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PubMed2006

Effects of central or peripheral leptin administration on norepinephrine turnover in defined fat depots.

Leptin preserves lean tissue but decreases adipose tissue by increasing lipolysis and/or inhibiting lipogenesis. The sympathetic nervous system (SNS) is a primary regulator of lipolysis, but it is not known if leptin increases norepinephrine turnover (NETO) in white adipose tissue. In this study, we examined the effect of leptin administered either as a chronic physiological dose (40 microg/day for 4 days from ip miniosmotic pumps) or as an acute injection in the third ventricle (1.5 microg injected two times daily for 2 days) on NETO and the size of brown and white fat depots in male Sprague Dawley rats. NETO was determined from the decline in tissue norepinephrine (NE) during 4 h following administration of the NE synthesis inhibitor alpha-methyl-para-tryrosine. The centrally injected leptin-treated animals demonstrated more dramatic reductions in food intake, body weight, and fat pad size and an increase in NETO compared with the peripherally infused animals. Neither route of leptin administration caused a uniform increase in NETO across all fat pads tested, and in both treatment conditions leptin decreased the size of certain fat pads independent of an increase in NETO. Similar discrepancies in white fat NETO were found for rats pair fed to leptin-treated animals. These results demonstrate that leptin acting either centrally or peripherally selectively increases sympathetic outflow to white fat depots and that a leptin-induced change in fat pad weight does not require an increase in NETO.

Adipose Tissue, White↗

PubMed2006

Serotonin-type 3 receptors mediate intestinal lipid-induced satiation and Fos-like immunoreactivity in the dorsal hindbrain.

Several gastrointestinal stimuli, including some intestinal nutrients, have been shown to exert their satiating effect via activation of serotonin type-3 (5-HT(3)) receptors. The presence of lipids in the small intestine potently suppresses food intake; however, whether 5-HT(3) receptors play a role in this response has not been directly examined. Therefore, using the selective 5-HT(3) receptor antagonist ondansetron, we tested the hypothesis that duodenal infusion of lipid suppresses intake of both sucrose solution and chow through 5-HT(3) receptor activation. Rats duodenally infused with 72 and 130 mM Intralipid suppressed 1-h 15% sucrose intake by 33 and 67%, respectively. Suppression of sucrose intake by 72 mM Intralipid was significantly attenuated by ondansetron at all doses tested (0.5, 1.0, 2.0, and 5.0 mg/kg ip), whereas the lowest effective dose of ondansetron to attenuate suppression of intake by 130 mM Intralipid was 1.0 mg/kg. Furthermore, infusion of 130 mM Intralipid suppressed 1- and 4-h chow intake by 35 and 20%, respectively. Ondansetron administered as low as 0.5 mg/kg significantly attenuated 1-h Intralipid-induced suppression of chow intake and completely reversed the suppression by 4 h. Administration of ondansetron alone did not alter sucrose or chow intake compared with vehicle injection at any time. Finally, to test whether Intralipid-induced neuronal activation of the dorsal vagal complex is mediated by 5-HT(3) receptors, Fos-like immunoreactivity (Fos-LI) was quantified in ondansetron-pretreated rats following intestinal lipid infusion. Ondansetron (1 mg/kg) significantly attenuated duodenal intralipid-induced Fos-LI in the dorsal hindbrain. These data support the hypothesis that 5-HT(3) receptors mediate both satiation, as well as hindbrain neuronal responses evoked by intestinal lipids.

Animals↗

PubMed2002

Site-specific modulation of LPS-induced fever and interleukin-1 beta expression in rats by interleukin-10.

