Abstract

Cardiac output (CO), heart rate (HR), stroke volume (SV), dorsal aortic blood flow (DABF), dorsal aortic blood pressure (P_DA) and plasma electrolytes were monitored in stanniectomized and sham-operated freshwater eels over a 3-week period; branchial shunting and systemic resistance (R_SYS) were estimated. DABF was significantly reduced by 45% from 11·72±0·48 (control) to 6·55±0·41 (n=6; day 21) ml.min⁻¹.kg⁻¹ within 3 weeks after the removal of the corpuscles of Stannius. This large reduction in blood flow was due to a 25% decrease in CO and a 100% increase in estimated branchial shunting which preceded the fall in CO. CO was decreased from 16·07 ±0·31 (control) to 11·91 ±1 (n=6; day 21) ml.min⁻¹.kg⁻¹ through a reduction in SV; there was no significant change in HR. Estimated branchial shunting, a relative measure of branchial arterio-venous blood flow, corresponded to 2·53±0·18 ml.min⁻¹.kg⁻¹ (control; n=12), which represents 16% of baseline CO. Ventral and dorsal aortic pulse flows also decreased following stanniectomy. The decrease in DABF occurred in conjunction with a reduction in P_DA which was measured for 12 days in a separate group of eels. Baseline P_DA (3·03 ±0·1 kPa) significantly decreased by 15% to 2·55 ±0·13 kPa 4 days after stanniectomy. However, this fall in P_DA was transient and accompanied by an elevation in derived R_SYS. These results support the hypothesis that the corpuscles of Stannius are closely linked to cardiovascular regulation in freshwater eels. Electrolyte changes (hypercalcemia, hypomagnesia, hyperkalemia and hyponatremia) were temporally coupled to the changes in blood flows. Impaired cardiovascular function and altered patterns of blood flow to osmoregulatory organs such as the gills, kidney and skin may have led to some or all of the electrolyte disturbances which followed stanniectomy.

Journal of Endocrinology (1995) 145, 181–194

SUMMARY

The effects were studied of cortisol, corticosterone and aldosterone on the concentrations of sodium and potassium in muscle and blood plasma and on water content of muscle in the fresh-water rainbow trout (Salmo gairdneri).

These steroids appeared to cause a loss in plasma sodium throughout the 96 hr. experimental period. An initial rise in muscle sodium was observed during the first 24 hr. after commencement of the treatments. The subsequent decline in muscle sodium was interrupted by a transient rise followed by a continuing decline.

The effect of these hormones on the potassium concentrations in plasma was variable, although there was a significant rise in the potassium concentration in muscle during the period of decline in sodium concentration.

The significance of these results in relation to the possible enhanced adrenocortical activity of the trout during adaptation to a marine environment is discussed.

SUMMARY

Developing marine birds, but not mature ones, when maintained on sea water failed to grow at the same rate as those maintained on fresh water. In both developing and mature birds maintained on sea water the size of the adrenal glands and supraorbital nasal glands showed dramatic increases. The significance of these changes is discussed in relation to both the results of other workers and our recent work on the salt-loaded domestic duck.

Abstract

Angiotensin II (ANG II)-mediated catecholamine release and its possible contribution to the pressor response was assessed in baroreceptor-denervated rats.

Neonatal male Sprague-Dawley rats were injected with the sympatholytic drug, guanethidine monosulphate (50 mg/kg s.c., 6 days/week) for 40 days. Plasma catecholamine concentrations were measured using a ³H-radioenzymatic assay as follows: (a) before and 30 s after the injection of saline or ANG II (79·3 pmol/kg i.v.), at the peak of the pressor response, then 50 s and 80 s thereafter, in guanethidine-treated (GUAN) and saline-injected (SHAM) rats, and (b) before and after adrenalectomy (ADX), following the same time-sequence for ANG II as in (a). Peak pressor responses to graded doses of ANG II (6·6, 26·4, 53·0 and 79·3 pmol/kg i.v.) were measured in GUAN+ADX and ADX rats. Destruction of peripheral sympathetic nerves was confirmed by measurements of plasma noradrenaline (NA), adrenaline (AD) and dopamine (DA) concentrations and by changes in pressor responses and heart rates following i.v. doses of tyramine.

ANG II induced significantly (P<0·05) greater pressor responses in GUAN+ADX rats than in ADX rats, especially after the 53·0 and 79·3 pmol/kg doses. Plasma AD concentrations increased within seconds after the pressor response to ANG II in both GUAN and SHAM rats but there was no change in plasma NA or DA concentrations (P<0·05). ANG-II-mediated AD release from the adrenal medulla may contribute to the overall pressor action of the peptide.

