EFFECT OF HYPOPHYSECTOMY AND A LOW SODIUM DIET ON THE VOLUMES OF THE GLOMERULAR ZONE, FASCICULAR AND RETICULAR ZONES AND MEDULLA OF RATS

1965 ◽  
Vol 50 (3) ◽  
pp. 486-492 ◽  
Author(s):  
Richard A. Miller

ABSTRACT Direct measurements of volume of the glomerular zone, fascicular and reticular zones and medulla were made in normal and hypophysectomized rats. All zones of the cortex and the medulla atrophied after hypophysectomy. However, while medullary and glomerular atrophy was proportional to the decrease in body weight, fascicular atrophy exceeded the loss in body weight. Hypertrophy of the glomerular zone occurred in rats fed a sodium deficient diet for 5 to 28 days beginning 14 days after hypophysectomy. Hence the volume of the glomerular zone is probably independent of the pars distalis, since the glomerular zone does not atrophy after hypophysectomy and can be stimulated to hypertrophy after it and the infundibular process are removed. Calculation of mass from areas in a mid-section by the Bahn formula and from direct measurements of volume yielded similar values for the mass of the fascicular zone. However, mean values for glomerular mass and for medullary mass were each significantly different. None the less, there was a high correlation between values, and the percent changes in mass of the glomerular zone resulting from the sodium deficiency were similar. Hence, the Bahn formula seems to be a useful shortcut procedure for detecting changes in the mass of the several regions of the cortex.

1965 ◽  
Vol 50 (3) ◽  
pp. 493-496 ◽  
Author(s):  
Richard A. Miller

ABSTRACT The weights of the several zones of the adrenal cortex and the medulla were calculated from their areas in the midsection of adrenals from hypophysectomized rats injected with carbon tetrachloride, with formalin, or fed a low sodium diet, for varying periods of time. It was found that the glomerular zone of the rats so stressed was significantly heavier than that of hypophysectomized controls. The data suggest that the glomerular zone can be stimulated to enlarge by stress in the absence of the pars distalis and corticotrophin.


1970 ◽  
Vol 47 (2) ◽  
pp. 243-250 ◽  
Author(s):  
M. PALKOVITS ◽  
W. DE JONG ◽  
B. VAN DER WAL ◽  
D. DE WIED

SUMMARY Hypophysectomy abolishes the aldosterone secretory response to sodium deficiency in rats. Sodium deficiency causes a significant increase in plasma renin activity in chronically hypophysectomized rats which is of the same order as that found in intact animals. Long-term treatment with either adrenal maintenance doses of corticotrophin (ACTH) or with growth hormone (STH) did not affect the low rate of aldosterone production of hypophysectomized rats on a sodium-deficient diet. However, ACTH and STH given simultaneously restored the aldosterone secretory response to sodium deficiency in chronically hypophysectomized rats. The plasma renin activity of hypophysectomized rats on a sodium-deficient or a normal diet remained unaltered during treatment with either ACTH or STH or with the two hormones given simultaneously. This was also reflected in the systolic blood pressure of rats which, under the conditions used, did not change when the animals were sodium-deficient, or after hypophysectomy or hormone treatment. These results indicate that the effect of STH, in restoring the aldosterone secretory response to sodium deficiency in the presence of adrenal maintenance doses of ACTH in chronically hypophysectomized rats, is independent of changes in the renin-angiotensin system.


1978 ◽  
Vol 58 (4) ◽  
pp. 597-604
Author(s):  
C. Y. PANG ◽  
L. D. CAMPBELL ◽  
G. D. PHILLIPS

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.


1981 ◽  
Vol 96 (3) ◽  
pp. 361-369 ◽  
Author(s):  
Cornelia Seifert ◽  
Wolfgang Oelkers

Abstract. Unknown pituitary factor(s) apart from ACTH may participate in the regulation of aldosterone (aldo) secretion in man. We investigated whether the 'sensitization' of the zona glomerulosa against angiotensin II (A II) by sodium deficiency was mediated by the pituitary gland. A II was infused in stepwise increasing doses (2, 4, 8 ng/kg/min) into 5 normal subjects (N) and into 8 patients with hypopituitarism (H) before and after 4 days on a low sodium diet. Mean cumulative sodium balance after the low sodium diet was − 145 mm in N and − 165mm in H. Plasma-aldo and aldo-exretion rate on the normal sodium diet were slightly lower in H than in N but rose less than normal during sodium depletion in H. Plasma A II and renin activity on normal sodium were slightly higher in H than in N, but the increase on the low sodium diet was blunted in H. The stimulation of plasmaaldo by A II infusion was similar in both groups on the normal sodium diet. In both groups, the response of P-aldo to A II infusion was greater in the sodium deplete than in the replete state, although 'sensitization' was slightly less marked in H than in N. This may be due to the blunted rise of plasma-A II after sodium loss in H, which may also account for abnormalities in the blood pressure response in the H group. Altogether, the results speak against a direct involvement of the pituitary gland in 'sensitization', but an indirect influence through unexplained abnormalities in renin secretion is possible.