Bacterial lipopolysaccharide (LPS) induces fever that is mediated by pyrogenic cytokines such as interleukin (IL)-1 beta. We hypothesized that the anti-inflammatory cytokine IL-10 modulates the febrile response to LPS by suppressing the production of pyrogenic cytokines. In rats, intravenous but not intracerebroventricular infusion of IL-10 was found to attenuate fever induced by peripheral administration of LPS (10 microg/kg iv). IL-10 also suppressed LPS-induced IL-1 beta production in peripheral tissues and in the brain stem. In contrast, central administration of IL-10 attenuated the febrile response to central LPS (60 ng/rat icv) and decreased IL-1 beta production in the hypothalamus and brain stem but not in peripheral tissues and plasma. Furthermore, intravenous LPS upregulated expression of IL-10 receptor (IL-10R1) mRNA in the liver, whereas intracerebroventricular LPS enhanced IL-10R1 mRNA in the hypothalamus. We conclude that IL-10 modulates the febrile response by acting in the periphery or in the brain dependent on the primary site of inflammation and that its mechanism of action most likely involves inhibition of local IL-1 beta production.

Animals↗

PubMed1982

Dissociation of dipsogenic and pressor responses to chronic central angiotensin II in rats.

Chronic intracerebroventricular (icv) infusion of angiotensin II (ANG II) (6 micrograms/h) in rats resulted in a sustained 70-mmHg rise in blood pressure during 7 days of treatment. A marked dipsogenic response preceded the maximal rise in blood pressure, peaked at 24 h, and returned to control by the 5th day. Urinary sodium excretion rose on the 1st day of infusion but thereafter was not different from that of vehicle-infused rats. ANG II-infused rats showed a small but significant kaliuresis, a fall in serum osmolality (5.5 mosmol/kg), but no change in plasma Na+, K+, or glucose. Rats infused with the same dose of ANG II intravenously showed a small, 8-mmHg rise in blood pressure, but none of the changes noted after icv ANG II. Plasma renin activity was suppressed in rats infused with ANG II by both routes. We conclude that the pressor, dipsogenic, and renal excretory effects of icv ANG II are mediated centrally and cannot be explained by leakage of the peptide into the systemic circulation. Furthermore, the pressor and dipsogenic effects of ANG II become clearly dissociated during chronic icv infusion.

Angiotensin II↗

PubMed1986

Angiotensin and Na appetite of sheep.

The effect of both intravenous (iv; 24 micrograms/h) and intracerebroventricular (ivt; 3.8 micrograms/h) infusion over 1-2 days of angiotensin II (ANG II) on Na intake of both Na-replete and -deplete sheep (i.e., 22 h loss of parotid saliva) was observed. In Na-replete sheep with continuous access to water and 2-h daily access to 0.5 M NaCl solution, both iv and ivt ANG II caused an increase in Na intake. The increase in Na intake caused by iv or ivt ANG II was preceded by a Na deficit due to increased urinary Na excretion. The increase in Na intake was eliminated by the continuous return of urine. In Na-deplete sheep with continuous access to water and 2-h daily access to 0.6 M NaHCO3 solution, iv ANG II caused no change in Na loss but a small increase in Na intake during the 1st day of infusion. The ivt ANG II caused no change in Na loss or in Na intake. The iv ANG II caused a small and inconsistent increase in water intake in Na-replete sheep but did not cause any change in water intake of Na-deplete sheep. The ivt ANG II caused a large increase in water intake in both Na-replete and -deplete sheep. In both Na-replete and -deplete sheep, iv ANG II did not alter cerebrospinal fluid or plasma [Na] or osmolality but decreased plasma [K]. The ivt ANG II decreased both cerebrospinal fluid and plasma [Na] and osmolality. The results of the present experiments are consistent with the proposition that the ANG II-induced Na appetite in sheep is largely due to an ANG II-induced Na loss preceding the development of appetite.

Angiotensin II↗

PubMed1988

Angiotensin-related sodium appetite and thirst in cattle.

