Role of endogenous central opioid mechanisms in maintenance of body sodium balance

1995 ◽  
Vol 268 (3) ◽  
pp. R723-R730 ◽  
Author(s):  
D. R. Kapusta ◽  
J. C. Obih
Keyword(s):  
Sodium Intake ◽  
Dietary Sodium ◽  
Opioid Antagonist ◽  
Sodium Balance ◽  
Sodium Restriction ◽  
Sprague Dawley ◽  
Intracerebroventricular Infusion ◽  
Sprague Dawley Rats ◽  
Body Sodium

The role of endogenous central opioids in the regulation of renal function was studied in Sprague-Dawley rats. In metabolism studies, changes in sodium balance were examined during normal dietary sodium intake (days 1-7; Na+ of 174 meq/kg) and sodium restriction (days 8-14; Na+ of 4.0 meq/kg). The influence of endogenous central opioids was investigated by repeating the protocol in the same rats during intracerebroventricular infusion of the opioid antagonist naltrexone methylbromide (NMBR). Intracerebroventricular NMBR did not alter sodium balance in rats fed normal sodium chow. In contrast, on low-sodium days 8 and 9, rats exhibited a more negative sodium balance during intracerebroventricular NMBR (day 8; -1,191 +/- 37 mu eq) compared with respective predrug control levels (day 8; -641 +/- 39 mu eq). Subcutaneous NMBR did not alter renal adaptation to sodium restriction. Thus central opioids are not involved in the maintenance of sodium balance during normal sodium intake. However, when dietary sodium is restricted, central opioid pathways are activated as a mechanism to maximally retain sodium.

scholarly journals Sites and sources of sympathoexcitation in obese male rats: role of brain insulin

2020 ◽  
Vol 318 (3) ◽  
pp. R634-R648 ◽  
Author(s):  
Zhigang Shi ◽  
Ding Zhao ◽  
Priscila A. Cassaglia ◽  
Virginia L. Brooks
Keyword(s):  
Insulin Receptors ◽  
Male Rats ◽  
Melanocortin Receptor ◽  
Sprague Dawley ◽  
Intracerebroventricular Infusion ◽  
Sprague Dawley Rats ◽  
Y1 Receptors ◽  
The Brain ◽  
Obese Male

In males, obesity increases sympathetic nerve activity (SNA), but the mechanisms are unclear. Here, we investigate insulin, via an action in the arcuate nucleus (ArcN), and downstream neuropathways, including melanocortin receptor 3/4 (MC3/4R) in the hypothalamic paraventricular nucleus (PVN) and dorsal medial hypothalamus (DMH). We studied conscious and α-chloralose-anesthetized Sprague-Dawley rats fed a high-fat diet, which causes obesity prone (OP) rats to accrue excess fat and obesity-resistant (OR) rats to maintain fat content, similar to rats fed a standard control (CON) diet. Nonspecific blockade of the ArcN with muscimol and specific blockade of ArcN insulin receptors (InsR) decreased lumbar SNA (LSNA), heart rate (HR), and mean arterial pressure (MAP) in OP, but not OR or CON, rats, indicating that insulin supports LSNA in obese males. In conscious rats, intracerebroventricular infusion of insulin increased MAP only in OP rats and also improved HR baroreflex function from subnormal to supranormal. The brain sensitization to insulin may elucidate how insulin can drive central SNA pathways when transport of insulin across the blood-brain barrier may be impaired. Blockade of PVN, but not DMH, MC3/4R with SHU9119 decreased LSNA, HR, and, MAP in OP, but not OR or CON, rats. Interestingly, nanoinjection of the MC3/4R agonist melanotan II (MTII) into the PVN increased LSNA only in OP rats, similar to PVN MTII-induced increases in LSNA in CON rats after blockade of sympathoinhibitory neuropeptide Y Y1 receptors. ArcN InsR expression was not increased in OP rats. Collectively, these data indicate that obesity increases SNA, in part via increased InsR signaling and downstream PVN MC3/4R.