The vasculature became more sensitive to ANG II at a time when NA and DA depletion occurred following sympathectomy and/or adrenalectomy. This heightened sensitivity to ANG II was not due to a decrease in circulating ANG II in sympathectomized rats because even though plasma renin activity fell from 6·54 ±0·52 to 3·77 ±0·26 ng ANG I/ml per h it remained within the normal range.

Journal of Endocrinology (1994) 142, 19–28

Abstract

Somatostatin has been suggested to influence the somatotrophic axis outside the central nervous system, in reducing GH-induced IGF-I mRNA and IGF-I generation. This study aimed to determine whether such effects were mediated via the GH receptor (GHR). GH-deficient dwarf rats aged 45–47 days (n=8 per group) received twice daily subcutaneous injections of octreotide (1 mg/kg) (group O), saline (group S), octreotide (1 mg/kg) plus bovine GH (0·25 mg/kg) (group OG), or bovine GH (0·25 mg/kg) plus saline (group G) for 10 days.

Octreotide-treated animals had less weight gain compared with saline-treated animals, but not when GH cotreated (group OG vs G). Octreotide had an overall effect on decreasing length gain (P<0·01). Serum IGF-I (ng/ml) was reduced by octreotide (group O 171 ±11, group S 239 ± 20, P<0·01; group OG 283 ± 30, group G 362 ± 10, P<0·001), as was serum insulin (P<0·001). A significant decrease in hepatic and muscle IGF-I mRNA expression was found as expected, yet this was not associated with decreased hepatic GHR expression. Rather, an increase in hepatic ¹²⁵I-bovine GH specific binding was observed (P<0·001) and, in GH-cotreated animals (OG), hepatic GHR and GH binding protein (GHBP) mRNA expression were also increased by octreotide by approximately 40%. In muscle, octreotide was associated with an approximately 30% decrease in GHBP mRNA and no effect on GHR mRNA.

This study suggests that the suppressive effects of octreotide on IGF-I metabolism, at least in liver, are not mediated via down-regulation of GHR expression, but more likely by direct effects on IGF-I expression.

Journal of Endocrinology (1996) 149, 223–231

Abstract

The majority of IGF-I circulates in a large (150 kDa) ternary complex with IGF-binding protein-3 (IGFBP-3) and a non-IGF-binding acid-labile subunit. The secretion of ternary complex into the circulation from liver has been considered to be GH-dependent; however, recent data indicate that GH does not directly regulate hepatic IGFBP-3 synthesis. To examine the role of insulin in regulating plasma IGFBP-3 levels, postpubertal male GH-deficient (dw/dw) rats were treated every 8 h with injections (s.c.) of 0·9% saline, 20 μg insulin/day, 200 μg hIGF-I/day, or 20 μg insulin/day plus 200 μg hIGF-I/day, for 10 days with the animals being killed 2–3 h after the final injection. Hypoglycaemia was not observed in any of the treatment groups. hIGF-I treatment increased longitudinal growth and weight gain (P<0·05), while insulin treatment had no effect. Plasma IGF-I levels were increased in groups treated with hIGF-I (P<0·05), while insulin treatment resulted in a reduction (P<0-05): saline=267·1 ± 15·6 (ng/ml ± s.e.m.), insulin=219·3 ± 17·5, hIGF-I=391·7 ± 17·6, insulin plus hIGF-I=357·5 ± 31·8. Hepatic IGF-I mRNA expression was increased in insulin-treated dw/dw rats in comparison with hIGF-I-treated animals (P<0·05) but not in comparison with saline control or the combined treatment groups. Plasma levels of intact IGFBP-3, measured by ligand blot analysis, were increased in all treatment groups compared with saline (P<0·05): saline=100·0 ± 9·4% (% of saline ± s.e.m.), insulin=149·9 ± 17·5%, hIGF-I= 191·4 ± 17·3%, insulin plus hIGF-I=205·4 ± 15·3%. The levels of the 28/32 kDa IGFBPs and IGFBP-4 in plasma were increased by hIGF-I treatment (P<0·05) but not by insulin treatment. Hepatic specific ¹²⁵I-bovine GH binding was not significantly different in any of the treatment groups. This study provides the first evidence in non-diabetic animals that insulin regulates hepatic IGF-I mRNA expression, plasma IGF-I and plasma IGFBP-3 levels in the GH-deficient state without changes in hepatic GH receptors. The divergent response of plasma IGF-I and IGFBP-3 levels to insulin treatment in the present study may indicate an effect of insulin on the clearance of IGF-I from the circulation.

Journal of Endocrinology (1996) 150, 67–76