Cows depleted of Na by loss of saliva from a parotid fistula for 46 h had an avid appetite for Na solution. They drank 21.0 +/- 1.6 liter of 0.3 M NaHCO3-NaCl solution during 2 h of access but little or no water during that time. Solutions of angiotensin II or captopril were infused for 3 h intravenously or into a lateral ventricle (intracerebroventricular) beginning 1 h before access to Na solution. Intravenous angiotensin II increased Na intake (to 26.8 +/- 2.9 liter, P less than 0.01) but did not alter water intake. Intracerebroventricular angiotensin II increased water intake but did not alter Na intake. Intravenous captopril reduced Na intake (to 11.0 +/- 2.1 liter, P less than 0.001) and concurrent intravenous angiotensin II prevented the reduction but concurrent intracerebroventricular angiotensin II did not. Intracerebroventricular captopril did not alter Na or water intake. Intravenous captopril reduced to zero the water intake during the hour before Na access, and concurrent intravenous angiotensin II prevented that reduction also. The dipsogenic action of intracerebroventricular angiotensin II was potentiated by intravenous captopril. The results of these experiments suggest that if angiotensin II receptors involved in the mechanism regulating Na appetite are in the brain, they are accessible only from the blood, e.g., in circumventricular organs. Thirst was inhibited by reduction of angiotensin II in blood but was stimulated only by angiotensin II acting inside the blood-brain barrier.

Angiotensin II↗

PubMed1992

Atrial natriuretic peptide does not alter cerebrospinal fluid formation in sheep.

Because the choroid plexus has been shown to have a high density of atrial natriuretic peptide (ANP) binding sites, we investigated the effect of intracerebroventricular and intravenous administrations of ANP on cerebrospinal fluid (CSF) formation. CSF formation rate was measured in conscious sheep with a dye-dilution method using blue dextran 2000 as an indicator substance. During the experiment animals were partially restrained in a sling, and their ventricular systems were perfused with artificial CSF containing the indicator substance. ANP (alpha-human ANP) administered centrally at rates of 0.015-15 ng/min, resulting in CSF ANP concentrations ranging from physiological to pharmacological CSF hormone levels, was found not to influence CSF formation. Similarly, intravenous administration of ANP at a rate of 10 ng.kg-1.min-1 did not affect CSF formation, i.e., decreases in CSF formation rate in all experiments involving ANP administration were not significantly different from those observed in time control experiments. Our results suggest that ANP does not significantly affect CSF production in sheep. It is possible that the lack of effect of ANP on CSF formation is associated with the predominance in the choroid plexus of clearance receptors over biologically active receptors.

Animals↗

PubMed1998

Role of angiotensin in renal sympathetic activation in nephrotic syndrome.

The effect of type 1 angiotensin II receptor antagonist treatment (losartan) on cardiac baroreflex regulation of renal sympathetic nerve activity (RSNA) and renal sodium handling in rats with nephrotic syndrome was examined. After intravenous losartan administration, with arterial pressure normalized by intravenous methoxamine, basal RSNA was decreased 14 +/- 3% in arterial baroreceptor-intact rats and by 21 +/- 5% in arterial baroreceptor-denervated rats. Intracerebroventricular losartan, which did not affect arterial pressure, decreased basal RSNA activity by 15 +/- 1%. Both intravenous and intracerebroventricular losartan augmented the renal sympathoinhibitory response to acute volume loading, and this was associated with an enhanced natriuretic response to the acute volume load. In nephrotic syndrome, acute losartan administration improved cardiac baroreflex regulation of RSNA, which was associated with improved ability to excrete acute sodium loads.

Angiotensin II↗

PubMed1998

Central alpha2-receptor mechanisms contribute to enhanced renal responses during ketamine-xylazine anesthesia.

We have recently developed an experimental approach to study central opioid control of renal function in anesthetized rats. This model system uses the intravenous infusion of the alpha2-agonist xylazine to enhance basal levels of urine flow rate and urinary sodium excretion in ketamine-anesthetized rats. This study examined the contribution of central and peripheral alpha2-adrenergic receptor mechanisms in mediating the enhanced renal excretory responses produced by xylazine. In ketamine-anesthetized rats, the enhanced levels of urine flow rate and urinary sodium excretion produced by the intravenous infusion of xylazine were reversed by the intravenous bolus injection of the alpha2-adrenoceptor antagonist yohimbine but not by the alpha1-adrenoceptor antagonist terazosin. In separate animals the intracerebroventricular administration of yohimbine only reduced urine flow rate by approximately 50% but did not alter urinary sodium excretion. The decrease in urine flow rate produced by intracerebroventricular yohimbine was reversed by the intravenous injection of a selective V2-vasopressin receptor antagonist. In a separate group of ketamine- and xylazine-anesthetized rats, the bilateral microinjection of yohimbine into the hypothalamic paraventricular nucleus (PVN) also significantly decreased urine flow rate by 54% without altering urinary sodium excretion. The microinjection of the beta-adrenoceptor antagonist propranolol into the PVN did not alter either renal excretory parameter. These results suggest that during intravenous infusion, xylazine increases urine flow rate by activating alpha2-adrenergic receptors in the PVN, which in turn decrease vasopressin release. The ability of alpha-adrenergic mechanisms in the PVN to selectively influence the renal handling of water, but not sodium, may contribute to the reported dissociation of the natriuretic and diuretic responses of alpha2-adrenoceptor agonists.

