The effect on drinking in the rat of intravenous infusion of angiotensin, given alone or in combination with other stimuli of thirst

Abstract

SUMMARY1. Intravenous infusion of angiotensin causes rats which are in water balance to drink water.2. The mean amount of angiotensin needed to initiate drinking was 291 + 4-6 jtg/kg (S.E. of mean) in twenty normal rats, and 15-7 + 241 ,g/kg in thirty-four nephrectomized rats.3. The nephrectomized rat is therefore more sensitive to this action of angiotensin than the rat with intact kidneys.4. The rates of infusion (0.05-3.0 jtg/kg-l min-) which cause drinking are comparable to those used to produce other effects in rats.5. Angiotensin restores the drinking response of the nephrectomized rat subjected to caval ligation to a value similar to that obtained in the uninfused normal rat subjected to caval ligation.6. The effects of angiotensin and hypertonic saline on drinking are additive when both substances are administered to nephrectomized rats.7. These experiments provide further support for the view that the renin-angiotensin system is concerned in extracellular thirst.

Renin‐like activity of the rat submaxillary gland: characterization and the effect of several drugs and stimuli

“…Interestingly, both tissues which contain renin activity, the kidney and the submaxillary gland, are essential for thirst induced by hypovolemia (Gutman & Benzakein, 1969;Gutman et al, 1971) and the renin-angiotensin system has been demonstrated to be a thirst-inducing stimulus (Fitzsimons & Simons, 1969).…”

Review: AT1-receptors in the central nervous system

“…Following the early demonstrations by Fitzsimons and colleagues that water drinking was a response to stimulation of the renin-angiotensin-aldosterone system 56 or to systematically-administered Ang II, 57 the question arose as to its site of action in the brain. How could a circulating peptide like Ang II, which is unable to cross the blood-brain barrier, induce water drinking?…”

Neuroendocrine Factors Influencing Polydipsia in Psychiatric Patients: An Hypothesis

“…In the next section, we examine data on angiotensin II (A-II). It is a known dipsogen in animals (Fitzsimons and Simons 1969), and in man, it is associated with dis orders with abnormal thirst (Yamamoto et al, 1986;Phillips et al 1985b). Dopamine-2 blockade by typical neuroleptics increases A-II-induced thirst in animals (Sumners et al 1981) and enhances peripheral response to A-II in man (Missale et a1.…”

“…Angiotensin II has a profound effect on thirst and drinking in animals. Angiotensin II injected intravenously (Fitzsimons and Simons 1969) and intraven· triculariy (Epstein et a1. 1970) causes a potent and im· mediate dipsogenic response.…”