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Abstract
The renal effects of arginine vasopressin and oxytocin were studied in the conscious unrestrained rat infused with 0·077 m NaCl. Peptides were infused at rates of 24 and 160 pmol/min (vasopressin) or 30 and 200 pmol/min (oxytocin) either alone or as a combination of the two lower or two higher doses. The rates of infusion were selected to give ratios of oxytocin:vasopressin similar to those seen in the plasma of euhydrated and dehydrated rats.
Vasopressin produced dose-dependent antidiuretic and natriuretic responses, the natriuresis commencing after 15–30 min infusion. Oxytocin produced dose-dependent diuretic and natriuretic responses, the natriuresis commencing within the first 15 min of infusion. Combined infusion of vasopressin and oxytocin produced dose-dependent antidiuretic responses which were comparable to those seen with vasopressin alone. The natriuretic response from combined infusion at the higher rate appeared to have the greater magnitude for individual 15-min periods of the vasopressin response combined with the longer duration of the oxytocin response. Although the total natriuretic response was therefore greater, this difference failed to reach significance.
Only the higher rates of infusion of vasopressin and oxytocin significantly increased the clearance of sodium, by 53 ± 23 and 62 ± 18% and glomerular filtration rate (GFR) by 23 ± 4 and 23 ± 4% respectively. The clearance of sodium during the combined hormone infusion was significantly greater (109 ± 21%), while the rise in GFR at 23 ± 5% was comparable to that seen when each hormone was given separately. Both fractional excretion of sodium and potassium excretion were also significantly elevated by this combined infusion, suggesting an additional tubular component to the response. Although no synergistic effect of neurohypophysial hormones on the antidiuresis was found in the conscious rat, they may act together to promote sodium excretion
Journal of Endocrinology (1995) 144, 441–448
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ABSTRACT
The peptides vasopressin-Gly and vasopressin-Gly-Lys-Arg occur as part of the sequence of the vasopressin-neurophysin precursor molecule and may be released from the hypothalamus and/or pituitary. [8-Lysine]-vasopressin-Gly (LVP-Gly) and [8-lysine]-vasopressin-Gly-Lys-Arg were administered i.v. to conscious, water-diuretic rats. The renal effects of the peptides were assessed by comparison with the actions of [8-lysine]-vasopressin (LVP) which was administered to separate groups of rats.
LVP-Gly and LVP-Gly-Lys-Arg were weakly antidiuretic. LVP-Gly-Lys-Arg was the more potent of the two peptides, but on a molar basis it only had about 10% of the antidiuretic activity of LVP. LVP-Gly and LVP-Gly-Lys-Arg at 10 pmol/h per 100 g body weight (equivalent to the maximal antidiuretic dose of LVP) slightly decreased (P < 0·001) urine flow without causing significant changes in urine osmolality.
LVP (10 pmol/h per 100 g body weight) promoted a marked natriuresis (P < 0·001 ) but LVP-Gly and LVP-Gly-Lys-Arg were not natriuretic, even at the dose which was markedly antidiuretic (100 pmol/h per 100 g body weight). Osmolal output decreased at all doses during administration of the extended peptides, but was not significantly changed in the control group or by LVP. Inulin clearance was decreased by about 30% during administration of both LVP and LVP-Gly-Lys-Arg at 100 pmol/h per 100 g body weight.
It is concluded that LVP-Gly and LVP-Gly-Lys-Arg show weak antidiuretic activities and that the effect on urine flow may be partly due to a decrease in glomerular filtration rate (GFR). The decrease in osmolal output produced by the peptides is also a likely consequence of an effect on GFR. It is suggested that LVP-Gly and LVP-Gly-Lys-Arg have a low potential for activation of tubular vasopressin receptors, as shown by the weak antidiuretic activity and lack of a natriuretic action, but that they have a relatively stronger action on glomerular vasopressin receptors.
