scholarly journals Physiological and Transcriptomic Changes in the Hypothalamic-Neurohypophysial System after 24 h of Furosemide-Induced Sodium Depletion

2020 ◽  
Vol 111 (1-2) ◽  
pp. 70-86 ◽  
Author(s):  
Sabrina G.V. Dutra ◽  
Alex Paterson ◽  
Livia R.N. Monteiro ◽  
Michael P. Greenwood ◽  
Mingkwan P. Greenwood ◽  
...  
Keyword(s):  
Gene Expression ◽  
Male Rats ◽  
Sodium Depletion ◽  
Water Excretion ◽  
Hypotonic Stress ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Body Sodium ◽  
Plasma Angiotensin ◽  
Transcriptomic Changes

<b><i>Background/Aims:</i></b> Furosemide is a loop diuretic widely used in clinical practice for the treatment of oedema and hypertension. The aim of this study was to determine physiological and molecular changes in the hypothalamic-neurohypophysial system as a consequence of furosemide-induced sodium depletion. <b><i>Methods:</i></b> Male rats were sodium depleted by acute furosemide injection (10 and 30 mg/kg) followed by access to low sodium diet and distilled water for 24 h. The renal and behavioural consequences were evaluated, while blood and brains were collected to evaluate the neuroendocrine and gene expression responses. <b><i>Results:</i></b> Furosemide treatment acutely increases urinary sodium and water excretion. After 24 h, water and food intake were reduced, while plasma angiotensin II and corticosterone were increased. After hypertonic saline presentation, sodium-depleted rats showed higher preference for salt. Interrogation using RNA sequencing revealed the expression of 94 genes significantly altered in the hypothalamic paraventricular nucleus (PVN) of sodium-depleted rats (31 upregulated and 63 downregulated). Out of 9 genes chosen, 5 were validated by quantitative PCR in the PVN (upregulated: Ephx2, Ndnf and Vwf; downregulated: Caprin2 and Opn3). The same genes were also assessed in the supraoptic nucleus (SON, upregulated: Tnnt1, Mis18a, Nr1d1 and Dbp; downregulated: Caprin2 and Opn3). As a result of these plastic transcriptome changes, vasopressin expression was decreased in PVN and SON, whilst vasopressin and oxytocin levels were reduced in plasma. <b><i>Conclusions:</i></b> We thus have identified novel genes that might regulate vasopressin gene expression in the hypothalamus controlling the magnocellular neurons secretory response to body sodium depletion and consequently hypotonic stress.

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.

Chronic low-sodium diet in rats: responses to severe heat exposure

1985 ◽  
Vol 58 (1) ◽  
pp. 152-156 ◽  
Author(s):  
R. P. Francesconi ◽  
R. W. Hubbard
Keyword(s):  
Heat Stress ◽  
Thermal Sensitivity ◽  
Heat Exposure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Male Rats ◽  
Control Group ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Severe Heat Stress

To determine the effects of sodium (Na+) deficiency on the responses to severe heat stress (35.5 degrees C), immature (mean wt 150.4 g) male rats (n = 21) were fed a low-Na+ diet for 71 days. Rates of weight gain and food consumption were significantly (P less than 0.001) reduced in the low-Na+ group, whereas water consumption was unaffected. Prior to heat exposure circulating Na+ levels were unaffected by dietary Na+ restriction, but both circulating potassium (K+) and hematocrit levels were significantly (P less than 0.001) increased. After 24-h exposure to severe heat stress, circulating Na+ levels did manifest a significant (P less than 0.001) decrement in the low-Na+ group. K+ levels increased significantly (P less than 0.01) in the control group after 6 h of heat exposure but remained depressed in comparison with the low-Na+ group after 48 and 72 h. Although plasma renin activity (PRA) was not increased by chronic consumption of the low-Na+ diet or by severe heat exposure in the control group, severe heat stress in the low-Na+ group did elicit significant (P less than 0.005) increments in PRA after 24 h of exposure. Alternatively, plasma aldosterone levels were significantly (P less than 0.001) elevated by both the low-Na+ diet and heat stress. We concluded from these studies that chronic consumption of the low-Na+ diet had severe effects on hematologic, endocrinological, and thermoregulatory variables as well as thermal sensitivity to prolonged and sedentary exposure to severe heat stress.

Pressor resistance to vasopressin in sodium depletion, potassium depletion, and cirrhosis

1986 ◽  
Vol 251 (3) ◽  
pp. R525-R530 ◽  
Author(s):  
B. M. Murray ◽  
M. S. Paller
Keyword(s):  
Pressor Response ◽  
Potassium Depletion ◽  
Pressor Effect ◽  
Sodium Depletion ◽  
Sprague Dawley ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Sprague Dawley Rats ◽  
Low Potassium ◽  
Baroreceptor Reflexes

Resistance to the pressor effects of angiotensin II, but not norepinephrine, has been observed in sodium depletion, potassium depletion, and cirrhosis. We tested the response to arginine vasopressin (AVP) in each of these conditions. Male Sprague-Dawley rats were made sodium depleted with furosemide and a low-sodium diet for 3 days, potassium depleted by feeding a low-potassium diet for 14-21 days, or cirrhotic by inhalation of carbon tetrachloride for 8 wk. In conscious rats, the pressor response to graded doses of AVP was reduced in sodium depletion by 27-43% compared with control rats. Sodium-depleted rats were also found to have enhanced baroreceptor reflexes, since the decrease in heart rate for a given increase in mean arterial pressure was greater than in control rats. When the ganglionic blocker pentolinium tartrate was given to sodium-depleted rats the pressor response to AVP was restored to control levels. In potassium-depleted rats the pressor response to AVP was 21-52% lower than that in controls, whereas cirrhotic rats also had a blunted response to AVP (14-41% lower than control). However, there was no evidence in either of these two states of enhanced baroreceptor activity, and pretreatment with pentolinium tartrate did not restore the pressor response to normal. Therefore, although resistance to the pressor effect of AVP was found in all three conditions, the mechanism of this effect was different in sodium depletion compared with potassium depletion and cirrhosis. We conclude that resistance to the pressor action of AVP in sodium depletion was secondary to resetting of the baroreceptors.