Adrenergic alpha-Agonists↗

PubMed1999

Effect of adrenocorticotrophic hormone on sodium appetite in mice.

A main vector of the effects of stress is secretion of corticotrophin releasing factor (CRF), adrenocorticotrophin (ACTH), and adrenal steroids. Systemic administration of ACTH (2.8 microgram/day sc) for 7 days in BALB/c mice caused a very large increase of voluntary intake of 0.3 M NaCl equivalent to turnover of total body sodium content each day. Intracerebroventricular infusion of ACTH (20 ng/day) had no effect. Intracerebroventricular infusion of ovine CRF (10 ng/h for 7 days) caused an increase of sodium intake. The large sodium appetite-stimulating effect of systemic ACTH was not influenced by concurrent systemic infusion of captopril (2 mg/day). Induction of stress by immobilization of mice on a running wheel caused an increase in Na appetite associated with a 50% decrease of thymus weight, indicative of corticosteroid effects. The present data suggest that stress and the hormone cascade initiated by stress evoke a large sodium appetite in mice, which may be an important survival mechanism in environmental conditions causing stress.

Adrenocorticotropic Hormone↗

PubMed2001

Circulating angiotensin II mediates sodium appetite in adrenalectomized rats.

We investigated the role of circulating ANG II in sodium appetite after adrenalectomy. Adrenalectomized rats deprived of their main access to sodium (0.3 M NaCl) for 9 h drank 14.1 +/- 1.5 ml of the concentrated saline solution in 2 h of access. Intravenous infusion of captopril (2.5 mg/h) during the last 5 h of sodium restriction reduced sodium intake by 77 +/- 12% (n = 5) without affecting the degree of sodium depletion and hypovolemia incurred during deprivation. Functional evidence indicates that this dose of captopril blocked production of ANG II in the peripheral circulation, but not in the brain; that is, injection of ANG I into the lateral brain ventricle stimulated intake of both water and 0.3 M NaCl. Intravenous infusion of ANG II (starting 10-15 min before 0.3 M NaCl became available) in adrenalectomized, captopril-treated rats restored both sodium intake and blood pressure to values seen in rats not treated with captopril. Longer (20 h) infusions of captopril in 22-h sodium-restricted rats also blocked sodium appetite, but reduced or prevented sodium depletion. Intravenous infusion of ANG II after these long captopril infusions stimulated sodium intake, but intake was less than in controls not treated with captopril. These results indicate that most or all of the sodium appetite of adrenalectomized rats is mediated by circulating ANG II.

Adrenalectomy↗

PubMed2001

Constitutive activation of STAT-3 and downregulation of SOCS-3 expression induced by adrenalectomy.

