Search Results
Search for other papers by N. Wongsurawat in
Google Scholar
PubMed
Search for other papers by H. J. Armbrecht in
Google Scholar
PubMed
Search for other papers by T. V. Zenser in
Google Scholar
PubMed
Search for other papers by L. R. Forte in
Google Scholar
PubMed
Search for other papers by B. B. Davis in
Google Scholar
PubMed
ABSTRACT
Growth hormone stimulates intestinal calcium absorption. This action has been linked to vitamin D metabolism. We have investigated the effects of hypophysectomy and GH treatment on renal metabolism of 25-hydroxycholecalciferol (25-OH-D3). Renal hydroxylation of 25-OH-D3 was measured in vitro using the renal slice technique. Experiments were performed in young F344 rats fed a vitamin D-replete, low calcium diet for 4 weeks. In hypophysectomized rats, renal conversion of 25-OH-D3 to 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) was markedly reduced compared with sham-operated rats. Renal conversion of 25-OH-D3 to 24,25-(OH)2D3 was markedly increased in hypophysectomized rats compared with sham-operated rats. Treatment of hypophysectomized rats with rat GH (rGH) for 10 days resulted in a significant increase in renal conversion of 25-OH-D3 to 1,25-(OH)2D3 and a significant decrease in conversion to 24,25-(OH)2D3. Rat GH treatment caused no significant changes in serum levels of immunoreactive parathyroid hormone. Serum calcium concentrations were similar in all groups, and serum phosphorus was low in hypophysectomized rats. Treatment of hypophysectomized rats with ovine GH for 6 days caused changes which were much less pronounced than those induced by rGH. Renal conversion of 25-OH-D3 to 1,25-(OH)2D3 and 24,25-(OH)2D3 correlated well with growth rate (weight gain). These results suggest that GH, either directly or indirectly, modulates renal metabolism of 25-OH-D3.
J. Endocr. (1984) 101, 333–338
Search for other papers by H Grønbæk in
Google Scholar
PubMed
Search for other papers by B Nielsen in
Google Scholar
PubMed
Search for other papers by J Frystyk in
Google Scholar
PubMed
Search for other papers by H Ørskov in
Google Scholar
PubMed
Search for other papers by A Flyvbjerg in
Google Scholar
PubMed
Abstract
IGF-I acts as a renotropic factor in early streptozotocin-induced diabetes. Somatostatin analogue (octreotide) treatment initiated at the onset of diabetes prevents kidney IGF-I accumulation and renal growth. Seven days of octreotide treatment initiated after 3, 5, 7 or 9 days of untreated diabetes was investigated. Diabetic renal hypertrophy was followed by renal hyperplasia. Compared with placebo-treated diabetic rats, the earliest octreotide intervention was followed by a greater reduction in renal growth compared with intervention later on (days 3 to 10, 12%; days 5 to 12, 10%; days 7 to 14, 9%; days 9 to 16, 6%; P<0·05). Octreotide treatment was unable to reduce protein accumulation and kidney DNA increase consistently. No difference in glomerular volume fraction or total glomerular volume was observed between placebo- and octreotide-treated diabetic rats. Octreotide treatment was followed by reduced kidney and serum IGF-I especially following early intervention, while no effect over that of diabetes was observed in the later intervention periods. The results confirm the notion that initial renal IGF-I accumulation is a prerequisite for early diabetic kidney hypertrophy in rats and show that delayed octreotide treatment cannot reverse renal and glomerular growth which is already manifest.
Journal of Endocrinology (1995) 147, 95–102
Search for other papers by J. P. ASHBY in
Google Scholar
PubMed
Search for other papers by F. W. HEATON in
Google Scholar
PubMed
SUMMARY
The influence of magnesium deficiency on cyclic AMP metabolism was investigated in rats on diets of normal and low calcium content. Magnesium deficiency itself did not significantly affect either the basal concentration or the parathyroid hormone-stimulated formation of cyclic AMP in the renal cortex.
Magnesium-deficient rats with hypercalcaemia excreted more cyclic AMP in the urine, but similar rats that developed hypocalcaemia on low calcium intake excreted less than their respective controls. The former type of animals also tended to accumulate more cyclic AMP in the renal cortex in response to the injection of a standard dose of parathyroid hormone, whereas rats of the latter type accumulated less. The activity of parathyroid hormone-stimulated renal cortical adenylate cyclase in vitro was increased by magnesium and reduced by calcium under most conditions, but with low concentrations of magnesium small amounts of calcium had a stimulatory effect. These observations suggest that cyclic AMP metabolism is influenced by metabolic disorders developing secondary to magnesium deficiency.
Search for other papers by J. L. ARTETA in
Google Scholar
PubMed
Clamping of the renal vessels gives rise to a reflex change of circulation at the level of the vascular zone innervated by the splanchnic nerves.