Renal nerves in renal adaptation to dietary sodium restriction

1983 ◽  
Vol 245 (3) ◽  
pp. F322-F328 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin
Keyword(s):  
Renal Denervation ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Body Sodium ◽  
Renal Adaptation

To assess the physiologic importance of the renal nerves in the renal mechanisms for the maintenance of body sodium balance, renal adaptation to normal and low sodium diet was evaluated in conscious Sprague-Dawley male rats before and 8 days after recovery from bilateral surgical-pharmacological renal denervation. Renal denervation was confirmed in every rat at the end of the study by absence of renal vasoconstriction to splanchnic nerve stimulation and loss of renal tissue norepinephrine content. Daily sodium balance, defined as the difference between dietary sodium intake and urinary sodium excretion, was positive with the normal sodium diet before and after bilateral renal denervation. Prior to bilateral renal denervation, changing to the low sodium diet was associated with a diminishingly negative sodium balance for 3 days that became progressively positive thereafter. After bilateral renal denervation, changing to the low sodium diet was associated with a continuous and progressively negative sodium balance. We conclude that intact renal innervation is required for normal renal sodium conservation and maintenance of body sodium balance during dietary sodium restriction.

scholarly journals Role of endogenous peripheral opioid mechanisms in renal function.

1994 ◽  
Vol 4 (10) ◽  
pp. 1792-1797
Author(s):  
G F DiBona ◽  
S Y Jones
Keyword(s):  
Renal Function ◽  
Adaptive Response ◽  
Dietary Sodium ◽  
Opioid Antagonist ◽  
Sodium Restriction ◽  
Hypertensive Rats ◽  
Functional Responses ◽  
Spontaneously Hypertensive ◽  
Opioid Mechanisms

The role of endogenous peripheral opioid mechanisms in renal function was evaluated in normotensive and hypertensive rats. Intravenous naloxone methylbromide, a quaternary opioid antagonist with limited ability to cross the blood-brain barrier, was used to inhibit endogenous peripheral opioid mechanisms. In normotensive rats, the opioid antagonist impaired the normal renal adaptive response to dietary sodium restriction. In spontaneously hypertensive rats, the opioid antagonist did not affect the renal functional responses to acute environmental stress. These data indicate that, depending on the nature of the intervention, a role for endogenous peripheral opioid mechanisms in the renal function responses may be identified.

Role of renal nerves in maintaining sodium balance in unrestrained conscious rats

1985 ◽  
Vol 249 (6) ◽  
pp. F819-F826 ◽  
Author(s):  
E. Fernandez-Repollet ◽  
C. R. Silva-Netto ◽  
R. E. Colindres ◽  
C. W. Gottschalk
Keyword(s):  
Blood Pressure ◽  
Renal Denervation ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Sodium Restriction ◽  
Low Sodium ◽  
Dietary Sodium Restriction

This study was designed to investigate the effects of bilateral renal denervation on sodium and water balance, the renin-angiotensin system, and systemic blood pressure in unrestrained conscious rats maintained on a normal- or low-sodium diet. Renal denervation was proven by chemical and functional tests. Both bilaterally denervated rats (n = 18) and sham-denervated rats (n = 15) maintained positive sodium balance while on a normal sodium intake. Both groups were in negative sodium balance for 1 day after dietary sodium restriction was instituted but were in positive sodium balance for the following 9 days. Systolic blood pressure was higher in sham-denervated (115 +/- 3 mmHg) than in denervated rats (102 +/- 3 mmHg) while on a normal diet (P less than 0.05) and remained so during sodium restriction. Plasma renin concentration (PRC) and plasma aldosterone concentration (PAC) were significantly diminished in the denervated rats during normal sodium intake (P less than 0.05). After dietary sodium restriction, PRC increased in both groups but remained significantly lower in the denervated rats (P less than 0.05). Following dietary sodium restriction, PAC also increased significantly to levels that were similar in both groups of rats. These results demonstrate that awake unrestrained growing rats can maintain positive sodium balance on a low sodium intake even in the absence of the renal nerves. However, efferent renal nerve activity influenced plasma renin activity in these animals.

