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Saturday, December 4, 2010

EXTRACELLULAR THIRST STIMULI

EXTRACELLULAR THIRST STIMULI
Although the amount of fluid in the extracellular fluid (ECF) compartment is less than that in the cells, it is vital that the ECF be conserved to avoid debilitating changes in the volume and pressure of fluid in the blood vessels. The effects of extracellular fluid loss can include fainting, caused by insufficient blood reaching the brain. The behavioural response of drinking in response to hypovolaemia, a disorder consisting of a decrease in the volume of blood circulation, ensures that plasma volume does not fall to dangerously low levels.
There are a number of ways that ECF volume can be depleted experimentally, including haemorrhage, lowering sodium content in the diet, and excessive sweating, urine production or salivation. Two main thirst-inducing systems are activated by hypovolaemia. One is the renin–angiotensin system mediated by the kidneys. When reductions in blood pressure or volume are sensed by the kidneys, the enzyme renin is released, leading to the production of the hormone angiotensin II which stimulates copious drinking A second thirst-inducing system activated by hypovolaemia is implemented by receptors in the heart. For example, reducing the blood flow to the heart in dogs markedly increases water intake (Ramsay et al., 1975). It is still not clear precisely where such cardiac receptors are located. But it seems likely that they are located in the venous circulation around the heart, since the compliance (i.e. the ability to change diameter) of these vessels is high, making them responsive to changes in blood volume. Information from these receptors is probably carried to the central nervous system via the vagosympathetic nerves, from where information is relayed to the brain and drinking behaviour can be regulated.

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