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Biomedical subjects

A N Epstein

Publications and source records attributed to A N Epstein.

90 records · Page 5Linked to original sources
PubMed1970

Drinking induced by injection of angiotensin into the rain of the rat.

1. When applied directly to the brain, angiotensin II amide, as either the valine(5) octapeptide, causes rats in normal fluid balance to drink water.2. The drinking response to angiotensin injections is copious, rapid, repeatable within the same test session, and stable over months of testing in the same animal.3. The response is motivationally potent and specific. After injection the animals move directly to the source of water and drink. There is typically no preliminary hyperactivity or subsequent depression. The animals do not eat, gnaw or exhibit other behaviours that are not normally seen during spontaneous drinking. The injections rouse sleeping animals to drink and interrupt eating in animals deprived of food for two days.4. The region of the brain that is most sensitive to angiotensin includes the anterior hypothalamus, the preoptic region, and the septum including the nucleus accumbens.5. Intracranial renin elicited drinking. Bradykinin and vasopressin did not, nor did adrenaline, noradrenaline or aldosterone. In the most sensitive region, sites positive for angiotensin also yielded drinking to carbachol.6. Responses were obtained with 5 ng (ca. 5 p-mole) and occurred reliably with 50 ng angiotensin or more. The dose-response curve for amount drunk rose from 5 to 100 ng and levelled off thereafter. Angiotensin is therefore the most potent dipsogen known and is effective at doses that are reasonably within the concentration range for circulating endogenous angiotensin.7. Injections into the sensitive region of doses of angiotensin that were effective for drinking did not produce peripheral haemodynamic changes in lightly anaesthetized rats.8. This work strengthens the suggestion that angiotensin is a natural hormone of drinking behaviour that participates in extracellular thirst by its release from the kidney and subsequent direct action on a specific chemoreceptive region in the anterior diencephalon and limbic lobe.

Aldosterone↗
PubMed1968

Showering as a coolant for rats exposed to heat.

Rats exposed to heat learn to take showers and thus defend themselves against hyperthermia; thereafter the rate of showering is a direct function of ambient temperature. The showering effectively replaces spreading of saliva as the major defense against heat in desalivate rats, and appears to be highly preferred to the use of saliva by the intact animal. Since rats will work to obtain heat when cold, it is now clear that learned behavior is effective and physiologically appropriate for thermoregulation at temperatures both above and below the neutral range.

Adaptation, Physiological↗
PubMed1966

Severe impairment of heat-induced saliva-spreading in rats recovered from lateral hypothalamic lesions.

A method has been devised to record saliva-spreading on fur and skin by rats in the heat. Normal males and females increase saliva-spreading with increasing ambient temperatures. Rats recovered from lateral hypothalamic lesions do not spread saliva in the heat, confirming the inference drawn from studies of their drinking behavior that their saliva production is severely impaired. Recovered lateral rats do produce saliva when injected with pilocarpine. The failure to salivate is, therefore, a result of the lateral hypothalamic lesions and is not due to an incompetence of the glands.

Animals↗
PubMedDate not supplied

The development in infant rats of kassinin's potent and selective control of cell-dehydration thirst.

In infant rats, kassinin exerts its antidipsogenic effect in the very early stages of neonatal life (2nd-3rd day). The inhibition of cell-dehydration drinking appears in rats of 2 days, and attains adult levels in pups of 9 days. Instead, the thirsts induced by suckling deprivation or by intracerebroventricular angiotensin II are inhibited by kassinin precociously (3rd day), but are unaffected by it in rats of 12-15 days. Kassinin also inhibits milk intake very early (3rd day) and this effect also disappears at 12 days of age. The pattern of ontogenetic results described here may be that of a brain kassinin-like tachykinin that, in the course of the development of the neural structures on which it acts, gains potent and selective control of cell-dehydration thirst.

Angiotensin II↗
PubMedDate not supplied

Neurokinin A is a specific and precocious inhibitor of water intake in neonatal rats.

Neurokinin A (NKA), which selectively inhibits only cellular dehydration (CD)-induced drinking in adult rats, exerts a more general antidipsogenic effect in pups in which it also inhibits drinking induced by angiotensin II (AII) or suckling deprivation (SD). The inhibition of drinking is precocious (1st-3rd day) and never involves the intake of milk. The inhibition of CD-induced drinking increases with age, while that of AII- or SD-induced drinking progressively decreases and disappears on day 12-15. In the rat, NKA is therefore a precocious and selective inhibitor of drinking behavior and its selectivity is achieved ontogenetically.

Aging↗
PubMedDate not supplied

Neurohormonal control of salt intake in the rat.

Steroids (aldosterone and testosterone) and peptides of cerebral origin (angiotensin II and the tachykinins) control the salt intake of the rat. They arouse or suppress the behavior and they produce lifelong enhancements of NaCl intake. Need-induced salt intake (salt appetite or salt hunger), which is the consequence of sodium deficiency, is aroused by a synergy within the brain of cerebral angiotensin II and aldosterone. And prior episodes of sodium depletion produce enhancements of subsequent salt appetites, but only if the prior depletions were accompanied by angiotensin II and aldosterone action. Need-free salt intake, which occurs daily when the rat is in positive sodium balance is also enhanced by prior activations of angiotensin II and aldosterone. Both need-induced and need-free salt intake are suppressed by intracranial tachykinins. Nonmammalian tachykinins (eledoisin, physalaemin, kassinin) are both antidipsogenic and antinatriorexigenic, but amino-senktide, an analog of the mammalian tachykinin substance P with selective affinity for the NK 3 receptor, appears to be a selective antinatriorexigenic agent, and could provide a rational therapy for chronic over-consumption of salt.

Aldosterone↗
PubMedDate not supplied

Control of salt intake by steroids and cerebral peptides.

Steroids (aldosterone and testosterone) and peptides of cerebral origin (angiotensin II and the tachykinins) control the salt intake of the rat. They arouse or suppress the behaviour and produce life-long enhancements of NaCl intake. Need-induced salt intake (salt appetite or salt hunger), which is the consequence of sodium deficiency, is aroused by a synergy within the brain of cerebral angiotensin II and aldosterone. And prior episodes of sodium depletion produce enhancements of subsequent salt appetites, but only if the prior depletions were accompanied by angiotensin II and aldosterone action. Need-free salt intake, which occurs daily when the rat is in positive sodium balance, is inherently high in the rat and is organized in the perinatal period by aromatized testosterone which suppresses the intake of the male. It is also enhanced by prior activations of angiotensin II and aldosterone. Both need-induced and need-free salt intake are suppressed by intracranial tachykinins. Non-mammalian tachykinins (eledoisin, physalaemin, kassinin) are both antidipsogenic and antinatriorexigenic, but amino-senktide, an analogue of the mammalian tachykinin substance P with selective affinity for the NK 3 receptor, appears to be a selective antinatriorexigenic agent, and could provide a rational therapy for chronic overconsumption of salt.

Aldosterone↗