J. Endocr. (1986) 108, 255–260
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Departments of Medicine-Renal Electrolyte Division, Pharmacology and Chemical Biology, Department of Veterinary Clinical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
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Escherichia coli . PLoS ONE 9 e84013 . ( doi:10.1371/journal.pone.0084013 ) Khandelwal et al. 2009 Khandelwal P Abraham SN Apodaca G 2009 Cell biology and physiology of the uroepithelium . American Journal of Physiology. Renal Physiology 297
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ABSTRACT
Six male volunteers were infused with arginine (0·5 g/kg body weight) over 30 min, after an overnight fast and water deprivation. There was a significant decrease in renal phosphate clearance (P<0·025) and urinary cyclic adenosine monophosphate (cAMP) output (P<0·025) during the 60- to 90-min period after the beginning of the infusion; both returned to the preinfusion basal levels within 150 min. The plasma levels of parathyroid hormone (PTH) were not affected by the infusion and remained unchanged during the subsequent 150 min. Plasma levels of arginine vasopressin (AVP) were also not significantly affected although plasma osmolality increased by 6–9 mmol/kg in all subjects. The infusion resulted in a diuresis, and a fall in urine osmolality but a decrease in free-water clearance; creatinine clearance was not affected. Six other subjects were given a bolus of 230 i.u. PTH intravenously, and 20 days later this was repeated during an infusion of arginine (0·5 g/kg body weight). There was a significant decrease in urinary phosphate (P< 0·025) and cAMP excretion (P<0·05) when PTH was given with arginine. It is suggested that arginine blocks the action of PTH on the proximal renal tubule but not that of vasopressin on the distal nephron and collecting ducts.
J. Endocr. (1986) 111, 501–506
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ABSTRACT
The effects of cortisol on hepatic and renal gluconeogenic enzyme activities were investigated in sheep fetuses during late gestation and after experimental manipulation of plasma cortisol levels by fetal adrenalectomy and exogenous infusion of cortisol. Hepatic and renal gluconeogenic enzyme activities increased with increasing gestational age in parallel with the normal rise in fetal cortisol levels towards term (146± 2 days). For the majority of enzymes this increase in activity towards term was prevented when the prepartum cortisol surge was abolished by fetal adrenalectomy and stimulated prematurely in fetuses younger than 130 days by exogenous infusion of cortisol. When the data from all the fetuses were combined irrespective of treatment or gestational age, there were significant positive correlations between the log plasma cortisol concentration in utero and the activities of glucose-6-phosphatase, fructose diphosphatase, phosphoenolpyruvate carboxykinase and aspartate transaminase in the fetal liver and kidney, and pyruvate carboxylase in the fetal liver but not in the kidney. No correlation was observed between log plasma cortisol and alanine aminotransferase activity in either fetal liver or kidney. These findings show that cortisol is a physiological regulator of most of the fetal gluconeogenic enzymes and enhances the glucogenic capacity of the sheep fetus during late gestation.
Journal of Endocrinology (1993) 137, 213–222
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ABSTRACT
Basolateral membranes were prepared from rat renal cortex by density gradient centrifugation. Their purity was confirmed by electron microscopy and by marker enzyme enrichment. The basolateral membrane preparation was shown to be derived predominantly from the proximal renal tubule by measurement of hormone-stimulated adenylate cyclase; marked stimulation of adenylate cyclase was found with parathyroid hormone, but not with isoprenaline, antidiuretic hormone or calcitonin. A single class of specific high-affinity [3H]angiotensin II-binding site was identified in the basolateral membrane preparation which, after correction of results for tracer degradation, showed equilibrium dissociation constant of 0·23 nmol/l and binding site concentration of 485·8 fmol/mg protein.
Binding sites for [3H]angiotensin II were measured in basolateral membranes prepared from rats fed diets with a low, normal or high sodium content. A trend of increased binding site density with reduced sodium intake was found which did not reach statistical significance. No effect on affinity was demonstrated. Treatment of rats on a low-sodium diet with captopril (500 mg/l drinking water) caused a significant reduction in binding site density; no effect on affinity was demonstrated.
These findings suggest that the density of angiotensin II receptors at this site is altered by the activity of the renin-angiotensin system.
Journal of Endocrinology (1989) 122, 499–507
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ABSTRACT
Twenty patients with chronic renal failure were studied before and after haemodialysis. Plasma atrial natriuretic peptide (ANP) concentrations were markedly elevated (P < 0·01) before dialysis in comparison with healthy control subjects. After haemodialysis the plasma ANP concentration was lower in 19 patients (P < 0·01) but remained above the normal range in all but three cases. Systolic and diastolic blood pressure and body weight fell during dialysis but none of these changes correlated with the reduction of the plasma ANP concentration. Chromatographic analysis of plasma extracts indicated that α-ANP is the predominant circulating molecular form. The increase in concentration of ANP in plasma between dialyses, at a time when many patients are susceptible to sodium and water overload, and its return towards normal after dialysis supports the putative role of ANP as a circulating factor released in response to sodium and water accumulation.