Removal of adrenal steroids by adrenalectomy (ADX) slows or reverses the development of many forms of obesity in rodents, including those that are leptin or leptin receptor deficient. Obesity is associated with hyperleptinemia and leptin resistance. We hypothesized that glucocorticoids impair leptin receptor signaling and that removal thereof would activate the Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling pathway. The inhibitory effect of leptin (2.5 microg icv) on food intake was enhanced in ADX rats. A combination of ribonuclease protection assays, RT-PCR, Western blots, and mobility shift assays was used to evaluate the leptin signaling pathway in whole hypothalami from sham-operated, ADX and corticosterone-replaced ADX (ADX-R) Sprague-Dawley rats that were treated acutely with either saline vehicle or leptin intracerebroventricularly. ADX increased the expression of leptin receptor mRNA, increased STAT-3 mRNA and protein levels, induced constitutive STAT-3 phosphorylation and DNA binding activity, and also reduced suppressor of cytokine signaling-3 (SOCS-3) mRNA and protein levels. ADX and leptin treatment increased STAT-3 phosphorylation, but with no concomitant increase in DNA binding activity. Leptin and ADX decreased NPY mRNA expression, but their combination did not further decrease NPY mRNA. Corticosterone supplementation of ADX rats partially reversed many of these effects. In conclusion, ADX through activation of STAT-3 and inhibition of SOCS-3 activates the JAK-STAT signaling pathway. These effects most probably explain the ability to prevent the development of obesity by removal of adrenal steroids.

Acute-Phase Proteins↗

PubMed1982

Distribution of two model amino acids from cerebrospinal fluid to brain and blood.

Ventriculocisternal perfusions of anesthetized rabbits were performed for 1-3 h with solutions containing radioactively labeled alpha-aminoisobutyric acid (AIB), cycloleucine (CYCL), and sucrose. Serial brain samples were taken at the conclusion of the perfusion period and assayed for radioactivity. Tissue concentration profiles were constructed from these data; tissue distribution spaces and diffusion coefficients (Dt) plus brain capillary transfer constants were estimated from the profiles. The Dt of sucrose was somewhat larger at 1 h than at 2 and 3 h. Tissue distribution spaces of 300-400% were found with AIB after 3 h. Inclusion of 5 mM AIB in the perfusate produced markedly lower tracer AIB spaces. The tissue distribution spaces of CYCL ranged from 100 to 400% and depended on the concentration of CYCL in the perfusate. A brain-to-blood transfer half time of 7.5 min was measured for CYCL. These findings demonstrate that sizable cellular uptake of CYCL and AIB occurs, that these processes are concentration dependent, and that the rates of influx and efflux across brain capillaries are similar.

Amino Acids↗

PubMed1986

Effect of beta-endorphin on fetal breathing movements in sheep.

It has been suggested that endogenous opioids, such as beta-endorphin (beta-EP), act to depress respiration in the fetus and newborn. We have investigated the effect of infusing beta-EP either intravenously or into a lateral cerebral ventricle on breathing movements and electrocortical activity in eight fetal lambs between 116 and 133 days gestation. Intravenous infusion of beta-EP (200 or 500 micrograms over 1 h) increased plasma beta-EP concentrations 2- to 230-fold and was associated with a small decrease in the percent time spent breathing, from 57.8 +/- 9.1 to 51.3 +/- 8.2%/h (n = 6 exp). There was no change in the amount of high- or low-voltage electrocortical activity. Intracerebroventricular beta-EP infusion (1 or 2 micrograms beta-EP/min for 120 min) was not associated with any change of breathing movements (n = 5 exp) during the period of the infusion. However, in four experiments, in the 6-h period after the end of the beta-EP infusion there were episodes of 2-4 h when the percent time per hour spent breathing exceeded 70%. Electrocortical activity increased in amplitude and distinct episodes of high- and low-voltage activity were sometimes lost in these experiments. We conclude that high concentrations of beta-EP in plasma or cerebrospinal fluid do not totally suppress fetal breathing directly in the fetal lamb.

Animals↗

PubMed1981

Infratentorial arachnoid cysts in children.

8 Children surgically treated for posterior fossa arachnoid cyst are described. In all the cases an enlarging head was the presenting sign; intracranial hypertension was evident in 6 patients; 2 children were clinically regarded as being affected by 'arrested' hydrocephalus. Preoperative subarachnoid lumbar infusion tests (8 cases) and prolonged intraventricular CSF pressure recordings (2 cases) demonstrated abnormal CSF dynamics in 6 cases. Ultramicroscopic examinations of the cyst wall (4 cases) suggest alterations in the anatomical arrangement of the arachnoid membrane, which supports the hypothesis of maldevelopment as the origin of the lesion.

Arachnoid↗

PubMed1982

Differential clearance of neurophysin and neurohypophysial peptides from the cerebrospinal fluid in conscious guinea pigs.

