Patients with Fe-deficiency anaemia are often afflicted by hypotension. However, the mechanism of secondary hypotension in Fe-deficiency anaemia is unknown. To investigate the pathogenesis of secondary hypotension in Fe-deficiency anaemia, we examined the effects of Fe deprivation on plasma aldosterone concentration and blood pressure in rats. A total of forty 4-week-old male Sprague–Dawley rats were assigned into four treatment groups of ten each for the 4-week study: Fe-deficient group (FD), Zn-deficient group (ZD), Fe/Zn-deficient group (FZD) and control group (CON). At days 26 and 27, blood pressure was measured by the tail-cuff method. Plasma aldosterone concentration was determined by ELISA. The data were analysed by Tukey's multiple comparison test. Rats in the FZD had significantly lower mean blood pressure (P < 0·01) and diastolic blood pressures (P < 0·05) and plasma aldosterone concentration (P < 0·01) compared to the CON. These results suggest that blood pressure is decreased in Fe-deficiency anaemia combined with Zn deficiency partly due to decreased circulating aldosterone concentrations in addition to decreased haematocrit.

Prenatal growth is sensitive to the direct and indirect effects of maternal dietary intake; manipulation can lead to behavioural and physiological changes of the offspring later in life. Here, we report on three aspects of how a high-salt diet during pregnancy (conception to parturition) may affect the offspring’s response to high oral salt loads: (i) dietary preferences for salt; (ii) response to salt and water balance and aldosterone and arginine vasopressin (AVP) concentrations after an oral salt challenge; (iii) concentrations of insulin and leptin after an oral salt challenge. We used two groups of lambs born to ewes fed either a high-salt (13% NaCl) diet during pregnancy (S lambs; n = 12) or control animals born to ewes fed a conventional (0.5% NaCl) diet during pregnancy (C lambs; n = 12). Lambs were subjected to short- (5 min) and long-term (24 h) preference tests for a high-salt (13% NaCl) or control diet, and the response to an oral challenge with either water or 25% NaCl solution were also carried out. Weaned lambs born to ewes fed high salt during pregnancy did not differ in their preference for dietary salt, but they did differ in their physiological responses to an oral salt challenge. Results indicate that these differences reflect an alteration in the regulation of water and salt balance as the metabolic hormones, insulin and leptin, were not affected. During the first 2 h after a single salt dose, S lambs had a 25% lower water intake compared to the C lambs. S lambs had, on average, a 13% lower AVP concentration than the C lambs (P = 0.014). The plasma concentration of aldosterone was higher in the S lambs than in the C lambs (P = 0.013). Results suggest that lambs born to ewes that ingest high amounts of salt during pregnancy are programmed to have an altered thirst threshold, and blunted response in aldosterone to oral salt loads.

An option to increase the productivity of saline land is to graze sheep on salt-tolerant plants, which, during the summer/autumn period, can contain 20% to 25% of their dry matter as salt. This study assessed the impact of coping with high dietary salt loads on the reproductive performance of grazing ewes. From the time of artificial insemination until parturition, 2-year-old maiden Merino ewes were fed either a high-salt diet (NaCl 13% of dry matter) or control diet (NaCl 0.5% of dry matter). Pregnancy rates, lamb birth weights, milk composition and the plasma concentrations of hormones related to salt and water balance, and energy metabolism were measured. Leptin and insulin concentrations were lower (1.4 ± 0.09 v. 1.5 ± 0.12 ng/ml; (P < 0.05) and 7.2 ± 0.55 v. 8.2 ± 0.83 ng/ml; P < 0.02) in response to high-salt ingestion as was aldosterone concentration (27 ± 2.7 v. 49 ± 5.4 pg/ml; P < 0.05), presumably to achieve salt and water homeostasis. Arginine vasopressin concentration was not significantly affected by the diets, but plasma concentration of T3 differed during gestation (P < 0.02), resulting in lower concentrations in the high-salt group in the first third of gestation (1.2 ± 0.18 v. 1.3 ± 0.14 pmol/ml) and higher concentrations in the final third of gestation (0.8 ± 0.16 v. 0.6 ± 0.06 pmol/ml). T4 concentration was lower in ewes ingesting high salt for the first two-thirds of pregnancy (162 ± 8.6 v. 212 ± 13 ng/ml; P < 0.001). No substantial effects of high salt ingestion on pregnancy rates, lamb birth weights or milk composition were detected.

Summary

Background and objective: This study was undertaken to investigate the role played by antidiuretic hormone (ADH), the renin–angiotensin system and atrial natriuretic factor (ANF) in the oliguria in patients undergoing spinal fusion.

Methods: Sixteen patients undergoing posterior spinal fusion using isoflurane and fentanyl (n = 8) or sufentanil (n = 8) had renin, aldosterone, ADH and ANF measurements.