PATHOPHYSIOLOGICAL CHANGES IN PLASMA AND BODY COMPSITION OF YOUNG POULTS FED A SODIUM-DEFICIENT DIET

1978 ◽  
Vol 58 (4) ◽  
pp. 597-604
Author(s):  
C. Y. PANG ◽  
L. D. CAMPBELL ◽  
G. D. PHILLIPS
Keyword(s):  
Tap Water ◽  
Basal Diet ◽  
Plasma Sodium ◽  
Deficient Diet ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Body Sodium ◽  
Ad Libitum ◽  
Water Contents

Significantly lower feed intake, higher water intake and depressed growth rate were observed in poults under 30 days of age offered ad libitum a low (0.05%) sodium diet and tap water compared to control poults offered the same basal diet containing 0.25% added sodium. Mortality with dehydration occurred mainly between 2 and 3 wk of age in poults fed the low sodium diet. Significant pathophysiological changes in poults fed low sodium diet compared with the control on days 9–30 were: lower plasma sodium, chloride and osmolal concentrations; higher plasma contents of uric acid and total protein; higher packed cell volume; and lower body sodium and water contents. Indications of extracellular dehydration and intracellular hydration and decreased glomerular filtration rate in sodium-deficient poults are discussed. Plasma and body composition of poults fed the low sodium diet returned to normal 1 wk after the poults were offered a normal (0.25%) sodium diet and tap water ad libitum.

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.

Role of the renin-angiotensin system in the adaptation of aldosterone biosynthesis to sodium restriction in the rat

1980 ◽  
Vol 94 (3) ◽  
pp. 381-388 ◽  
Author(s):  
Eva Tarján ◽  
András Spät ◽  
Tamás Balla ◽  
Annamária Székely
Keyword(s):  
Renin Angiotensin System ◽  
Plasma Sodium ◽  
Sodium Depletion ◽  
Angiotensin System ◽  
Aldosterone Level ◽  
Renin Angiotensin ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

Abstract. The purpose of the present study was to evaluate the role of the renin-angiotensin system in the secretion of aldosterone during restriction of dietary sodium intake. Rats were kept on control or low-sodium diet for one week. On the 7th morning of diet osmotic minipumps filled with the angiotensin converting enzyme inhibitor (CEI) SQ 20,881, or empty pumps, were implanted subcutaneously (sc). The rats were sacrificed 23 h later. Peripheral blood was analyzed for hormones and electrolytes. Adrenal capsular tissue (z. glomerulosa) was incubated for the determination of the conversion of [3H]corticosterone to [3H]aldosterone. Sodium depletion had no effect on plasma sodium, but it increased potassium concentration. Infusion of CEI had no significant effect on plasma electrolytes. Plasma renin activity was increased both by sodium depletion and CEI. The mean serum aldosterone level was twelve times higher in sodium depleted animals than in controls. Aldosterone level was reduced by about 60 per cent in CEI-infused animals both on control and low-sodium diet. The conversion of corticosterone to aldosterone was significantly stimulated by sodium deprivation. This effect was also inhibited by the CEI SQ 20,881.

scholarly journals Differential gene expression in response to low sodium diet in dogs: potential impact on cardiac function

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Caroline Ojaimi ◽  
Nobuhiro Suematsu ◽  
Gabor Kaley ◽  
Fabio A Recchia ◽  
Thomas H Hintze
Keyword(s):  
Gene Expression ◽  
Cardiac Function ◽  
Differential Gene Expression ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Differential Gene ◽  
Potential Impact

Splanchnic and renal contributions to circulatory homeostasis in sodium depletion

1983 ◽  
Vol 245 (4) ◽  
pp. H573-H579 ◽  
Author(s):  
S. F. Echtenkamp ◽  
J. O. Davis ◽  
R. H. Freeman ◽  
J. R. Dietz ◽  
D. Villarreal
Keyword(s):  
Blood Flow ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Significant Rise ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Indwelling Catheters ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Arterial Blood

Chronic sodium depletion is a state of reduced cardiac output in which the renin-angiotensin system is actively involved in maintenance of mean arterial blood pressure (MAP). Angiotensin II (ANG II) blockade with saralasin is known to produce renal vasodilation and a decrease in MAP in the sodium-deplete dog. In this study conscious trained dogs with chronic indwelling catheters were sodium depleted with diuretics plus a low sodium diet. Hepatic blood flow (HBF) and renal blood flow (RBF) were determined concurrently by the clearances of bromosulfophthalein and p-aminohippurate, respectively. When compared with the sodium-repleted state, the depleted dogs had reduced HBF with no change in MAP or RBF. In addition, the hepatic renin clearance and percent hepatic renin extraction were reduced. When saralasin was given intravenously to the depleted dogs, the response was a decrease in MAP with a concurrent decrease in both renal and splanchnic vascular resistances. The increased plasma renin activity during saralasin was accompanied by increased hepatic renin extraction but no significant rise in hepatic renin clearance. Saralasin also resulted in a large decrease in the urinary excretion of prostaglandin E2. This study provides evidence that increased plasma ANG II levels are responsible for the increased splanchnic vascular resistance during chronic sodium depletion.

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