Bilateral cutting of the splanchnic nerves and of the inferior part of the sympathetic chain at the level of the thorax prevents the reflex, and annuls the protective action of clamping the vascular pedicles of the kidney.
Renal lesions are not absolutely necessary for the production of alloxan diabetes, but may aggravate diabetes, probably by adding the toxic effects of retention of urine.
Search for other papers by S Omer in
Google Scholar
PubMed
Search for other papers by J Shan in
Google Scholar
PubMed
Search for other papers by DR Varma in
Google Scholar
PubMed
Search for other papers by S Mulay in
Google Scholar
PubMed
We tested the hypothesis that pregnancy might increase diabetes-associated nitric oxide (NO) production and renal hyperfiltration. Two weeks following i.v. streptozotocin (40 mg/kg), mean arterial pressure (MAP) was not modified by diabetes; glomerular filtration rate (GFR), renal plasma flow (RPF) and filtration fraction (FF) were higher in pregnant than in virgin controls and increased by diabetes to a greater extent in pregnant than in virgin rats. Urinary volume (UV), creatinine, albumin and sodium (UNaV) were significantly increased by diabetes. Diabetes led to an increase in renal, cardiac, aortic and uterine but not in placental NO synthase activities. Infusion of NG-nitro-l-arginine (l-NA) caused a dose-dependent reduction in GFR, RPF, plasma NO2-/NO3-, UV and UNaV; in general, diabetes increased these effects to a greater extent in pregnant than in virgin rats. l-NA increased MAP in all groups of rats but did not alter FF. Diabetes did not alter responses of thoracic aorta rings to vasoconstrictor effects of phenylephrine and the vasorelaxant effects of sodium nitroprusside but increased endothelium-dependent relaxant effects of acetylcholine. In general the effects of diabetes of 7 days duration were similar to those described above for diabetes of 14 days duration. These data suggest that diabetes-associated renal hyperfiltration and NO production are augmented by pregnancy.
Search for other papers by H Gronbaek in
Google Scholar
PubMed
Search for other papers by B Nielsen in
Google Scholar
PubMed
Search for other papers by B Schrijvers in
Google Scholar
PubMed
Search for other papers by I Vogel in
Google Scholar
PubMed
Search for other papers by R Rasch in
Google Scholar
PubMed
Search for other papers by A Flyvbjerg in
Google Scholar
PubMed
It was recently discovered that the streptozotocin (STZ)-diabetic mouse model is characterised by GH hypersecretion in contrast to the STZ-diabetic rat, the former thus mimicking the changes in GH in human type 1 diabetes. Inhibition of circulating and renal IGF-I by long-acting somatostatin analogues reduces renal and glomerular growth and urinary albumin excretion in diabetic rats. The aim of the present study was to examine renal and glomerular growth in early experimental diabetes in mice along with changes in the GH/IGF-I axis following treatment with the somatostatin analogue octreotide. Balb/C(a) mice were randomised into non-diabetic controls, placebo-treated and octreotide-treated diabetic (50 microg/day) mice and examined 7 and 14 days after induction of diabetes. There was no effect of octreotide treatment on body weight, glycaemic control or food intake. However, octreotide treatment significantly inhibited renal and glomerular growth by the end of the study period when compared with placebo treatment. In addition, octreotide prevented an increase in kidney IGF-I by day 7. GH hypersecretion was observed in the diabetic groups but octreotide treatment reduced GH levels compared with placebo treatment by day 14. No significant differences in serum or kidney IGF-binding protein-3 levels were observed between placebo- and octreotide-treated diabetic mice. In conclusion, this new diabetic mouse model mimicking human type 1 diabetes is characterised by GH hypersecretion and the somatostatin analogue octreotide is able to prevent renal and glomerular growth, probably mediated through changes in circulating GH and local kidney IGF-I levels.
Search for other papers by I. CHESTER JONES in
Google Scholar
PubMed
Search for other papers by D. K. O. CHAN in
Google Scholar
PubMed
Search for other papers by J. C. RANKIN in
Google Scholar
PubMed
SUMMARY
A method for the study of renal function and measurement of mean ventral and dorsal aortic blood pressure for the freshwater and seawater-adapted eel, and during transfer of the animal from fresh water to sea-water, is described.
Freshwater eels have higher resting blood pressure, p-aminohippuric acid (PAH) and inulin clearance rates and urine flow than seawater eels. Urine from freshwater animals has low Na, K, Ca, Mg and Cl concentrations, while the clearance rate of inorganic phosphate exceeded that of inulin. Urine from seawater animals has high Na, Ca, Mg and Cl concentrations while that of inorganic phosphate was low. Clearance rates for Ca and Mg greatly exceeded those of inulin.