Results: Compared to the non-oliguric patients, the oliguric patients had a higher number of fused vertebrae 10.5 ± 1.3 vs. 9.0 ± 0.5 (P = 0.01) and higher renin values at 12 h (3.3 ± 3.2 vs. 0.7 ± 0.6 ng L−1 s−1, P = 0.04). Hormonal values that had a significant correlation with intraoperative diuresis were: renin at 0.5 h (r2 = 0.26, P = 0.04), aldosterone at 0.5 h (r2 = 0.30, P = 0.03) and ANF at 0.5 h (r2 = 0.32, P = 0.02). Those that had a significant correlation with the mean postoperative diuresis were: renin at 6 h (r2 = 0.29, P = 0.03), 8 h (r2 = 0.26, P = 0.04) and 12 h (r2 = 0.31, P = 0.03), aldosterone at 6 h (r2 = 0.54, P = 0.001), 8 h (r2 = 0.40, P = 0.01) and 12 h (r2 = 0.32, P = 0.03), ADH at 24 h (r2 = 0.38, P = 0.01) and ANF at 6 h (r2 = 0.26, P = 0.045). Using stepwise regression, excluding hormonal values, only two continuous variables had a significant correlation with the mean postoperative diuresis: the number of fused vertebrae (P = 0.02) and the length of surgery (P = 0.02).

Conclusion: Activation of the renin–angiotensin system is the major cause of the early intraoperative oliguria. ADH and the renin–angiotensin system are both involved in the pathophysiology of postoperative oliguria in patients undergoing spinal fusion.

Elderly patients with hyperkalaemia often have low concentrations of plasma renin and aldosterone, perhaps secondary to reduced glomerular filtration and sympathetic insufficiency. The endocrine response to surgical stress and volume expansion during anaesthesia was studied in seven elderly patients with hyperkalaemia (mean age 87.7±SD 5.3 years), 18 elderly patients without hyperkalaemia (86.5±5.5 years), and 18 younger patients (52.6±7.2 years) as controls. Base-line values, in hyperkalaemic elderly patients, for plasma renin activity and plasma aldosterone concentration were 0.8±0.3 ng mL−1 h−1 and 2.8±0.8 pg mL−1 respectively (significantly lower than in the younger patients), and 287±42 pg mL−1 for plasma atrial natriuretic peptide levels, which were significantly higher. The plasma renin activity and aldosterone concentrations in elderly patients with hyperkalaemia were at all times lower, but not significantly, than those of the elderly patients without hyperkalaemia. The atrial natriuretic peptide concentrations (351±48 pg mL−1) in the hyperkalaemic elderly were significantly higher 90 min after induction of anaesthesia than in the normokalaemic elderly (108±38 pg mL−1). Hormone concentrations in the hyperkalaemic patients did not change during anaesthesia, but plasma atrial natriuretic peptide concentrations increased significantly in the normokalaemic elderly, and plasma renin activity and aldosterone of the younger patients increased significantly during anaesthesia. These results indicate that plasma renin activity, and the concentrations of aldosterone and of atrial natriuretic peptide in elderly patients with hyperkalaemia are unresponsive to surgical stress and volume expansion.

The effect of changes in dietary Na+ intake on plasma aldosterone levels and electrogenic amiloride-sensitive Na+ transport (Iamil) was studied in the rat distal colon. Five groups of rats were fed on diets containing different amounts of Na+. Estimated Na+ intake ranged from about 400–80000 ?equiv Na+ /kg body weight (BW) per d. Both variables investigated, Iamil and plasma aldosterone, depended non-linearly on Na+ intake. Reduction of the daily Na+ intake increased plasma aldosterone levels and if these levels reached the value 200 pg/ml or more then Iamil was induced. The corresponding Na+ intake was 1300 ?equiv Na+/kg BW per d. Iamil was not observed at lower aldosterone levels and higher Na+ intakes. Aldosterone infusion for 7 d produced similar changes in Iamil compared with dietary Na+-depleted animals and made the estimation of maximum transport capacity of Iamil possible. We conclude that Iamil operates only if Na+ intake decreases below minimal Na+ requirement in growing rats and that the maximum transport capacity of this pathway is reached only after very severe Na+ deprivation.

Recent studies have shown that faecal residue (dry weight) and Na and K increase with increasing levels of dietary fibre, an effect which may be related to unstirred layers that slow absorption and the flow rate of chyme through the gastrointestinal tract. Salts of Na are the primary osmotic components of chyme and influence both retention of fluid in the bowel and transit of fluid from the small to the large intestine. The present study examines the chronic effects of dietary Na and K intake on faecal Na, K and residue excretion. Male Sprague-Dawley rate were given 12–13 g feed/d (control (g/kg): Na 4, K 8.5) for 1 week, followed by a 4-week period where Na or K intake was altered (0.01–3 times control levels). These diets altered chronic (> 1 week) faecal residue excretion and affected Na and K excretion by 8-, 310-and 2100-fold respectively. Low dietary Na reduced faecal Na and residue; K excretion was doubled during week 1, but fell over weeks 2–4 despite a 4–5-fold increase in plasma aldosterone. Chronic high dietary Na increased faecal Na, residue and K despite a 60% decrease in plasma aldosterone. Chronic low dietary K decreased faecal Na, K and residue and plasma aldosterone. Chronic high dietary K did not alter faecal Na and K despite increased faecal residue and a 4–5-fold increase in plasma aldosterone. Faecal water was unchanged by diet, paralleling changes in faecal residue. Analyses of the results provide systematic models of chronic regulation of faecal Na, K and residue excretions. When plasma aldosterone is low (< 160 ng/I), weekly faecal residue excretion is equal to 3.6 g (fibre intake was 2.6–2.7 g/week) + 2.6 g/mmol Na, and K excretion is equal to 0.55 mmol/mmol Na. When plasma aldosterone is high (> 1500 ng/I) weekly faecal residue excretion is equal to 2.3 g + 2.6 g/mmol Na, and K excretion is equal to 0.7 mmol/week + 0.55 mmol/mmol Na.