THE ROLE OF GROWTH HORMONE AND THYROXINE IN NEPHROGENIC HYPERTENSION AND CARDIAC HYPERTROPHY IN HYPOPHYSECTOMIZED RATS

1967 ◽  
Vol 45 (6) ◽  
pp. 993-1000 ◽  
Author(s):  
Margaret Beznak

There was no indication of slowly developing hypertension and cardiac hypertrophy in hypophysectomized rats upon treatment with desoxycorticosterone and salt loading following unilateral nephrectomy. This was the case in both younger (less than 100 g) and older (220–260 g) male rats. However, the weight of the heart and kidney, the blood pressure, and the rate and output of the heart of normal and hypophysectomized rats following unilateral nephrectomy and treatment with desoxycorticosterone and salt loading were not too different when the hypophysectomized rats were given growth hormone and thyroxine. This agrees with the earlier conclusion that thyroxine and growth hormone are required in hypophysectomized rats for the development of hypertension and any significant enlargement of the heart, whether from aortic constriction or from nephrogenic causes.

1956 ◽  
Vol 184 (3) ◽  
pp. 563-566 ◽  
Author(s):  
Margaret Beznák

Of three growth hormone preparations only one (PGH 163-208A, Armour) restored cardiac hypertrophy and hypertension on aortic constriction in hypophysectomized rats near to the level seen in normal rats. The same aortic constriction caused no increase in the weight of the heart and no hypertension in untreated hypophysectomized rats and in similar rats treated with a bovine growth hormone preparation (R 285-174, Armour) or crystalline growth hormone (Dr. Li, Berkeley). The different action of the three preparations was not connected with their effect on appetite and on body growth. ACTH, 5 mg/rat/day, caused adrenal hypertrophy in hypophysectomized rats without raising their blood pressure. The weight of the heart and particularly the blood pressure after aortic constriction were, however, greater in hypophysectomized rats treated with ACTH than in their nontreated controls.


1955 ◽  
Vol 33 (1) ◽  
pp. 985-994 ◽  
Author(s):  
Margaret Beznák

The aortae of groups of normal and hypophysectomized rats were constricted with rings of five different sizes (0.93, 0.83, 0. 74, 0.71, and 0.63 mm. diameter). In normal rats constriction caused an increase in heart weight and blood pressure which was the greater the narrower the constriction. If constriction exceeded 0.74 mm., cardiac hypertrophy reached extremely high values, while the blood pressure was lower than in groups with less constriction. The blood pressure response to Adrenalin or Infundin increased in proportion to the degree of constriction down to 0.74 mm.; greater constriction reduced the response. In hypophysectomized rats no degree of aortic constriction produced hypertension or cardiac hypertrophy, yet the increase in blood pressure after Adrenalin or Infundin was as great as in the normal intact rats.


1963 ◽  
Vol 25 (4) ◽  
pp. 473-482 ◽  
Author(s):  
HELEN E. C. CARGILL THOMPSON ◽  
G. P. CREAN

SUMMARY 1. The effects of feeding, hormone administration, unilateral nephrectomy and adrenalectomy on width of tibial cartilage and total body weight in intact and hypophysectomized young male rats were measured. 2. Unilateral nephrectomy and adrenalectomy have no effect on the cartilage width of both intact and hypophysectomized rats, although adrenalectomy causes a loss in weight in the intact rat. 3. Intact rats, both young and adult, fed enough to maintain but not to put on weight, show a reduction of cartilage width to hypophysectomized levels. 4. Growth hormone alone (1 mg. and 3 mg./day for 14 days) causes a marked increase in cartilage width but only a 50–60% increase in total body weight in the hypophysectomized rat. 5. Adrenocorticotrophin (ACTH: 2 i.u./day for 14 days) causes a significant reduction in both cartilage width and total body weight in the hypophysectomized rat. 6. Thyrotrophin (TSH: 1 i.u./day) and Prolactin (1 mg. and 2 mg./day) caused significant increases in both total body weight and cartilage width in the hypophysectomized rat. 7. Luteinizing hormone (LH: 0·01 mg./day) together with follicle stimulating hormone (FSH: 1·0 mg./day) caused a significant increase in body weight, but had no effect on cartilage width in the hypophysectomized rat. 8. Both doses of combined hormones (growth hormone, ACTH, TSH, prolactin, FSH and LH administered together) caused a marked increase in cartilage width and a smaller increase in total body weight in the hypophysectomized rat.


