INFLUENCE OF THE ANTERIOR PITUITARY ON THE ALDOSTERONE SECRETORY RESPONSE TO DIETARY SODIUM RESTRICTION IN THE RAT

1968 ◽  
Vol 42 (3) ◽  
pp. 465-475 ◽  
Author(s):  
T. C. LEE ◽  
B. van der WAL ◽  
D. de WIED
Keyword(s):  
Anterior Pituitary ◽  
Normal Diet ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Aldosterone Production ◽  
Hypophysectomized Rats ◽  
Dietary Sodium Restriction ◽  
Long Acting ◽  
Intact Rats

SUMMARY Studies of the rate of aldosterone production in vitro of adrenals of rats hypophysectomized before dietary sodium restriction showed that hypophysectomy not only prevented the increases in aldosterone production observed in intact, Na-deprived rats, but also depressed the level of aldosterone production to below that of intact rats maintained on a normal diet. Rats hypophysectomized for a similar period of time but maintained on the normal diet showed a similar decrease. Experiments on adeno- and neuro-hypophysectomized rats indicated that the pituitary factor required for the normal mineralocorticoid response to dietary sodium restriction resides in the anterior pituitary. Treatment of hypophysectomized rats during dietary sodium restriction with doses of a long-acting corticotrophin (ACTH) prevented adrenal atrophy and maintained a normal glucocorticoid response to intravenous injections of ACTH, but failed to increase aldosterone production rates in vitro to levels above that of intact rats on a normal diet; it also failed to restore the enhanced adrenocortical sensitivity to the stimulating effect of aldosterone production of intravenously injected ACTH which is characteristic of acutely hypophysectomized, Na-deficient rats. Treatment with anterior pituitary powder (8–12 mg./day) for similar periods, however, restored the aldosterone production of adrenals in vitro of hypophysectomized, Na-deprived rats to levels nearly indistinguishable from those of acutely hypophysectomized, Na-deprived controls. The same doses of anterior pituitary powder were shown not to have any demonstrable effect on the aldosterone production of adrenals in vitro of intact rats on a normal diet. These results are interpreted as indicating the existence of a pituitary factor other than ACTH which stimulates aldosterone secretion. This factor does not appear to act directly on the adrenal cortex or to stimulate the secretion of specific glomerulotropic substances, but probably exerts its effect by maintaining the normal functional capacity of some as yet undefined tissues which secrete glomerulotropic substances in response to dietary sodium restriction.

EFFECT OF GROWTH HORMONE ON THE ALDOSTERONE SECRETORY RESPONSE TO SODIUM RESTRICTION IN CORTICOTROPHIN-MAINTAINED HYPOPHYSECTOMIZED NEPHRECTOMIZED RATS

1971 ◽  
Vol 51 (2) ◽  
pp. 369-374 ◽  
Author(s):  
M. PALKOVITS ◽  
J. J. T. W. A. STRIK ◽  
W. de JONG ◽  
D. de WIED
Keyword(s):  
Growth Hormone ◽  
Plasma Potassium ◽  
Secretory Response ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Sodium Deficiency ◽  
Aldosterone Production ◽  
Hypophysectomized Rats ◽  
Previously Treated

SUMMARY The rate of aldosterone production in vitro by adrenal glands from rats hypophysectomized 7 days previously, treated with corticotrophin (ACTH) and subjected to dietary sodium restriction for 2 weeks, was decreased 6 h after nephrectomy. However, 18 h and 48 h after nephrectomy there was a marked increase in the rate of aldosterone production in vitro. In addition there was a rise in the plasma potassium concentration. These results indicated that in order to detect whether the influence of growth hormone on aldosterone secretory response to sodium restriction in hypophysectomized rats was mediated by the kidney, studies had to be performed within 6 h after removal of the kidneys. Since the effect of growth hormone on aldosterone production requires 2 days to develop (Palkovits, de Jong, van der Wal & de Wied, 1971), rats hypophysectomized 54 h previously were used. The kidneys were removed 6 h before decapitation. In these animals, the administration of growth hormone in the presence of ACTH restored the aldosterone secretory response to sodium deficiency. The results suggest that growth hormone maintains the aldosterone secretory response to sodium restriction in hypophysectomized rats in the absence of the kidneys.

Ion transport by the pig colon: effects of theophylline and dietary sodium restriction

1982 ◽  
Vol 60 (7) ◽  
pp. 929-935 ◽  
Author(s):  
R. A. Argenzio ◽  
Deborah Lebo
Keyword(s):  
Ion Transport ◽  
Normal Diet ◽  
Loop System ◽  
Electrolyte Transport ◽  
Dietary Sodium ◽  
Secretory Process ◽  
Sodium Restriction ◽  
Basal Rate ◽  
Dietary Sodium Restriction

The effect of theophylline on colonic electrolyte transport was examined in an isolated, static loop system of the pig colon. The presence of theophylline abolished the net absorption of Na and water and increased the net secretion of HCO3. The net absorption of Cl or acetate was unaffected. In pigs adapted to a saltfree diet, the net absorption of Na was increased twofold from that observed in pigs fed the normal diet; however, the basal rate of net HCO3 secretion was unchanged. In the presence of theophylline, the saltfree diet restored net Na absorption to control levels, whereas the theophylline-induced increase in the rate of net HCO3 secretion was sustained. Results suggest that the relative rates of net Na and HCO3 transport are partially controlled by independent systems and indicate that normal rates of net absorption can be restored in the presence of a parallel secretory process.

