Hormone studies in Myxine glutinosa: failure of calcitonin to influence urine flow or plasma and urine electrolyte balance.

Hagfish, Myxine glutinosa, were used in a series of experiments to determine a possible role for calcitonin in plasma and urine electrolyte balance. Individual animals were anaesthetised and implanted with polythene cannulae for monitoring blood pressure and for infusion/injection. Urine was collected by manual palpation of the body surface whilst blood samples were withdrawn from the lateral sinus. Following injection of either 1.25 or 3.75 micrograms kg body wt-1 calcitonin, there was no significant change in either the plasma or urine composition of sodium, potassium, calcium, or magnesium ion levels. These results indicate that calcitonin may not be involved in electrolyte homeostasis in Myxine.

Hormone studies in Myxine glutinosa: effects of the eicosanoids arachidonic acid, prostaglandin E1, E2, A2, F2 alpha, thromboxane B2 and of indomethacin on plasma cortisol, blood pressure, urine flow and electrolyte balance.

Hagfish, Myxine glutinosa, were used in an investigation of the possible effects of various eicosanoids and the prostaglandin synthetase inhibitor indomethacin, on cortisol production, blood pressure control, urine flow and electrolyte balance. Cortisol levels in plasma of untreated control animals and plasma from animals 1 h following injection of 50 micrograms kg-1 prostaglandin E1, E2, A2, F2 alpha TXB2 and indomethacin were not detectable. However, plasma cortisol levels rose to between 10 and 26 pg ml-1 1 h following injection of either 50 micrograms kg-1 arachidonic acid or prostaglandin E2. This rise was similar in magnitude to that produced 1 h following administration of 50 micrograms kg-1 porcine ACTH. The resting dorsal aortic blood pressure of between 3.50 and 3.75 mmHg was reduced on average by 50% for 12-15 min when animals received 10 micrograms kg-1 arachidonic acid, prostaglandin E1, E2, A2, and TXB2 and was effectively reduced to zero for 20 min or more following 50 micrograms kg-1 of these eicosanoids. Similar doses of prostaglandin F2 alpha, however, evoked an increase in blood pressure (19-33%) whilst indomethacin was without effect. Control measurements of urine flow in Myxine were estimated to be between 540 and 660 microliters h-1 kg-1. There was a marked reduction in urine output following the arterial vasodepression induced by arachidonic acid, prostaglandin E1, E2, A2 and TXB2 in doses of 10 micrograms kg-1, an effect which became even more pronounced following injection of 50 micrograms kg-1 quantities, leading in some cases to complete anuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic, renal, and steroidogenic actions of prostaglandins E1, E2, A2, and F2 alpha in European eels.

Seawater-adapted eels were implanted with both venous and arterial cannulae and catheterised. Prostaglandin in 0.9% glucose saline was given either by 10 microliters injection or by infusion (40 ng/min) while blood pressure recordings and blood samples were taken from the dorsal aorta. Glomerular filtration rates were calculated from the clearance of [3H]inulin, renal plasma flow from the clearance of PAH, and functional tubular mass from measurements of glucose reabsorption maxima (TmG). Cortisol levels were measured by radioimmunoassay. Injections of prostaglandin E1, E2, and A2 (0.01-10 ng/kg body wt) induced transient reductions in dorsal aortic blood pressure whilst concentrations of between 10 and 100 ng/kg body wt caused both prolonged vasodepression and glomerular antidiuresis, with decreased TmG and CPAH. Fractional excretion of electrolytes remained unchanged. Doses of 10-50 micrograms/kg body wt caused an initial glomerular diuresis, increased TmG and CPAH but were without effect on the fractional excretion of the filtered load. This diuretic action was followed by a longer period of antidiuresis. The vasodepression during 24 hr prostaglandin infusion became less severe after an initial 2-hr period, indicating a degree of tachyphylaxis. Prostaglandin F2 alpha in doses of 10-50 micrograms/kg body wt was slightly vasopressor but with no obvious effect on kidney function. All prostaglandins so far used, given either by infusion or injection caused a significant increase in cortisol production. These results suggest that prostaglandins may play similar roles throughout a range of vertebrates.

Depression of sodium, chloride and calcium ions in the plasma of goldfish (Carassius auratus) and immature freshwater- and seawater-adapted eels (Anguilla anguilla L.) after acute administration of salmon calcitonin.

Goldfish showed a significant reduction in their plasma sodium and calcium levels 1 h after receiving 50 i.u. calcitonin per kg body weight. When 100 i.u. calcitonin were injected there was a significant fall in circulating levels of both sodium and calcium and also of chloride ions compared with those found in untreated control animals. Administration of calcitonin to immature eels adapted to either freshwater or seawater conditions showed no significant change in plasma ion composition at doses of 10 i.u. per kg body weight or less. However, doses of 50 and 100 i.u. caused significant reductions in plasma sodium, chloride and calcium ion levels compared with sham-injected control animals. When immature eels were given 100 i.u. calcitonin per kg body weight there were significant reductions in the plasma levels of sodium, chloride and calcium ions but the timing of these changes was slightly different. In freshwater-adapted eels, the depression of plasma sodium was seen after 30 min and lasted for up to 2 h, whilst depression of plasma chloride and calcium was not seen until 1 h after injection. In addition, whilst the lowering of plasma chloride ions lasted up to 2 h after injection, the plasma calcium had returned to the preinjection control level by this time. In seawater-adapted eels the depression of sodium, chloride and calcium levels was seen at 30 min and the effect continued for up to 2 h after injection when the depression was no longer apparent.