During transfer from fresh water to sea-water there was an initial fluctuation in blood pressure, urine flow and PAH and inulin clearance rates which lasted about 2 hr. Thereafter these gradually declined to values observed for the seawater-adapted animal.
The significance of PAH and inulin clearance rates in the study of renal function in the eel and in teleosts in general is discussed.
Search for other papers by J. N. MILLS in
Google Scholar
PubMed
Search for other papers by S. THOMAS in
Google Scholar
PubMed
Search for other papers by K. S. WILLIAMSON in
Google Scholar
PubMed
SUMMARY
The magnitude of the influence of endogenous adrenal steroids upon renal excretion of electrolytes has been assessed by observing the changes on administering spironolactone, which blocks, at least in part, the effect of steroids upon the kidney. The findings indicate that endogenous steroids exert a sodium-retaining effect in subjects asleep at night, recumbent or standing in the afternoon, and ambulant and perhaps also recumbent in the morning. Endogenous steroids also promote chloride reabsorption, but the changes are usually smaller. Changes in excretion of potassium and hydrion have been less convincingly demonstrated, but it is believed that sodium reabsorption is by ion exchange for potassium and hydrion, as well as in association with chloride.
If the subject maintains the recumbent posture for 5 hr. from midday, the influence—and probably the production—of endogenous steroids declines steadily, but it is maintained if he stands. The contribution of steroids to the altered renal behaviour on changing posture has been assessed; the low sodium excretion on standing is in part due to a non-adrenal, presumably haemodynamic factor, and in part to aldosterone secretion; and on standing there is a modest but significant fall in potassium excretion due to the non-adrenal factor.
Search for other papers by B. Auf'mkolk in
Google Scholar
PubMed
Search for other papers by R.-D. Hesch in
Google Scholar
PubMed
ABSTRACT
The stimulation of cyclic AMP production by human renal cortical membranes in the presence of the GTP analogue 5′-guanylimidodiphosphate and a calcium chelator represents a homologous assay system for the evaluation of biologically active parathyroid hormone (bioPTH) in human serum. Bioactive PTH was raised above normal (normal range: undetectable to 4·6 pmol human PTH(1–34) per 1) in 13/17 (76%) patients with primary hyperparathyroidism, in 5/6 (83%) patients with surgically proven hyperparathyroidism secondary to chronic renal failure, in 4/5 (80%) patients with hyperparathyroidism secondary to hypocalcaemia, in all three patients with pseudohypoparathyroidism, in 5/17 (29%) patients with osteoporosis and in 1/9 (11%) patients with renal stones and/or hypercalciuria. Bioactive PTH correlated positively with immunoreactive PTH (iPTH) measured with a radioimmunoassay predominantly recognizing the middleand carboxyl-terminal region of the PTH molecule (r = 0·503, P<0·001). A positive correlation (r = 0·572, P<0·05) was found between values of serum calcium and bioPTH in the group with primary hyperparathyroidism. Immunoreactive PTH did not correlate significantly with calcium in this group. In the other patients except those who had chronic renal failure, a negative correlation between serum calcium and both bioPTH and iPTH was observed (P<0·01). When alkaline phosphatase was compared with bioPTH in all patients, the correlation was positive (r = 0·390, P<0·01); no significant correlation existed between iPTH and alkaline phosphatase in the patients studied. When comparing the metabolic status of the bones with bioPTH, there was a higher incidence of severe bone lesions in those patients with primary hyperparathyroidism who had extremely raised levels of bioPTH. In osteoporosis no simple relationship was apparent.
J. Endocr. (1986) 108, 9–15
Search for other papers by C. Pippard in
Google Scholar
PubMed
Search for other papers by P. H. Baylis in
Google Scholar
PubMed
ABSTRACT
The effect of rat prolactin on rat renal Na+-K+-ATPase activity was investigated by a cytochemical technique. Rat prolactin caused stimulation of Na+-K+-ATPase activity only in the outer medulla of the kidney, and not in renal cortical structures. Peak enzyme activity in cultured rat renal segments occurred after tissue had been exposed to rat prolactin for 2 min, and the time of maximal stimulation did not vary with the concentration of prolactin. There was a curvilinear response in Na +-K+-ATPase activity over the rat prolactin concentration range, 0·04–40 ng/1, but higher prolactin concentrations caused inhibition of enzyme activity. Na+-K+-ATPase response was totally blocked by specific rat prolactin antiserum. Human prolactin had no consistent effect on rat medullary Na+-K+-ATPase activity. Addition of specific tri-iodothyronine and arginine vasopressin antisera to rat prolactin was without effect, confirming that the stimulatory action of rat prolactin on Na+-K+-ATPase was not due to contamination with these hormones which are known to stimulate this enzyme.
J. Endocr. (1986) 108, 95–99
