of action

The transport of sodium is a process that occurs in the
kidney. Diuretic drugs inhibit this process specifically in the nephron
functional unit of kidney. Burg et al. Furosemide is a weak acid,
actively secreted into the proximal convoluted tubule, and exerts its effect
from inside of luminal surface of the ascending limb of Henle’s loop. According
to Hanze et al. Furosemide cause increased urinary loss of
sodium, chloride, calcium, magnesium and to a lesser extent potassium in man
and these effects are independent of glomerular filtration rate. It is evident
therefore that furosemide increases urinary loss of several ion species and is
not specific for sodium alone.

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According to Aurbach et al. The renal reabsorption
of calcium is controlled by parathyroid hormone, and that this hormone acts at
a cellular level through a cyclic 3′,5′-adenosine monophosphate (cAMP)
dependent system.

Important evidence on the renal action of furosemide has
been provided by Burg et al. using the thick ascending limb of Henle’s
loop from rabbits. These authors have shown that active transport of chloride
is the driving force for ionic movement in this part of the nephron, the
chloride being passively followed by sodium ions.


This transport process is inhibited by the presence of 10
-5 or 10 -6 M furosemide in the luminal fluid. We know that the inhibition of
ionic reabsorption from Henle’s loop is one of the major effects of furosemide in
the human kidney, and this has the effect of reducing concentrating ability in
patients who receive it (Anderton and Kincaid-Smith, 1971).

In dogs, furosemide in large doses has been shown to
inhibit sodium

reabsorption in the proximal tubule (Seldin et al., 1966),
and it seems

likely that a similar phenomenon is seen in the human

We have used the isolated bladder of the toad, Bufo
marinus, as a

model system to investigate the cellular mode of action
of furosemide.

This tissue actively transports sodium which is passively
followed by

chloride ions. Sodium transports from the urine into the

epithelial cells consists of two components, a passive
component and a

carrier mediated component (Ferguson and Smith, 1972).
This entry

step appears to be rate-limiting in the transepithelial
flow of sodium.

Sodium transport across the tissue is stimulated by
vasopressin, which

increases this rate of sodium entry into the epithelial
cells. It is important

to outline the biochemical steps by which vasopressin is

to increase entry of sodium. It is unnecessary to go into
all the evidence

for and against the idea that the effects of vasopressin
on sodium transport

are mediated by cAMP, and the following is the generally

sequence of biochemical events.

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