Vasopressin sensitive H[lowered 2]O transport system of canine renal medulla

Date

1975

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Abstract

  1. Cyclic AMP production in response to 8-Lysine vasopressin is a biphasic effect. A net twofold increase in cyclic AMP is observed in response to 8.6 x 10[raised -9]M hormone concentration. 2) Vasopressin stimulates H[lowered 2]O transport but has no effect on Na+ transport at the above concentration. There is a lag of about 0.75 minutes between the time when maximal value of cyclic AMP is achieved and increased H[lowered 2]O transport is observed. This time difference may be due to time required for translocation of cyclic AMP from basilar to apical surface, where it has its effect. 3) The vasopressin stimulated H[lowered 2]O transport is oubain sensitive. 1 mM oubain completely abolishes the vasopressin effect. This indicates the necessity of an osmotic gradient to achieve H[lowered 2]O transport in response to vasopressin. 4) In hypertonic medium (1500 mOsm/kg) though there is decrease in absolute concentration of cyclic AMP, percent increase over control in response to vasopressin is the same as in isotonic medium. The time course of cyclic AMP production is shifted indicating that phase 'I' is stabilized and accounts for all the cyclic AMP production. Phase 'II' is completely inhibited. There is no lag between cyclic AMP production and increased H[lowered 2]O transport in response to vasopressin. This may be because of the reduction in cell volume in hypertonic medium obliterates the necessity of translocation of cyclic AMP and hence the H[lowered 2]O effect is more rapid. 5) Further, the magnitude of vasopressin stimulated H[lowered 2]O transport in hypertonic medium is not significantly different from that in isotonic medium. This indicates that though cyclic AMP may be critical to trigger the increase in permeability of the apical surface the net amount of water transported is a function of osmotic gradient across the apical and basilar surfaces only. 6) Ca[raised +2] inhibits hormone binding to its receptor, thus blocking both vasopressin stimulated cyclic AMP production and H[lowered 2]O transport. There is no cyclic AMP independent vasopressin stimulated H[lowered 2]O transport observed. 7) Colchicine disrupts microtubules and blocks vasopressin action at a step after the production of cyclic AMP. A minimum of 30 min. preincubation in colchicine containing medium is essential for it to block the hydroosmotic effect of vasopressin. 10 mM dibutryl cyclic AMP can not stimulate H[lowered 2]O transport in presence of colchicine. This indicates that microtubules and apical membrane interactions within the tubular cell is critical for transtubular flow of H[lowered 2]O.

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Kidneys

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