The clearance of neurohypophysial peptides from cerebrospinal fluid (CSF) in conscious unrestrained guinea pigs. 125I-labelled peptides were detectable in the cisterna magna within 2 min of their intracerebroventricular injection, reaching peak concentrations 10-15 min post-injection and declining exponentially over the next hour. 125I-oxytocin (125I-OT) and 125I-vasopressin (125(I-AVP) were cleared at similar rates, whereas 125I-labelled neurophysin (125I-NP) disappeared significantly more slowly; mean half-times of clearance (t1/2) from cisternal CSF were 28, 24 and 46 min, respectively. 125I-NP was cleared at the same rate as 3H-inulin (t1/2 40 min), as was an antibody to OT (anti-OT, t1/2 37 min). Intracerebroventricular infusions of iodinated peptides produced constant levels in CSF within 3 h. 125I-AVP reached lower plateau levels and disappeared twice as fast as 125I-NP, although the apparent equilibrium distribution space was the same for both peptides. Although NP was cleared half as fast as OT or AVP, this difference was not sufficient to account for the large molar excess of NP over the nonapeptides in guinea pig CSF. There is an effective blood/CSF barrier to neurohypophysial peptides in the guinea pig; intravenous infusions of OT or porcine NP did not raise the CSF levels of these peptides (measured by specific radioimmunoassays) except when very high concentrations were maintained in peripheral plasma. However, single intravenous injections of anti-OT produced low but significant titres in CSF, persisting for several days.

Animals↗

PubMed1983

Clearance of vasopressin from cerebrospinal fluid to blood in chronically cannulated Brattleboro rats.

The antidiuretic effects of intravenous (i.v.) and intracerebroventricular (i.c.v.) infusions of vasopressin (AVP) were compared in chronically cannulated conscious Brattleboro rats. AVP infused i.c.v. for 6 h reduced urine volume and increased urinary Na+ and K+ concentrations. These antidiuretic responses to i.c.v. AVP were dose related in the range 3-12 ng/h and were delayed and prolonged when compared with i.v. infusions (0.33-3 ng/h) of this peptide. Comparison of the dose-response curves for both routes of administration demonstrated that the antidiuretic response to i.c.v. infusion of AVP was approximately 10-fold lower than to AVP given intravenously. Since measurable amounts of AVP-like material appeared in the urine during the antidiuretic response, we conclude that a significant amount of AVP infused into the cerebroventricular system reaches the bloodstream in a biologically active form.

Animals↗

PubMed1990

Additive effects of atrial natriuretic peptide and angiotensin II on luteinizing hormone and prolactin release in female rats.

The present experiments were designed to assess the effects of central administration of atrial natriuretic peptide (ANP), alone or in conjunction with angiotensin II (AII), on luteinizing hormone (LH) and prolactin release in ovarian steroid-primed female rats. Intracerebroventricular injection of ANP (200 ng/2 microliters over 1 min) induced an increase in plasma LH levels without significantly affecting prolactin release. Injection of AII (50 ng/2 microliters over 1 min) also resulted in an increase in LH levels and, in addition, reduced plasma prolactin titers. Coinjection of ANP and AII did not elevate LH levels beyond that achieved by either peptide alone, but produced a further suppression in prolactin levels than that seen with AII alone. Water intake induced by AII was attenuated by coadministration of ANP. In a second protocol utilizing lower doses of the peptides delivered by infusion, either ANP (800 ng/h; 13.3 ng/min) or AII (200 ng/h; 3.3 ng/min) alone produced 100% increases in LH levels. Coinfusion of the peptides induced an additive (250%) increase in plasma LH titers. In this protocol, the release of prolactin was unaffected by infusion of the peptides, either alone or as a comixture. Water intake induced by AII infusion was attenuated by coadministration of ANP. Taken together, these experiments demonstrate that, in contrast to the antagonistic interaction of ANP and AII on water intake, the peptides affect reproductive hormone secretion in the same direction and, under particular experimental conditions, display additive effects in stimulating LH and inhibiting prolactin release.

Angiotensin II↗