Regulation of arterial pH during fresh water to sea water transfer in the rainbow trout Salmo gairdneri

1976 ◽  
Vol 53 (2) ◽  
pp. 157-160 ◽  
Author(s):  
R.S. Milne ◽  
D.J. Randall
Keyword(s):  
Rainbow Trout ◽  
Fresh Water ◽  
Sea Water ◽  
Water Transfer ◽  
Salmo Gairdneri ◽  
Arterial Ph

Effects of ergocryptine, prolactin, and growth hormone on survival and ion regulation in rainbow trout, Salmo gairdneri

1978 ◽  
Vol 56 (11) ◽  
pp. 2394-2401 ◽  
Author(s):  
K. J. Brewer ◽  
B. A. McKeown
Keyword(s):  
Growth Hormone ◽  
Rainbow Trout ◽  
Fresh Water ◽  
Sea Water ◽  
Salmo Gairdneri ◽  
Elevated Plasma ◽  
Ion Regulation ◽  
Simultaneous Injection ◽  
Ion Concentrations ◽  
Peripheral Action

Ergocryptine, an ergot alkaloid that suppresses prolactin (PRL) secretion and also affects growth hormone (GH) levels in mammals, was injected into juvenile rainbow trout, Salmo gairdneri, averaging 8 to 31 g. In fresh water the drug caused few fatalities but lowered plasma Na+, plasma Ca2+, muscle K+, muscle Mg2+, and haematocrit values. The simultaneous injection of low doses of PRL or GH did not significantly modify the results obtained with the drug alone except for an increase in muscle Mg2+ levels. This suggests a possible peripheral action of the drug.Ergocryptine caused the death of S. gairdneri in dilute sea water, while in certain circumstances PRL and GH prevented mortalities. In this medium the drug caused elevated levels of plasma Ca2+ and muscle K+. The simultaneous injection of ergocryptine plus PRL in hyperosmotic media produced an elevated plasma Na+ concentration but a decrease in intracellular Na+ content and concentration.The results suggest that PRL is not critical for the survival of S. gairdneri in fresh water but may still be necessary to maintain body ion concentrations. In hyperosmotic media, however, PRL and GH may be essential for survival and may act on general metabolic processes rather than specific osmoregulatory organs.

Ionic Regulation in Rainbow Trout (Salmo Gairdneri) Adapted to Fresh Water and Dilute Sea Water

1979 ◽  
Vol 83 (1) ◽  
pp. 181-192
Author(s):  
F. B. EDDY ◽  
R. N. BATH
Keyword(s):  
Rainbow Trout ◽  
Fresh Water ◽  
Sea Water ◽  
Salmo Gairdneri ◽  
Ionic Regulation ◽  
Tissue Concentrations ◽  
Plasma Ions ◽  
Full Strength ◽  
Water Values ◽  
Eventual Death

Small rainbow trout (5–20 g) adapt to salinities of up to at least 22‰ but not to full strength sea water. In adapted fish plasma ions are regulated nearthe fresh water values, but there is an ionic invasion of the tissues, particularly by Cl− in muscle cells. Analysis of ionic regulation in adapted fish indicates that balance is maintained mainly by expending energy on Cl− regulation. Fish in full strength sea water can no longer regulate Na+ or Cl− in plasma or tissues, which results in high tissue concentrations of these ions and eventual death.

Uptake and Loss of Potassium by Rainbow Trout (Salmo Gairdneri) in Fresh Water and Dilute Sea Water

1985 ◽  
Vol 118 (1) ◽  
pp. 277-286 ◽  
Author(s):  
F. B. EDDY
Keyword(s):  
Rainbow Trout ◽  
Red Blood Cells ◽  
Fresh Water ◽  
Blood Cells ◽  
Sea Water ◽  
Specific Activity ◽  
Whole Body ◽  
Salmo Gairdneri ◽  
Potassium Influx

Potassium turnover was studied in rainbow trout, Salmo gairdneri Richardson, adapted to fresh water or 22% sea water using 42K and 86Rb. Potassium space of the whole body increased with time and was about 5 mmol kg−1 after 20h, while Rb+ space under the same conditions was only about 0.5 mmol kg−1, indicating slow penetration of body K+ by Rb+, especially in muscle and red blood cells. Potassium influx, measured by decrease in specific activity of the medium, was 0.07 mmol kg−1 h−1 in fresh water and 0.48 mmol kg−1 h−1 in 22 % sea water; the values for efflux were comparable, indicating that unfed fish are able to maintain K+ balance. In both fresh water and dilute sea water, K+ fluxes are 5% or less of the simultaneous Na+ and Cl− fluxes. The mechanism for K+ fluxes is discussed in terms in K+-ATPases.

scholarly journals Adaptational Responses of Rainbow Trout to Lowered External Nacl Concentration: Contribution of the Branchial Chloride Cell

1989 ◽  
Vol 147 (1) ◽  
pp. 147-168 ◽  
Author(s):  
STEVE F. PERRY ◽  
PIERRE LAURENT
Keyword(s):  
Rainbow Trout ◽  
Surface Area ◽  
Fresh Water ◽  
Primary Response ◽  
Chloride Cell ◽  
Whole Body ◽  
Salmo Gairdneri ◽  
Apical Surface ◽  
Ionic Fluxes ◽  
Area 5

1. Whole-body ionic fluxes and gill chloride cell (CC) morphology were monitored in rainbow trout (Salmo gairdneri) exposed acutely or chronically to natural fresh water (NFW; [Na+]=0.120 mmoll−1; [Cr]=0.164 mmoll−1) or artificially prepared fresh water with reduced [NaCl] (AFW; [Na+]=0.017 mmoll−1; [CT]=0.014 mmoll−1). 2. Net fluxes of Na+ (JnetNa) and Cl− (JnetCl) became extremely negative (indicating net NaCl loss to the environment) upon immediate exposure to AFW exclusively as a result of reduced NaCl influx (JinNa and JinNa). JnetNa and JnetCl were gradually restored to control rates during prolonged (30 days) exposure to AFW. 3. The restoration of JnetCl in AFW was due both to increased JinCl and to reduced Cl− efflux (JoutCl) whereas the primary response contributing to the restoration of JnetNa a t was an increase of JNain. 4. The total apical surface area of branchial CCs exposed to the external environment increased markedly after 24 h in AFW and remained elevated for 1 month as a consequence of enlargement of individual CCs and, to a lesser extent, increased CC density. JinNa and JinNa were correlated significantly with total CC apical surface area. 5. Plasma cortisol levels rose transiently in fish exposed to AFW. Treatment of NFW-adapted fish with cortisol for 10 days (a protocol known to cause CC proliferation) caused pronounced increases in JinCl and JinNa, as measured in both NFW and AFW. 6. These results suggest that an important adaptational response of rainbow trout to low environmental [NaCl] is cortisol-mediated enlargement of branchial epithelial CCs which, in turn, enhances the NaCl-transporting capacity of the gill as a result of the proliferation of Na+ and Cl− transport sites.

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