Functional evidence for subfornical organ-intrinsic conversion of angiotensin I to angiotensin II.
(25/1487)
Using extracellular electrophysiological recording in an in vitro slice preparation, we investigated whether ANG I can be locally converted to the functionally active ANG II within the rat subfornical organ (SFO). ANG I and ANG II (10(-8)-10(-7) M) excited approximately 75% of all neurons tested with both peptides (n = 25); the remainder were insensitive. The increase in firing rate and the duration and the latency of the responses of identical neurons, superfused with equimolar concentrations of ANG I and ANG II, were not different. The threshold concentrations of the ANG I- and ANG II-induced excitations were both 10(-9) M. Inhibition of the angiotensin-converting enzyme by captopril (10(-4) M; n = 8) completely blocked the ANG I-induced excitation, a 10-fold lower dose was only effective in two of four neurons. The AT1-receptor antagonist losartan (10(-5) M; n = 6) abolished the excitation caused by ANG I and ANG II. Subcutaneous injections of equimolar doses of ANG I and ANG II (200 microliters; 2 x 10(-4) M) in water-sated rats similarly increased water intake by 2.4 +/- 0.5 (n = 16) and 2. 7 +/- 0.4 ml (n = 20) after 1 h, respectively. Control rats receiving saline drank 0.07 +/- 0.06 ml under these conditions. Pretreatment with a low dose of captopril (2.3 x 10(-3) M) 10 min before the injection of ANG I caused a water intake of 2.8 +/- 0.5 ml (n = 10), whereas a high dose of captopril (4.6 x 10(-1) M) suppressed the dipsogenic response of ANG I entirely (n = 11). These data provide direct functional evidence for an SFO-intrinsic renin-angiotensin system (RAS) and underline the importance of the SFO as a central nervous interface connecting the peripheral with the central RAS. (+info)
Amiloride-sensitive sodium signals and salt appetite: multiple gustatory pathways.
(26/1487)
In the rat, the ionic specificity of Na+ appetite is thought to rely on amiloride-sensitive Na+ signals conveyed by the chorda tympani (CT) nerve. We evaluated whether robust Na+ appetite relies exclusively on CT-mediated amiloride-sensitive Na+ signals. Amiloride dramatically reduced sham drinking of NaCl (41.9 +/- 9.0 vs. 6.9 +/- 3.7 ml, 0.1 M NaCl without vs. with 100 microM amiloride), which resulted in intake that was not different from intake of a non-Na+ salt solution (8.8 +/- 2.3 ml, 0.15 M KCl). In addition, intake of 0.1 M NaCl in CT-transected (CTX) rats was reduced (35.8 +/- 13.3 vs. 8.67 +/- 3.4 ml, sham-operated vs. CTX rats), but the addition of amiloride (100 microM) further reduced intake in CTX rats (0.5 +/- 0.29 ml). These data support the idea that amiloride-sensitive Na+ channels are the critical gustatory substrate for Na+ identification during Na+ appetite in the rat. However, the data indicate that these amiloride-sensitive signals are not conveyed exclusively by the CT nerve but by an additional afferent pathway. (+info)
Effect of dorsomedial hypothalamic nuclei knife cuts on ingestive behavior.
(27/1487)
Previous findings show that rats with electrolytic or excitotoxic lesions in the dorsomedial hypothalamic nucleus (DMN) are hypophagic and hypodipsic and have reduced ponderal and linear growth but normal body composition. DMN-lesioned (DMNL) rats also show altered ingestive responses to naloxone. The present study investigated the intrahypothalamic nerve pathways involved in these DMNL effects and the response of the pathways to deprivation challenges by placing knife cuts posterior (Post), lateral (Lat), ventral (Vent), dorsal, or anterior to the DMN or by administering sham operations. One major finding was that rats with Post or Vent were hypophagic (P < 0. 05) and had reduced body weight but responded normally to deprivation challenges. Post and Lat groups were hypodipsic (P < 0. 05), but plasma Na+, K+, and osmolality and 24-h post-water-deprivation drinking responses were similar in all groups. Naloxone did not suppress the intake of Post rats. It appears that the hypophagia and the reduced body weight after DMNL involve fibers entering or leaving the DMN from ventral and posterior directions, and they may be part of an opioid feeding system. (+info)
Cardiovascular changes associated with dehydration and drinking in unrestrained, lactating goats.
(28/1487)
The aim of this study was to investigate if the alertness connected with seeing water increased arterial blood pressure and heart rate to the same extent as the act of drinking, and if ingestion of warm water caused a different effect compared with ingestion of cool water on these cardiovascular variables. Seven goats of the Swedish domestic breed (Capra hircus) were used in a cross-over design. The animals were dehydrated for 24 h. They were allowed to watch water being prepared for 11-16 min, after which they were given access to warm (35 degrees C) or cool (15 degrees C) water. The goats drank 6.86 +/- 0.36 l of the warm water and 4.54 +/- 0.35 l of the cool water (P < 0.05) within the first hour. The arterial blood pressure, heart rate and activity of the animals were registered by an implanted telemetric device. Dehydration did not affect the cardiovascular variables, except before feeding in the morning, when the heart rate accelerated faster in dehydrated goats. Heart rate increased abruptly when dehydrated goats saw water being prepared, remained at the increased level during drinking and then slowly declined. It increased again during the afternoon feeding, to a level similar to that on control days, but between 18.00 and 06.00 h the heart rate was higher than during control nights. Blood pressure did not change when the goats saw water, but increased when they drank. On the morning following rehydration, the rise in heart rate in response to feeding was delayed compared with that during control and dehydration periods. It is concluded that seeing water caused arousal in the goats, resulting in an accelerated heart rate. The additional rise in blood pressure during the act of drinking appears to be a combination of excitement and sensory inputs from the pharyngeal region, causing a temporary activation of the sympathetic nervous system. (+info)
Serologic evidence of rickettsialpox (Rickettsia akari) infection among intravenous drug users in inner-city Baltimore, Maryland.