J. Endocr. (1986) 110, 193–196
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SUMMARY
1. Plasma cortisol concentrations, and the urinary output of free and conjugated Porter-Silber reacting steroids, 17-ketosteroids (17-KS), 'total 17-OH CS', urinary cortisone and cortisol, free and conjugated tetrahydrocortisone and cortisol were measured before and after a 1 l. water load.
2. The plasma cortisol concentration fell within 30 min of water ingestion, and tended to increase as diuresis declined.
3. There was a simultaneous increase in the urinary output of 17-KS, total 17-OH CS, and free Porter-Silber reacting steroids. In contrast, urinary excretion of glucuronide-conjugated corticosteroids did not increase during diuresis.
4. The implications of these findings are discussed and it is concluded that (a) the enhanced corticosteroid output during water diuresis is renal in origin, suggesting that tubular factors play a part in the excretion of these hormones; and (b) the role of the adrenal in the excretion of a water load is permissive.
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ABSTRACT
In previous studies, we have demonstrated that 1–10 fmol arginine vasopressin (AVP)/l maximally stimulates the activity of the enzyme Na+/K+-ATPase in the rat renal medullary thick ascending limb (MTAL) of Henle's loop after 4 or 10 min of stimulation when measured using a cytochemical bioassay. We have tested the hypothesis that this stimulation is mediated by the V2 receptor in the MTAL. A cytochemical bioassay was used to investigate the effect of specific V1 and V2/V1 antagonists and a synthetic V2 agonist [1-deamino,8-d-arginine]-vasopressin (dDAVP), on the activity of Na+/K+-ATPase. There was no effect of the V1 antagonist (1 fmol-1 μmol/l) in inhibiting the activity of Na+/K+-ATPase stimulated by 1 fmol AVP/l. In contrast, 100 pmol of the V2/V1 antagonist/l significantly (P < 0·001) inhibited the stimulation of Na+/K+-ATPase activity by 1 fmol AVP/l from 55·5±4·3 (s.e.m.) to 31·9±1·6 mean integrated extinction (MIE) after 4 min of stimulation and from 67·0±3·2 to 36·9±0·7 MIE after 10 min of stimulation. Similarly, the stimulation of Na+/K+-ATPase by 10 fmol dDAVP/l was inhibited by the V2/V1 antagonist from 55·1±1·0 to 26·1±0·5 MIE after 4 min of stimulation.
We conclude that the stimulation of Na+/K+-ATPase by AVP is mediated by the V2 receptor in the rat renal MTAL.
Journal of Endocrinology (1990) 127, 213–216
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ABSTRACT
The effect of potassium (K)-free medium on the stimulation of cyclic AMP (cAMP) production by arginine vasopressin (AVP) and forskolin was examined in rat renal papillary collecting tubule cells in culture. All experiments were performed in the presence of 3-isobutyl-l-methylxanthine (0·5 mmol/l). Cellular cAMP levels in response to 1 nmol and 0·1 μmol AVP/1 were 430·9 ± 42·1 (s.e.m.) and 501·8± 43·6 fmol/μg protein per 10 min respectively; these levels were significantly (P <0·01) higher than those in the vehicle-treated group (126·6 ± 23·3 fmol/μg protein per 10 min). The cellular cAMP response to 1 nmol AVP/1 was significantly attenuated after 24 and 72 h of exposure of cells to K-free medium, cellular concentrations of cAMP being 280·2 ± 37·1 and 233·0 ± 9·6 fmol/μg protein per 10 min respectively. The response of cAMP to AVP remained unchanged when the cells were preincubated with K-free medium for 1 h. Similarly, forskolin (20 nmol/l)-stimulated cellular cAMP production was also significantly impaired after 24 or 72 h of exposure of cells to K-free medium. When the cells preincubated in K-free medium were again exposed for 1 h to K-replete medium containing 5 mmol KC1/1, cellular cAMP production in response to AVP or forskolin recovered totally. Cellular protein and ATP content and cellular viability were not altered by exposure of cells to K-free medium for 24 h, and thus the impaired cAMP response to AVP or forskolin in the K-depleted cells was independent of altered cellular viability and source of ATP. The present results indicate that the K ion is an important factor for AVP– and forskolin-activated adenylate cyclase at the catalytic unit in the renal papillary collecting tubule cells.
J. Endocr. (1987) 113, 199–204