1997 ◽  
Vol 27 (2) ◽  
pp. 245-248 ◽  
Author(s):  
Enrico Lippi Ortolani

Fifteen lambs were fed diet with normal (0.11%) or deficient levels of sodium ( 0.035%), respectively, for five weeks on each diet. At the end of each period saliva was collected by three different methods: swabbing with a 5 x 5 x 1.25cm synthetic sponge, aspiration with a 15cm long plastic tube connected to a 20ml syringe and sucking with a 4mm x 45cm long plastic tube through a water-jet aspirator pump or an eletric motor pump. The volume of saliva collected/min and the salivary sodium: potassium ratio were analysed. Larger volume of saliva was obtained with the developed sucking apparatus than with the sponge or the syringe. There was no influence of the method of saliva collection on the values of salivary Na:K ratio in both periods. Nevertheless, the lower the sodium dietary level was, the smaller the salivary Na:K ratio. Five weeks of low sodium diet intake resulted in a decrease in the salivary Na:K ratio values by half. However, the lambs did not exhibit any clinical sign of sodium deficiency. The advantages of the developed method to collect saliva are discussed.


2019 ◽  
Vol 50 (1) ◽  
pp. 11-18
Author(s):  
Horacio J. Adrogué ◽  
Sreedhar Mandayam ◽  
Hocine Tighiouart ◽  
Nicolaos E. Madias

Background: The Edelman equation has long guided the expected response of plasma [Na+] to changes in sodium, potassium, and water balance, but recent short-term studies challenged its validity. Plasma [Na+] following hypertonic NaCl infusion in individuals on low-sodium diet fell short of the Edelman predictions supposedly because sodium restriction caused progressive osmotic inactivation of 50% of retained sodium. Here, we examine the validity of this challenge. Methods: We evaluated baseline total body water (TBW) and Na+ space following acute hypertonic NaHCO3 infusion in dogs with variable sodium and potassium stores, including normal stores, moderate depletion (chronic HCl feeding), or severe depletion (diuretics and dietary NaCl deprivation). Results: TBW (percentage body weight) averaged 65.9 in normals, 62.6 in HCl-induced metabolic acidosis and moderate sodium and potassium depletion, and 57.6 in diuretic-induced metabolic alkalosis and severe sodium and potassium depletion (p < 0.02). Na+ space (percentage body weight) at 30, 60, and 90 min postinfusion averaged 61.1, 59.8, and 56.1, respectively, in normals (p = 0.49); 70.0, 74.4, and 72.1, respectively, in acidotic animals (p = 0.21); and 56.4, 55.1, and 54.2, respectively, in alkalotic animals (p = 0.41). Absence of progressive expansion of Na+ space in each group disproves progressive osmotic inactivation of retained sodium. Na+ space at each time point was not significantly different from baseline TBW in normal and alkalotic animals indicating that retained sodium remained osmotically active in its entirety. However, Na+ space in acidotic animals at all times exceeded by ∼16% baseline TBW (p < 0.01) signifying an early, but nonprogressive, osmotic inactivation of retained sodium, which we link to baseline bone-sodium depletion incurred during acid buffering. Conclusions: Our investigation affirms the validity of the Edelman construct in normal dogs and dogs with variable sodium and potassium depletion and, consequently, refutes the recent observations in human volunteers subjected to dietary NaCl restriction.


Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3714
Author(s):  
Natale Musso ◽  
Federico Gatto ◽  
Federica Nista ◽  
Andrea Dotto ◽  
Zhongyi Shen ◽  
...  