1955 ◽  
Vol 33 (6) ◽  
pp. 985-994 ◽  
Author(s):  
Margaret Beznák

The aortae of groups of normal and hypophysectomized rats were constricted with rings of five different sizes (0.93, 0.83, 0. 74, 0.71, and 0.63 mm. diameter). In normal rats constriction caused an increase in heart weight and blood pressure which was the greater the narrower the constriction. If constriction exceeded 0.74 mm., cardiac hypertrophy reached extremely high values, while the blood pressure was lower than in groups with less constriction. The blood pressure response to Adrenalin or Infundin increased in proportion to the degree of constriction down to 0.74 mm.; greater constriction reduced the response. In hypophysectomized rats no degree of aortic constriction produced hypertension or cardiac hypertrophy, yet the increase in blood pressure after Adrenalin or Infundin was as great as in the normal intact rats.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Sheon Mary ◽  
Philipp Boder ◽  
Giacomo Rossitto ◽  
Lesley Graham ◽  
Kayley Scott ◽  
...  

Abstract Background and Aims Uromodulin (UMOD) is the most abundant renal protein secreted into urine by the thick ascending epithelial (TAL) cells of the loop of Henle. Genetic studies have demonstrated an association between UMOD risk variants and hypertension. Studies on UMOD overexpressing transgenic mice have shown that UMOD increases the tubular salt reabsorption via enhanced NKCC2 activity. We aimed to dissect the effect of salt-loading and blood pressure on the excretion of UMOD. Method Wistar-Kyoto (WKY) and stroke-prone spontaneously hypertensive (SHRSP) rats (n=8/sex/strain) were maintained on 1% NaCl for three weeks. Salt-loaded SHRSP were treated with nifedipine. Tubule isolation and ex vivo incubation with nifedipine were used to assess its direct effect on TAL. Results Urinary UMOD excretion was significantly reduced after salt loading in both strains (figure). In salt-loaded SHRSP, nifedipine treatment reduced blood pressure and urinary UMOD excretion. The reductions in urinary UMOD excretion were dissociated from unchanged kidney UMOD protein and mRNA levels, however, were associated with UMOD endoplasmic reticulum accumulation, thus suggesting secretion as a key regulatory step. Ex vivo experiments with TAL tubules showed that nifedipine did not have a direct effect on UMOD secretion. Conclusion Our data suggest a direct effect of salt on UMOD secretion independent of blood pressure and a potential role of endoplasmic reticulum stress on the control of UMOD secretion. The role of UMOD as a cardiovascular risk marker deserves mechanistic reappraisal and further investigations based on our findings.


Endocrinology ◽  
1998 ◽  
Vol 139 (3) ◽  
pp. 1067-1074 ◽  
Author(s):  
Varadaraj Chandrashekar ◽  
Andrzej Bartke

2006 ◽  
Vol 47 (4) ◽  
pp. 531-541 ◽  
Author(s):  
Thunder Jalili ◽  
Justin Carlstrom ◽  
Sun Kim ◽  
David Freeman ◽  
Huifeng Jin ◽  
...  

2013 ◽  
Vol 120 (6) ◽  
pp. 927-935 ◽  
Author(s):  
O. Lairez ◽  
T. Cognet ◽  
S. Schaak ◽  
D. Calise ◽  
C. Guilbeau-Frugier ◽  
...  

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