sodium diet (7 meq/day) for 9 days and then infused with the converting-enzyme inhibitor captopril (CAP, 14 micrograms.kg-1.min-1, 7 days) followed by CAP plus ANG II (10 ng.kg-1.min-1, 7 days). Mean arterial pressure (MAP) fell from a control of 88 +/- 4 (average for 5 days preceding CAP) to 65 +/- 3 mmHg during CAP. Infusion of ANG II along with CAP restored MAP to 97 +/- 5 mmHg. There were no significant differences in urine volume or sodium, potassium, chloride, or osmolar excretions between innervated and denervated kidneys during the control period, CAP infusion, or CAP plus ANG II infusion. Norepinephrine content was reduced by 99 +/- 1% in denervated kidneys. Because a differential response was not observed between innervated and denervated kidneys during ANG II blockade or infusion of ANG II, we conclude that the renal nerves do not play a major role in mediating the sodium-retaining effects of ANG II during chronic sodium restriction.

Role of brain serotonergic pathways and hypothalamus in regulation of renin secretion

1987 ◽  
Vol 253 (1) ◽  
pp. R179-R185
Author(s):  
E. Gotoh ◽  
K. Murakami ◽  
T. D. Bahnson ◽  
W. F. Ganong
Keyword(s):  
Plasma Renin ◽  
Dorsal Raphe ◽  
Raphe Nucleus ◽  
Renin Secretion ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Head Up Tilt ◽  
Dorsal Raphé

To investigate the role of brain serotonergic neurons in the regulation of renin secretion, we measured changes in plasma renin activity (PRA), and, in some instances, plasma renin concentration (PRC), plasma angiotensinogen, and plasma adrenocorticotropic hormone (ACTH) in rats with lesions of the dorsal raphe nucleus and lesions of the paraventricular nuclei, dorsomedial nuclei, and ventromedial nuclei of the hypothalamus. We also investigated the effects of p-chloroamphetamine (PCA), immobilization, head-up tilt, and a low-sodium diet in the rats with dorsal raphe, paraventricular, and dorsomedial lesions. Lesions of the dorsal raphe nucleus abolished the increase in PRA produced by PCA but had no effect on the increase produced by immobilization, head-up tilt, and a low-sodium diet. Paraventricular lesions, which abolish the increase in plasma ACTH produced by PCA, immobilization, and head-up tilt, decreased plasma angiotensinogen. The paraventricular lesions abolished the PRA and the PRC responses to PCA and the PRA but not PRC response to immobilization, head-up tilt, and a low-sodium diet. The ventromedial lesions abolished the PRA and PRC responses to PCA and did not reduce plasma angiotensinogen. The data suggest that paraventricular lesions depress angiotensinogen production by the liver and that the paraventricular and ventromedial nuclei are part of the pathway by which serotonergic discharges increase renin secretion. They also suggest that the serotonergic pathway does mediate the increases in renin secretion produced by immobilization, head-up tilt, and a low-sodium diet.

Control of adrenal cell proliferation by AT1 receptors in response to angiotensin II and low-sodium diet

1999 ◽  
Vol 276 (2) ◽  
pp. E303-E309 ◽  
Author(s):  
Pauline E. McEwan ◽  
Gavin P. Vinson ◽  
Christopher J. Kenyon
Keyword(s):  
Cell Proliferation ◽  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Ang Ii ◽  
Adrenal Cell ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Glomerulosa Cells

The effects of angiotensin II (ANG II), the angiotensin type 1 (AT1) receptor antagonist losartan, and low-sodium diet on rat adrenal cell proliferation were studied in vivo with immunocytochemistry. Both ANG II and low-sodium diet increased proliferation of endothelial cells of the zona glomerulosa. Losartan prevented ANG II-induced hyperplasia of glomerulosa cells but not the effects of a low-sodium diet. Glomerulosa cells after ANG II + losartan treatment appeared hypertrophied compared with those of controls. Proliferative effects of ANG II and low-sodium diet in the reticularis were blocked by losartan. No changes were seen in the fasciculata. Proliferation in the medulla was increased with losartan, was decreased by ANG II, but was unaffected by low-sodium diet. In conclusion, 1) cell hypertrophy and proliferation of glomerulosa cells are mediated by AT1 receptor-dependent and -independent processes, 2) proliferation of reticularis cells is controlled by AT1 receptors, and 3) reciprocal control of chromaffin cell proliferation by ANG II may involve indirect AT1-dependent processes.