Commercial rodent diets contain more sodium than rats need

2005 ◽  
Vol 288 (2) ◽  
pp. F428-F431 ◽  
Author(s):  
Wesley Martus ◽  
Dennis Kim ◽  
Jeffrey L. Garvin ◽  
William H. Beierwaltes
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Caloric Intake ◽  
Sodium Content ◽  
Dietary Sodium ◽  
Renal Physiology ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Pelleted Diet ◽  
Experimental Group

The dietary sodium requirements for rats have been a matter of debate. Our hypothesis was that normal commercial rodent chow contains sodium in excess of dietary needs and that this could have a significant impact on cardiovascular and renal physiology. To investigate dietary sodium requirements, 3-wk-old weanling Sprague-Dawley rats were fed a custom pelleted diet containing no sodium that was isocaloric to normal commercial rodent chow. These rats were provided with two drinking bottles; one contained water, and the other contained 0.5% NaCl. Thus they could choose and consume sodium as needed. Age-matched controls received normal pelleted Harlan Teklad 22/5 rodent diet (0.5% sodium content) and water ad libitum. Body weight and liquid intake were monitored over 7 wk until the rats were 10 wk old. At the end of the study, blood pressure was recorded. Weekly sodium intake in the experimental group was only 15% of that reported for rats fed normal rodent chow beginning in the first week postweaning. Growth was identical in the two groups (7.8 ± 0.1 vs. 7.6 ± 0.1 g/day), as was the total fluid volume intake. Blood pressure was significantly lower in the experimental rats compared with controls (96 ± 4 vs. 122 ± 4 mmHg, P < 0.05). These data suggest that, when given the choice, rats will consume significantly less sodium than provided in commercial chow, without any alteration in their growth rate. Rats fed standard commercial rodent chow may consume at least seven times more sodium than is necessary. This suggests commercial rodent diets may force excess sodium to accommodate caloric intake.

Temporal pattern of renin and aldosterone secretion in men: effects of sodium balance

1992 ◽  
Vol 262 (5) ◽  
pp. F871-F877 ◽  
Author(s):  
W. V. Vieweg ◽  
J. D. Veldhuis ◽  
R. M. Carey
Keyword(s):  
Sodium Intake ◽  
Time Lag ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Low Sodium

To investigate the pulsatile nature of basal and stimulated renin and aldosterone secretion, we sampled blood for plasma renin activity (PRA) and plasma aldosterone concentration at 10-min intervals for 24 h in nine normal supine human male subjects after equilibration in high- and low-sodium balance states. We evaluated serial hormonal measures by a quantitative waveform-independent deconvolution technique designed to compute the number, amplitude, and mass of underlying secretory bursts and simultaneously to estimate the presence and extent of basal secretion. For both PRA and aldosterone: 1) burstlike release accounted for greater than or equal to 60% of total secretion and tonic release for less than 40%; 2) there was an 80- to 85-min interpulse interval unchanged by sodium intake; 3) sodium restriction engendered an increase in plasma hormone concentrations by increasing the amount and maximal rate of hormone secreted per burst; 4) low dietary sodium also induced increases in basal hormone secretory rates, suggesting that there may be two regulatory processes driving renin and aldosterone secretion; and 5) PRA was significantly coupled to plasma aldosterone concentration by a 0-, 10-, or 20-min aldosterone lag time in both high- and low-sodium balance. We conclude that both renin and aldosterone are released via a predominantly burstlike mode of secretion; PRA and plasma aldosterone concentrations are positively coupled by a short time lag (0-20 min); and sodium restriction achieves an increase in mean PRA and plasma aldosterone concentration by selective amplitude enhancement of individual hormone secretory bursts and by increased tonic (interburst) basal secretory rates.