(29/1487)
We tested single serum samples from 631 intravenous (i.v.) drug users from inner-city Baltimore, Maryland for serologic evidence of exposure to spotted fever group rickettsiae. A total of 102 (16%) individuals had titers > or = 64 to Rickettsia rickettsii by an indirect immunofluorescence assay. Confirmation that infection was caused by R. akari was obtained by cross-adsorption studies on a subset of serum samples that consistently resulted in higher titers to R. akari than to R. rickettsii. Current i.v. drug use, increased frequency of injection, and shooting gallery use were significant risk factors for presence of group-specific antibodies reactive with R. rickettsii. There was a significant inverse association with the presence of antibodies reactive to R. rickettsii and antibodies reactive to the human immunodeficiency virus. This study suggests that i.v. drug users are at an increased risk for R. akari infections. Clinicians should be aware of rickettsialpox, as well as other zoonotic diseases of the urban environment, when treating i.v. drug users for any acute febrile illness of undetermined etiology. (+info)
Intracerebroventricular infusion of angiotensin II increases water and ethanol intake in rats.
(30/1487)
The influence of prolonged ingestion of ethanol on stimulation of water or ethanol intake by intracerebroventricular infusion of ANG II was evaluated in rats. Animals were maintained for 5-6 mo with either 10% ethanol solution or water as their only source of fluid. In both groups of rats, infusion of ANG II caused a large increase in water intake (7-fold) and a lesser increase in 10% ethanol intake (2-fold). The effect of ANG II on the volume of ethanol solution ingested, however, was inversely related to the concentration of the ethanol solution. As the concentration of ethanol solution was decreased, frequency and duration of drinking bouts increased. The intake of sweetened 10% ethanol solution or commercially produced wine during infusion of ANG II was similar to the intake of 10% ethanol and not related to taste preference. In conclusion, chronic consumption of ethanol solution did not appear to adversely effect ANG II stimulation of water intake. The intake of ethanol solution during infusion of ANG II was inhibited by a direct effect of ingested ethanol and/or by indirect effect from metabolized ethanol. (+info)
Impaired osmoregulatory responses in rats with area postrema lesions.
(31/1487)
Area postrema lesions (APX) in adult male rats produced a robust spontaneous intake of 0.5 M NaCl, as reported previously. The largest NaCl intakes (up to 108 ml/day) were observed when there was little incidental damage in the medial subnucleus of the nucleus of the solitary tract adjacent to the caudal and middle portions of the area postrema. Rats with discrete APX also drank substantial amounts of 0.5 M NaCl when access to saline was restricted to 7 h/day (up to 30 ml in 1 h, 48 ml in 7 h). Such large NaCl intakes stimulated considerable water ingestion and renal sodium excretion, but together these responses usually were insufficient for osmoregulation during the 7-h test period. After systemic administration of hypertonic NaCl solution, rats with APX excreted less Na(+) in urine and secreted less vasopressin and oxytocin than control rats did. The prominent salt appetite, insufficient thirst and natriuresis in response to an ingested NaCl load, and blunted natriuresis and neurohypophysial hormone secretion in response to an injected NaCl load, all indicate that osmoregulatory responses are impaired in rats after APX. (+info)
Association between preference for sweets and excessive alcohol intake: a review of animal and human studies.
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This report reviews a series of studies demonstrating a relationship between the consumption of sweets and alcohol consumption. There is consistent evidence linking the consumption of sweets to alcohol intake in both animals and humans, and there are indications that this relationship may be at least partially genetic in nature. Alcohol-preferring rats have a tendency to consume sucrose and saccharin solutions far beyond the limits of their normal fluid intake and this has been proposed to be a model of the clinical phenomenon known as loss of control. Furthermore, rats and mice, genetically bred to prefer alcohol, tend to choose more concentrated sweet solutions, compared to animals which do not prefer alcohol. Similar tendencies to prefer ultra-sweet solutions have been noted in studies of alcoholic subjects, with most alcoholics preferring sweeter sucrose solutions than do controls. Evidence also exists that those alcoholics who prefer sweeter solutions may represent a familial form of alcoholism. Finally, consumption of sweets and/or sweet solutions may significantly suppress alcohol intake in both animals and in alcoholics. Carbohydrate structure and sweet taste may contribute to this effect through different physiological mechanisms involving serotonergic, opioid, and dopaminergic functions. The possibility that there is concordance between sweet liking and alcohol consumption and/or alcoholism has theoretical, biological, and diagnostic/practical implications. (+info)