Adrenergic control of renin during dietary sodium deprivation in conscious dogs

1989 ◽  
Vol 256 (6) ◽  
pp. E863-E871 ◽  
Author(s):  
H. Hisa ◽  
Y. H. Chen ◽  
K. J. Radke ◽  
J. L. Izzo ◽  
C. D. Sladek ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Conscious Dogs ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Adrenergic Stimulation ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Dietary Sodium Restriction

These experiments evaluated the contribution of alpha- and beta-adrenergic stimulation to plasma renin activity (PRA) during early and long-term dietary sodium restriction, compared with normal sodium intake. Uninephrectomized conscious dogs with catheters in the aorta, vena cava, and remaining renal artery were studied during normal sodium diet (approximately 70 meq/day), after 2-3 days of low-sodium diet (5-7 meq/day), and after greater than or equal to 2 wk of low-sodium diet. Direct renal arterial (ira) infusion of phenoxybenzamine plus propranolol decreased PRA by similar proportions (39-48%) during all three states of dietary sodium intake. The PRA achieved after adrenergic blockade remained higher (P less than 0.05) during early and long-term sodium restriction than during normal sodium intake. The effect on PRA of ira infusion of propranolol alone was not different from that of phenoxybenzamine plus propranolol during normal or low-sodium diet, and the magnitude of decrease in PRA during low-sodium diet was the same whether propranolol (1 microgram.kg-1.min-1) was infused ira or intravenously. In summary, beta-adrenergic stimulation accounts for similar proportions of PRA during early and long-term dietary sodium restriction and during normal sodium intake. Renal alpha-adrenoceptors appear to play little or no role in control of PRA under these conditions.

scholarly journals Role of ANG II in mediating somatosensory-induced renal nerve-dependent antinatriuresis in the rat

1998 ◽  
Vol 275 (1) ◽  
pp. R194-R202 ◽  
Author(s):  
Chunlong Huang ◽  
Edward J. Johns
Keyword(s):  
Sodium Excretion ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Renal Nerves ◽  
Ang Ii ◽  
Renal Nerve ◽  
Somatosensory Stimulation ◽  
Two Stages ◽  
The Brain

This study examined the renal nerve-dependent renal hemodynamic and tubular responses to somatosensory stimulation in the anesthetized rat by use of subcutaneously applied capsaicin when the action of ANG II was blocked peripherally or selectively within the brain. Activation of skin somatosensory receptors caused a transient reversible 10–15% increase in blood pressure, and while renal perfusion pressure was regulated at control levels, there was a transient fall in urine flow and sodium excretion even though both renal blood flow and glomerular filtration rate were unchanged. These reflexly induced excretory responses were abolished when the renal nerves were sectioned. Administration of the ANG II AT1-receptor antagonist, losartan, either intravenously at 3 or 10 mg/kg or locally into the lateral cerebroventricles at 15 μg plus 7.5 μg/h, had no effect on capsaicin-induced vasopressor responses but blocked the reductions in urine flow and sodium excretion. These findings are consistent with ANG II being involved in at least two stages in the reflex, one centrally and one at the periphery.

Alterations in Cerebrospinal Fluid Angiotensin II by Sodium Intake in Patients with Essential Hypertension

1989 ◽  
Vol 77 (4) ◽  
pp. 389-394 ◽  
Author(s):  
Minoru Kawamura ◽  
Yuhei Kawano ◽  
Kaoru Yoshida ◽  
Masahito Imanishi ◽  
Satoshi Akabane ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Essential Hypertension ◽  
Sodium Intake ◽  
Ang Ii ◽  
Sodium Depletion ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

1. Angiotensin (ANG) levels were measured in the cerebrospinal fluid of 15 patients with essential hypertension on a high sodium diet for 1 week and on a low sodium diet for a further week. ANGs were determined using a system of extraction by Sep-Pak cartridges followed by h.p.l.c. combined with radioimmunoassay. 2. Sodium depletion resulted in increases of ANG II in the cerebrospinal fluid from 1.16 ± 0.38 (sem) to 1.83 ± 0.43 fmol/ml (P < 0.01) and of ANG III from 0.65 ± 0.11 to 0.86 ± 0.15 fmol/ml (P < 0.01). 3. The ANG II level in the cerebrospinal fluid was found to be unchanged and recovery of added ANG II was approximately 90%, even after incubation for 3 h, on both diets. Thus, it is unlikely that ANG II is produced or degraded in the cerebrospinal fluid in vitro. 4. There was no significant correlation between the cerebrospinal fluid and the plasma ANG II concentration on the low sodium diet. 5. These results suggest that the cerebrospinal fluid ANG II level increases with sodium depletion, and that the effect of the level of ANG II on the activity of the angiotensin-forming system in the central nervous system may be assessed by determination of ANG II in the cerebrospinal fluid in patients with essential hypertension.

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