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stimulate activity of the renal 1α-hydroxylase (1α(OH)ase) to increase the synthesis of 1,25(OH) 2 D. The kidney is one of the most important sites for physiologic regulation of serum phosphate; it controls urinary phosphate excretion to balance the
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It is well known that renal hypertrophy is induced by hyperthyroidism; however, the mechanism is not fully understood. We recently reported that cardiac hypertrophy in hyperthyroidism is mediated by enhanced cardiac expression of renin mRNA. The present study addresses the hypothesis that renal hypertrophy in hyperthyroidism is mediated by amplification of renal expression of renin mRNA. Twenty Sprague-Dawley rats were divided into control (n=5) and hyperthyroid groups by daily intraperitoneal injections of saline vehicle or thyroxine. The hyperthyroid group was subdivided further into hyperthyroid-vehicle (n=5), hyperthyroid-losartan (n=5), and hyperthyroid-nicardipine (n=5) groups by daily intraperitoneal injections of saline vehicle, losartan, or nicardipine. All rats were killed at 4 weeks, and the blood and kidneys were collected. The kidney-to-body weight ratio increased in the hyperthyroid groups (+34%). Radioimmunoassays and reverse transcriptase-polymerase chain reaction revealed increased renal renin (+91%) and angiotensin II (+65%) levels and enhanced renal renin mRNA expression (+113%) in the hyperthyroid groups. Losartan and nicardipine decreased systolic blood pressure to the same extent, but only losartan caused regression of thyroxine-induced renal hypertrophy. These results suggest that thyroid hormone activates the intrarenal renin-angiotensin system via enhancement of renal renin mRNA expression, which then leads to renal hypertrophy.
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The renal nerves of the left kidney of sodium-replete anaesthetized rats were stimulated for 30-min periods at 2–3 Hz (15 V, 0·2 ms). Renal blood flow was reduced by 22% and glomerular filtration rate by 14% which resulted in a rise in filtration fraction of 12%. Circulating plasma renin activity was increased by 30% during such nerve stimulation. In rats treated for 3–4 weeks with deoxycorticosterone acetate (DOCA) and saline (150 mm-NaCl) basal values of arterial blood pressure, renal blood flow, glomerular filtration rate and filtration fraction were not significantly different from those observed in sodium-replete rats. However, plasma renin activity was lower, being approximately one-third of that observed in sodium-replete animals. Stimulation of the renal nerves in rats treated with DOCA and saline resulted in a fall in renal blood flow of 32% and a much larger fall in glomerular filtration rate of 33% which resulted in no change in filtration fraction. Plasma renin activity was not changed by renal nerve stimulation in the animals treated with DOCA and saline. It is suggested that these renal responses provide evidence in the rat for a role of locally generated angiotensin II in regulating glomerular filtration rate during electrical activation of the renal nerves by causing preferential vasoconstriction of the efferent arteriole.
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actions of AII on the cardiovascular and renal systems before and after birth, while the AII type 2 (AT 2 ) receptor is primarily and widely expressed in fetal tissues and, although its function is less clear, it appears to be involved in the control of
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SUMMARY
The fasting serum phosphate level, the tubular maximal (Tm) phosphate reabsorption and the mean renal phosphate threshold were measured in 18 hyper- and six hypothyroid patients in comparison with 11 euthyroid control subjects. A significant increase of serum inorganic phosphate, phosphate Tm and of the mean renal phosphate threshold were found in hyperthyroidism. These findings suggest an increased tubular reabsorption of phosphate in hyperthyroidism. Four main possible mechanisms of such a renal handling of phosphate in thyroid disease are briefly mentioned although their acceptance needs more direct proof.
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ABSTRACT
The mechanism of water conservation is impaired in ageing mammals. An age-related defect in the release of vasopressin has been implicated but, more recently, attention has moved to the renal component of the water conservation mechanism. Previous studies using renal cells prepared from mice of different ages have shown that the threshold dose of vasopressin required to elicit a significant rise in cyclic AMP (cAMP) was greater in older animals. The dose–response curve was moved to the right in 35-month-old mice, i.e. the concentration of vasopressin required to give maximum cAMP output was increased. To investigate this further we examined the binding of vasopressin to renal medullary cells maintained in short-term culture, to determine whether the decreased response of cAMP levels to vasopressin is due to changes in hormone-receptor interaction. In 6-month-old male mice the dissociation constant (K d) was 2·38 nmol/l and the maximum binding of the hormone (Bmax) was 47·6 fmol/106 cells, and at 30 months of age K d was 2·37 nmol/l and Bmax was 47·0 fmol/106 cells. In female mice the changes were more complicated because the data for the 6-month-old mice could be split into two groups. It is concluded that there are no age-related differences in the numbers of receptors or their affinity for vasopressin, and that the decreased cAMP response is probably associated with post-receptor mechanisms in this species.