Objective: To evaluate the left ventricular mass (LVM) reduction induced by dietary sodium restriction. Patients and Methods: A simple sodium-restricted diet was advised in 138 treated hypertensives. They had to avoid common salt loads, such as cheese and salt-preserved meat, and were switched from regular to salt-free bread. Blood pressure (BP), 24-h urinary sodium (UNaV) and LVM were recorded at baseline, after 2 months. and after 2years. Results: In 76 patients UNaV decreased in the recommended range after 2 months and remained low at 2 years. In 62 patients UNaV levels decreased after 2 months and then increased back to baseline at 2 years. Initially the two groups did not differ in terms of BP (134.3 ± 16.10/80.84 ± 12.23 vs. 134.2 ± 16.67/81.55 ± 11.18 mmHg, mean ± SD), body weight (72.64 ± 15.17 vs. 73.79 ± 12.69 kg), UNaV (161.0 ± 42.22 vs. 158.2 ± 48.66 mEq/24 h), and LVM index (LVMI; 97.09 ± 20.42 vs. 97.31 ± 18.91 g/m2). After 2years. they did not differ in terms of BP (125.3 ± 10.69/74.97 ± 7.67 vs. 124.5 ± 9.95/75.21 ± 7.64 mmHg) and body weight (71.14 ± 14.29 vs. 71.50 ± 11.87 kg). Significant differences were seen for UNaV (97.3 ± 23.01 vs. 152.6 ± 49.96 mEq/24 h) and LVMI (86.38 ± 18.17 vs. 103.1 ± 21.06 g/m2). Multiple regression analysis: UNaV directly and independently predicted LVMI variations, either as absolute values (R2 = 0.369; β = 0.611; p < 0.001), or changes from baseline to +2years. (R2 = 0.454; β = 0.677; p < 0.001). Systolic BP was a weaker predictor of LVMI (R2 = 0.369; β = 0.168; p = 0.027; R2 = 0.454; β = 0.012; p = 0.890), whereas diastolic BP was not correlated with LVMI. The prevalence of left ventricular hypertrophy decreased (29/76 to 15/76) in the first group while it increased in the less compliant patients (25/62 to 36/62; Chi2p = 0.002). Conclusion: LVM seems linked to sodium consumption in patients already under proper BP control by medications.


1966 ◽  
Vol 44 (1) ◽  
pp. 13-20 ◽  
Author(s):  
B. Korecky ◽  
M. Beznak ◽  
M. Korecka

Heart–lung preparations (h.l.p.) were made in normal rats, hypophysectomized rats, and in hypophysectomized rats treated with either growth hormone or thyroxine or both. While mean arterial pressure was kept constant at 100 mm Hg, the flow into the heart was increased stepwise until cardiac output did not rise any further (maximum cardiac output (m.c.o.)). Hypophysectomy substantially decreased the m.c.o., even when expressed per kilogram body weight. Thyroxine treatment alone or with growth hormone completely restored the m.c.o. to normal. However, when the m.c.o. was calculated per gram of left ventricle weight, it did not reach the normal level in any of the hypophysectomized rats investigated. Growth hormone, on the other hand, raised the stroke volume (expressed per gram of left ventricle) of hypophysectomized rats without affecting the rate of the heart.


1972 ◽  
Vol 70 (1) ◽  
pp. 167-174 ◽  
Author(s):  
Artur Ber

ABSTRACT Hypophysectomy was performed at the same time as ovariectomy in 19 rats aged 6 weeks; in addition a fragment of the animal's own ovary was implanted into the greater omentum. The graft took but there was complete cessation of the growth of the implant and a decrease in body and uterine weights as compared to 15 ovariectomized controls of the same age killed after one month. This shows that the pituitary is indispensable for the growth of ovarian implants but not for their take. In 84 spayed rats aged 3 weeks with ovarian implants, methallibure (6 mg/day in a 0.2% solution of Tween 20) was given by gavage during one month. Some of them were treated with PMSG (20 IU/day), HCG (20 IU/day) or with oestradiol benzoate (0.05 mg/day) only or in combinations. As controls, there were 74 spayed rats with ovarian implants, seven of which received Tween 20, and 67 were untreated. No differences were found between the two control groups. Methallibure alone caused arrest of the development of the implants and uteri and a decrease in body weight. In the methallibure treated animals HCG stimulated the growth of the implant which was, however, smaller than that in the controls, while PMSG restored the weight of the implant even above that of the control rats. Oestradiol benzoate caused a further diminution in the size of the implants but augmented considerably the influence of HCG on the implants. It had no effect on the weight of the implant in rats treated with PMSG. It is concluded that FSH is the principal implant growth-promoting factor and that oestrogens appear to act in two directions. They decrease the gonadotrophin output from the pituitary thus inhibiting the growth of the implants, but in the presence of gonadotrophins they act directly on the implants, promoting their development.


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