THE ROLE OF A FEEDBACK MECHANISM IN THE REGULATION OF ALDOSTERONE SECRETION IN THE RAT

1973 ◽  
Vol 73 (2) ◽  
pp. 282-288
Author(s):  
L. Debreceni ◽  
B. Csete
Keyword(s):  
Marked Decrease ◽  
Feedback Regulation ◽  
Feedback Mechanism ◽  
The Other ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Aldosterone Production

ABSTRACT The effect of prolonged aldosterone and DOC treatment in the in vitro aldosterone production was studied in the rat. When the animals were supplied with food containing 16.5 mEq./100 g of sodium, both aldosterone and DOC treatment led to a marked decrease in aldosterone production. On the other hand, under dietary sodium restriction both aldosterone and DOC treatment failed to induce a suppression of the elevated aldosterone production. On the basis of these findings, it seems that a sufficient sodium supply of the organism is necessary for the control of aldosterone secretion either by an increase of aldosterone production or DOC treatment if any feedback regulation is involved in the mechanism controlling aldosterone secretion.

THE REGULATION OF ALDOSTERONE PRODUCTION IN NORMAL AND SODIUM-DEFICIENT RATS

1968 ◽  
Vol 41 (2) ◽  
pp. 179-188 ◽  
Author(s):  
M. F. D. CSÁNKY ◽  
B. van der WAL ◽  
D. de WIED
Keyword(s):  
Dietary Sodium ◽  
Sodium Balance ◽  
Standard Diet ◽  
Aldosterone Secretion ◽  
Deficient Diet ◽  
Enhanced Production ◽  
Aldosterone Production ◽  
High Doses ◽  
Long Acting

SUMMARY Aldosterone secretion of rats on a standard diet, as determined by the rate of aldosterone produced by adrenal tissue in vitro, was not affected by exposure to ether, by hypophysectomy or by nephrectomy. Administration of high doses of long-acting corticotrophin (ACTH; 1·5 units) to rats hypophysectomized 24 hr. previously also failed to affect the rate of aldosterone production in vitro in rats on the standard diet. Only hypophysectomy and nephrectomy in the same rat induced a significant decrease in aldosterone production in vitro 6 hr. after operation in rats fed the standard diet. Aldosterone production in vitro increased in rats fed a sodium-deficient diet. The increment was more pronounced in rats maintained on the diet for 14- than for 10-days. Hypophysectomy, or nephrectomy, caused no decrease in aldosterone production, when compared to sham-operated rats. However, hypophysectomy and nephrectomy together caused a marked decline in the rate of aldosterone production in vitro 6 hr. after operation as compared with sham-operated or non-operated rats. The administration of relatively small amounts of ACTH (8 m-u.) induced a marked increase in the rate of aldosterone production in vitro of intact, and hypophysectomized sodium-deficient rats. The results indicate that in the rat, as in other species, both the kidney and the pituitary contribute to the maintenance of the basal rate of aldosterone production in animals in normal sodium-balance and that these organs are responsible for the increased rate of aldosterone production in dietary sodium restriction. ACTH, however, though a potent stimulus for aldosterone secretion, appears only to augment the already enhanced production of aldosterone in the sodium-deprived rat.

Macula densa stimulation of renin is reversed by selective inhibition of neuronal nitric oxide synthase

1997 ◽  
Vol 272 (5) ◽  
pp. R1359-R1364 ◽  
Author(s):  
W. H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Normal Diet ◽  
Macula Densa ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Restricted Group ◽  
Dietary Sodium Restriction ◽  
Oxide Synthase ◽  
Stimulation Of

The neuronal isoform of nitric oxide synthase (nNOS) exists in the renal cortex predominantly in the macula densa, suggesting that nitric oxide (NO) derived from the macula densa plays a role in feedback regulation of renin in response to altered sodium metabolism. To determine if nNOS is a critical component in renin stimulation induced by dietary sodium restriction, rats received either normal sodium or a sodium-restricted diet (0.03%) for 7 days and subsequently were or were not treated with the selective inhibitor of nNOS 7-nitroindazole (7-NI) either acutely (50 mg/kg body wt ip) on the final day or chronically (20 mg/kg body wt ip 2 x/day) over the final 5 days. On the last day, rats were anesthetized with Inactin and fitted with arterial and renal venous catheters to collect blood and monitor blood pressure (BP) and a flow probe to measure renal blood flow (RBF). BP (105 vs. 108 mmHg) was similar in normal and low-sodium dietary groups, respectively, whereas RBF tended to be higher in the sodium-restricted group (6.5 +/- 0.3 vs. 7.6 +/- 0.4 ml.min-1.g kidney wt-1). Both renal venous renin (RR) and renin secretion rate (RSR) were elevated approximately fourfold by sodium restriction [RR = 5.8 +/- 0.8 vs. 20.5 +/- 2.7 ng angiotensin (ANG) I.ml-1.h-1; P < 0.001; RSR = 3.0 +/- 0.9 vs. 13.1 +/- 4.1 ng ANG I.h-1.min-1; P < 0.025]. Acute 7-NI did not change BP, RR, or RSR, but reduced RBF in sodium-restricted rats by 8% (P < 0.05). Chronic 7-NI had no effect on renin in rats on a normal diet, but reduced RR by one-half in the sodium-restricted group (to 9.9 +/- 1.6 ng ANG I-ml-1.h-1; P < 0.001) and reduced RSR to normal (diet) levels (to 3.9 +/- 1.4 ng ANG I.h-1.min-1; P < 0.05). Although selective NOS inhibition by 7-NI did not affect BP, RBF, or renin in control rats on a normal diet, chronic 7-NI reversed the stimulation of renin induced by dietary sodium restriction. These data suggest that nNOS-derived NO plays an important role in the macula densa during feedback stimulation of renin induced by dietary sodium restriction.

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.

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