Some particularities of sodium nitroprusside stimulatory effects on food intake.

It was previously shown that sodium nitroprusside (NP) stimulates food (FI) and water (WI) intakes when injected intraperitoneally (i.p.) in male rats deprived for 1-h of both food and water during day time. The present work shows that: 1) intramuscular NP increased only water intake; 2) when NP was i.p. injected simultaneously without 1-h deprivation it slightly reduced both intakes in the first 30 min but stimulated significantly FI between 30 and 60 min, and 3) it increased significantly FI even in absence of available water, while WI in absence of food was practically not affected. In conclusion NP effect on FI does originate mainly in the splanchnic area, it requires a latency of about 30 min, and stimulation of FI by NP triggers an increase in WI and not the other way around.

Effect of intraperitoneal nitroprusside and adrenergic agonists on food and water intake.

In previous works it was shown that catecholamine-induced hypodipsia is mediated by alpha1-adrenergic receptors while food intake (FI) inhibition supposes also beta-adrenergic participation. We used sodium nitroprusside (N) as a vasodilator, alone or mixed with various adrenergic agonists and measured FI and water intake (WI) in rats either deprived food and water overnight or in postprandial conditions after only 1 hour of deprivation in day time. N injected alone had no effect after overnight deprivation but diminished significantly norepinephrine (NE)-induced inhibition of both intakes, while epinephrine (E) inhibited only FI. In day time, N stimulated 30 min FI by 60% and WI by 84% in male but not in female rats. Isoproterenol (I) stimulated only WI (by 155%), while phenylephrine (P) and E inhibited it by 55%. In the presence of N, I increased WI even more (by 220%) but reduced FI. P + N and E + N increased FI by 41% and 128% as compared with P and E, respectively. Only P-induced inhibition of WI was canceled in presence of N. The results show that N, probably due to nitric oxide production, may induce hyperphagia and hyperdipsia in 1 hour-deprived male rats and also that catecholamine effects on FI and WI are differently modulated by N.

Norepinephrine inhibition of water and food intake: comparison with vasopressin effects.

UNLABELLED: In a previous publication we showed that intraperitoneally (IP) injected norepinephrine (NE) induces hypodipsia (hD) in rats by an alpha 1-adrenergic effect which might be due to splanchnic vasoconstriction. In the present work we administered two vasoconstrictive hormones: NE 250 ug/kg and arginine vasopressin (VP) 550 mU/kg either by IP or intramuscular (IM) route to fasted rats in two different thirst-inducing conditions: (a) water-deprivation; or (b) induced hyperosmolarity. IP NE inhibited significantly food and water intake under both conditions. IM NE did not affect food intake and elicited significantly less hD and this only in (a). VP did not affect food intake but induced hD regardless of the route of administration in (a) but not in (b). NE administrated to anesthetized rats after food and water deprivation increased arterial pressure by both routes while VP effect was weaker and more variable. IN CONCLUSION: blood pressure elevation may be implicated in the hD effect but IP NE elicits a specific splanchnic action; splanchnic-induced hypophagia is not necessarily related to water intake inhibition.

Specificity of alpha- and beta-adrenergic inhibition of water and food intake.

In previous publications from our laboratory it was shown that catecholamines (CA) injected intraperitoneally (IP) to fasted rats induce a transient inhibition of food intake. This effect seems to be both alpha- and beta-adrenergic. According to more recent data (20), IP CA also reduced water intake in water-deprived rats, and the effect is exclusively alpha-adrenergic. In order to obtain more information on the adrenergic specificity of the two inhibitory effects we measured the amount of food and water ingested during 30 min by male and female rats previously deprived of both food and water for 18 h. Three adrenergic agonists (norepinephrine, isoproterenol, and salbutamol) were injected IP after the administration (IP) of the following adrenergic antagonists: phentolamine, prazosin, yohimbine, propranolol, or metoprolol. Results showed that, under these experimental conditions, water intake inhibition was due exclusively to an alpha 1 effect, whereas food intake inhibition seemed to depend on alpha 1 and beta 1 actions plus some beta 2 participation. It is also suggested that blocking one type of receptors may enhance the responsiveness of the other type.

Effects of catecholamines on water intake in rats.

It is known that intraperitoneally (IP) injected adrenaline (A) inhibits food intake in otherwise hungry animals. In a recent work, Hinton et al. (6) showed that IP A also inhibits water intake in thirsty rats, concluding that A's effect is unspecific. We administered A IP or intramuscularly (IM) in different doses in rats made thirsty either by 18-h water deprivation or by subcutaneous injection of hypertonic saline or polyethylene glycol. IP A reduced water intake in all experimental conditions. A dose-related inhibition was observed in water-deprived animals. On the other hand, IM A showed a small effect only at the highest dose (50 micrograms/100 g body weight). When some of these experiments were repeated using noradrenaline (NA) and isoproterenol (IS), IM administration of either substance showed no effect. IP administration reduced water intake significantly only at the highest dose of NA (50 micrograms/100 g). It is concluded that water intake inhibition by catecholamines in rats made thirsty either by osmotic or by volumetric challenges is of porto-hepatic origin and, in contrast with food intake inhibition, has no beta-adrenergic component.

Ontogeny of alpha- and beta-adrenergic anorexia in rats.

The anorectic action of alpha- (phenylephrine) and beta- (isoproterenol) adrenergic agonists was studied in mildly deprived neonatal, weanling, prepubescent, and adult rats. Intraperitoneal phenylephrine produced a reduction of food intake at all ages but with reduced potency and with a maximum of 50% in neonates. Contrary to intramuscular epinephrine that has no effect on feeding at any age, intramuscular phenylephrine was as effective as intraperitoneal in neonates, probably because it is not as rapidly destroyed in tissues as epinephrine. However, in weanlings and adults intramuscular phenylephrine was much less anorectic than intraperitoneal, suggesting that this effect is exerted via the liver. Isoproterenol did not reduce milk intake at any age before adulthood. Lactate had no effect on milk intake before the age of 40 days. Thus catecholamine anorexia is a purely alpha-adrenergic effect in young rats and appears before the metabolic effect of lactate. beta-Adrenergic anorexia, on the other hand, can be obtained only after puberty, suggesting that the mechanism mediating it matures after the preparatory action of the sexual hormones.

Anorexia elicited by different catecholamines in rats.

Adrenaline (A) produces a strong anorexic effect, possibly by acting on hepatic receptors (nerve endings on hepatocytes). To study whether this is mediated by alpha- or beta-adrenergic mechanisms, or both, the anorexigenic effects of intraperitoneal injections of A, noradrenaline (NA) and isoproterenol (I) were studied under four different experimental conditions: (I) at the beginning of the dark period in rats fed ad libitum, or (II) on a 24 h-feeding/24 h-fasting schedule; (III) during the light period, under the same feeding schedule; (IV) after an acute 24 h fast. In condition I, the three catecholamines produced a marked decrease in feeding, slightly larger for A. In condition II (dark), they elicited a decrease in food intake about double that in condition III (light), their relative potencies also differed: A greater than I greater than NA in II and A greater than I = NA in III. In IV, the same relative potencies were obtained as in III. A mixture of half-doses of NA and I had the same effect in III and IV as either NA or I alone, suggesting that the alpha and beta effects are additive. However, even a mixture of the full doses of NA and I was not as effective as A in condition IV. This suggests that A is more potent than NA or I at stimulating hepatic adrenergic receptors that cannot be classified as either alpha or beta.