Enhanced adrenal renin and aldosterone biosynthesis during sodium restriction in TGR (mREN2)27

1994 ◽  
Vol 267 (4) ◽  
pp. E515-E520 ◽  
Author(s):  
S. Rubattu ◽  
I. Enea ◽  
D. Ganten ◽  
D. Salvatore ◽  
G. Condorelli ◽  
...  
Keyword(s):  
Adrenal Cortex ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Transgenic Rat ◽  
Sodium Restriction ◽  
Sprague Dawley ◽  
Low Sodium ◽  
Sd Rats

The aim of the study was to investigate the relationships between tissue renin and the steroid production in the adrenal cortex during dietary sodium restriction in the transgenic rat (TGR) (mREN2)27. Thus the effects of a 1-wk low-sodium intake (0.04% NaCl) were studied in 5-wk-old male TGR (n = 33, systolic blood pressure = 151 +/- 3 mmHg) and in 24 age- and sex-matched outbred normotensive Sprague-Dawley (SD) rats. Measurements of plasma and tissue hormones were obtained at 0, 4, and 7 days of a low-sodium diet. Sodium restriction caused sustained increases of adrenal renin activity (from 28.5 +/- 3.5 to 87.5 +/- 4.5 ng.mg protein-1.h-1 on day 7) and of adrenal renin mRNA (+63 +/- 13 and +43 +/- 7% on days 4 and 7, respectively), whereas plasma renin activity (from 3.3 +/- 0.3 to 4.4 +/- 0.6 ng.ml-1.h-1) and renal renin activity (from 0.85 +/- 0.25 to 0.7 +/- 0.4 microgram.mg protein-1.h-1) did not change. The stimulation of the adrenal renin-angiotensin system was associated with a large increase of the aldosterone synthase cytochrome P-450 mRNA (+165 +/- 35 and +184 +/- 44%, on days 4 and 7) and of plasma aldosterone levels (from 125 +/- 32 to 338 +/- 59 pg/ml, P < 0.01). In SD rats, in spite of a more consistent increase in renal and circulating renin, mineralocorticoid production did not increase significantly. These results demonstrate that the exaggerated biosynthesis of aldosterone in TGR during sodium restriction is associated with an activation of renin in the adrenal cortex but not in the kidney.

scholarly journals The Effects of Short-Term Changes in Sodium Intake on Plasma Marinobufagenin Levels in Patients with Primary Salt-Sensitive and Salt-Insensitive Hypertension

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1502
Author(s):  
Katarzyna Łabno-Kirszniok ◽  
Agata Kujawa-Szewieczek ◽  
Andrzej Wiecek ◽  
Grzegorz Piecha
Keyword(s):  
Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Sodium Intake ◽  
Left Ventricular ◽  
Primary Hypertension ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Short Term ◽  
Salt Loading ◽  
Dietary Sodium Restriction

Increased marinobufagenin (MBG) synthesis has been suggested in response to high dietary salt intake. The aim of this study was to determine the effects of short-term changes in sodium intake on plasma MBG levels in patients with primary salt-sensitive and salt-insensitive hypertension. In total, 51 patients with primary hypertension were evaluated during acute sodium restriction and sodium loading. Plasma or serum concentrations of MBG, natriuretic pro-peptides, aldosterone, sodium, potassium, as well as hematocrit (Hct) value, plasma renin activity (PRA) and urinary sodium and potassium excretion were measured. Ambulatory blood pressure monitoring (ABPM) and echocardiography were performed at baseline. In salt-sensitive patients with primary hypertension plasma MBG correlated positively with diastolic blood pressure (ABPM) and serum NT-proANP concentration at baseline and with serum NT-proANP concentration after dietary sodium restriction. In this subgroup plasma MBG concentration decreased during sodium restriction, and a parallel increase of PRA was observed. Acute salt loading further decreased plasma MBG concentration in salt-sensitive subjects in contrast to salt insensitive patients. No correlation was found between plasma MBG concentration and left ventricular mass index. In conclusion, in salt-sensitive hypertensive patients plasma MBG concentration correlates with 24-h diastolic blood pressure and dietary sodium restriction reduces plasma MBG levels. Decreased MBG secretion in response to acute salt loading may play an important role in the pathogenesis of salt sensitivity.