J. Endocr. (1987) 115, 379–385
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ABSTRACT
Diurnal variation in blood melatonin levels and renal melatonin excretion was monitored in five ewes by blood sampling and quantitative urine collection at 2-h intervals. A typical secretory pattern of melatonin was seen both in blood and urine levels and in the renal excretion of melatonin. Serum melatonin levels increased from daytime values of approximately 200 pmol/l to a mean of 800 pmol/l during darkness. Urine flow rate and urine osmolality did not show any clear diurnal rhythm.
To examine whether urine flow rate affects renal melatonin excretion at night, urine was collected in three consecutive 30-min fractions, and blood was sampled in the middle of each urine collection period when the sheep were in normal water balance or after hydration. Hydration increased urine flow rate over sixfold and decreased urine osmolality well below plasma osmolality. Glomerular filtration rate, measured as creatinine clearance, did not change. Serum melatonin concentrations did not differ between hydrated and non-hydrated sheep. However, urinary melatonin excretion was 1·1 ± 0·3 (s.e.m.) pmol/min at midnight in normal water balance, and significantly higher (2·6 ± 0·4 pmol/min) in the hydrated state.
In this study, the validity of urinary melatonin determinations as an indicator of pineal function was confirmed in normal water balance. In addition, our results suggest that a high tubular fluid load during diuresis increases urinary melatonin excretion because of decreased tubular reabsorption. This means that urine flow rate should be taken into consideration in studies where urinary melatonin levels are used as an index of production of the indole by the pineal gland.
Journal of Endocrinology (1993) 138, 445–450
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ABSTRACT
Standard renal clearance techniques were used to investigate the acute effects of TRH on kidney function in anaesthetized rats. A significant reduction in salt and water outputs, glomerular filtration rate and renal plasma flow was produced within 10 min of infusion of 12 μg TRH over 30 min. The rapidity of the response may suggest a direct effect of TRH on the renal vascular system.
J. Endocr. (1987) 113,445–448
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Abstract
The effect of insulin-like growth factor-I (IGF-I) administration on body weight gain and the rate of recovery of renal function was investigated in rats following an acute episode of renal ischaemia. Since the des(1–3)IGF-I and LR3IGF-I variant forms of IGF-I have been shown to be more potent than IGF-I, their effects were also examined. Acute renal failure was produced in male Sprague–Dawley rats by clamping both renal arteries for 45 min. Treatment was commenced at the time of renal artery occlusion with vehicle (0·1 mol acetic acid/l; control group), IGF-I (2·0 mg/kg per day), des(1–3)IGF-I (2·0 mg/kg per day) or LR3IGF-I (1·5 mg/kg per day) by s.c. osmotic pump, and continued for 7 days, with rats being held in metabolism cages. Glomerular filtration rate (GFR) was estimated by the use of 51Cr-EDTA continuously infused i.p. via osmotic pump. Following the episode of renal ischaemia, body weight gain and nitrogen retention were significantly improved in all three peptide-treated groups, and serum urea concentrations were reduced in the groups treated with IGF-I and des(1–3)IGF-I. However, there was no evidence of the variants having any increased potency over the growth effects of IGF-I itself. GFR was significantly reduced, urine output was increased and urinary concentrating ability was reduced in all groups compared with normal rats, with no significant effect of the IGF peptides being apparent.
A closer examination of the acute effects of LR3IGF-I on renal function was undertaken by measuring GFR for 3 days before and 3 days after renal ischaemia in two groups of rats, treated for the latter 3 days with either vehicle (controls) or LR3IGF-I (1·5 mg/kg per day). LR3IGF-I treatment following renal ischaemia resulted in a significantly greater fall in GFR than in controls, urinary osmolality was also significantly reduced, and fractional excretion of sodium was increased. In addition, there was histological evidence of a greater degree of tubular epithelial calcification in the kidneys of the rats treated with LR3IGF-I.
This study showed that administration of IGF peptides at doses sufficient to cause significant improvement in anabolic status did not improve renal function in rats following an acute episode of renal ischaemia. Indeed the LR3IGF-I variant of IGF-I had a deleterious effect on renal function in the early stage of the recovery period.
Journal of Endocrinology (1994) 140, 23–32
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SUMMARY
Extracts of porcine thyroid containing calcitonin produced increases in urinary flow and urinary electrolyte content when infused or injected into anaesthetized rabbits. This response occurred more rapidly after intraaortic than after intravenous injection and was accompanied by an increase in glomerular filtration rate (inulin clearance) and renal plasma flow (paraaminohippuric acid clearance).
Preparations of calcitonin failed to affect the short-circuit current in isolated frog skin.
Although an effect of calcitonin on renal tubular transport mechanisms cannot be excluded it seems likely that one mechanism responsible for the diuretic effect of this compound in the rabbit is an increase in renal blood flow.