scholarly journals Mild DOCA-salt hypertension: sympathetic system and role of renal nerves

2011 ◽  
Vol 300 (5) ◽  
pp. H1781-H1787 ◽  
Author(s):  
Sachin S. Kandlikar ◽  
Gregory D. Fink
Keyword(s):  
Control Period ◽  
Whole Body ◽  
Renal Nerves ◽  
Experimental Hypertension ◽  
Sympathetic Activation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Salt Hypertension ◽  
Hypertension Development

Excess sympathetic nervous system activity (SNA) is linked to human essential and experimental hypertension. To test whether sympathetic activation is associated with a model of deoxycorticosterone acetate (DOCA)-salt hypertension featuring two kidneys and a moderate elevation of blood pressure, we measured whole body norepinephrine (NE) spillover as an index of global SNA. Studies were conducted in chronically catheterized male Sprague-Dawley rats drinking water containing 1% NaCl and 0.2% KCl. After a 7-day surgical recovery and a 3-day control period, a DOCA pellet (50 mg/kg) was implanted subcutaneously in one group of rats (DOCA), while the other group underwent sham implantation (Sham). NE spillover was measured on control day 2 and days 7 and 14 after DOCA administration or sham implantation. During the control period, mean arterial pressure (MAP) was similar in Sham and DOCA rats. MAP was significantly increased in the DOCA group compared with the Sham group after DOCA administration ( day 14: Sham = 109 ± 5.3, DOCA = 128 ± 3.6 mmHg). However, plasma NE concentration, clearance, and spillover were not different in the two groups at any time. To determine whether selective sympathetic activation to the kidneys contributes to hypertension development, additional studies were performed in renal denervated (RDX) and sham-denervated (Sham-DX) rats. MAP, measured by radiotelemetry, was similar in both groups during the control and DOCA treatment periods. In conclusion, global SNA is not increased during the development of mild DOCA-salt hypertension, and fully intact renal nerves are not essential for hypertension development in this model.

Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension

1994 ◽  
Vol 267 (2) ◽  
pp. H751-H756 ◽  
Author(s):  
A. W. Cowley ◽  
E. Szczepanska-Sadowska ◽  
K. Stepniakowski ◽  
D. Mattson
Keyword(s):  
Body Weight ◽  
Arginine Vasopressin ◽  
Plasma Catecholamines ◽  
Plasma Osmolality ◽  
Sprague Dawley ◽  
Prolonged Administration ◽  
Chronic Stimulation ◽  
Sustained Hypertension ◽  
Sprague Dawley Rats

Despite the well-recognized vasoconstrictor and fluid-retaining actions of vasopressin, prolonged administration of arginine vasopressin (AVP) to normal animals or humans fails to produce sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. Conscious Sprague-Dawley rats with implanted catheters were infused with the selective V1 agonist, [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1), for 14 days in amounts that were acutely nonpressor. Blood pressure (MAP), heart rate (HR), body weight, and water intake (WI) were determined daily. Plasma AVP, plasma catecholamines norepinephrine and epinephrine, plasma osmolality, and electrolyte concentration were determined before and on days 1 and 7 of infusion. MAP increased significantly by 10.4 +/- 4.5 mmHg on day 1 and rose to 22 +/- 5 mmHg above control by day 14 (transient decrease on days 6-9) and then fell to control levels after the infusion was stopped. HR did not change significantly. Plasma AVP immunoreactivity increased from 2.5 +/- 0.3 to 10.9 +/- 2.1 pg/ml, whereas norepinephrine tended to fall only on day 1, with epinephrine only slightly elevated on day 7. No evidence of fluid retention was found, and rats lost sodium only on the first day of V1 agonist infusion. Body weight increased throughout the study but was unrelated to the changes of MAP. We conclude that chronic stimulation of V1 receptors results in sustained hypertension in rats.

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