Effects of interleukin-1 beta injections into the subfornical organ and median preoptic nucleus on sodium appetite, blood pressure and body temperature of sodium-depleted rats

2016 ◽  
Vol 163 ◽  
pp. 149-160 ◽  
Author(s):  
Diana R. Cerqueira ◽  
Hilda S. Ferreira ◽  
Andrei L.B.B. Moiteiro ◽  
Josmara B. Fregoneze
Keyword(s):  
Blood Pressure ◽  
Body Temperature ◽  
Interleukin 1 ◽  
Subfornical Organ ◽  
Interleukin 1 Beta ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Sodium Appetite

Hypothalamic neuronal histamine modulates physiological responses induced by interleukin-1 beta

1995 ◽  
Vol 269 (6) ◽  
pp. R1308-R1313 ◽  
Author(s):  
M. Kang ◽  
H. Yoshimatsu ◽  
S. Chiba ◽  
M. Kurokawa ◽  
R. Ogawa ◽  
...  
Keyword(s):  
Body Temperature ◽  
Intraperitoneal Injection ◽  
Histidine Decarboxylase ◽  
Interleukin 1 ◽  
Suppressive Effect ◽  
Ingestive Behavior ◽  
Interleukin 1 Beta ◽  
Hypothalamic Histamine ◽  
Food And Water Intake ◽  
Neuronal Histamine

Dynamic involvement of hypothalamic histamine in ingestive behavior and thermogenesis induced by interleukin-1 beta (IL-1 beta) was examined in rats. Intraperitoneal injection of 0.12 nmol/rat IL-1 beta decreased food and water intake and elevated body temperature. However, depletion of neuronal histamine induced by intraperitoneal injection of 160 mumol/rat alpha-fluoromethylhistidine, a suicide inhibitor of histidine decarboxylase (HDC), attenuated the suppressive effect of IL-1 beta on food intake, facilitated the suppressive effect on drinking, and enhanced the elevating effect on rectal temperature. Intraperitoneal injection of 0.12 nmol/rat IL-1 beta increased hypothalamic histamine turnover rate. The same dose of IL-1 beta also increased activity of HDC and histamine-N-methyltransferase (HMT). These results suggest that IL-1 beta may stimulate synthesis and release of hypothalamic histamine in presynaptic terminals by activation of HDC and facilitate degradation of extracellular histamine by activation of MHT. These changes in the dynamics of hypothalamic histamine modulate IL-1 beta-induced ingestive behavior and body temperature.

Cardiovascular effects of human recombinant interleukin-1 beta in conscious rats

1994 ◽  
Vol 266 (4) ◽  
pp. R1148-R1153 ◽  
Author(s):  
A. Bataillard ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Interleukin 1 ◽  
Renin Angiotensin System ◽  
Cardiovascular Effects ◽  
Interleukin 1 Beta ◽  
Pronounced Increase ◽  
Arterial Blood

Cardiovascular effects of human recombinant interleukin-1 beta (hrIL-1 beta) were investigated in normotensive rats using a computerized analysis of arterial blood pressure in conscious, unrestrained animals. Intravenous injection of hrIL-1 beta induced a rapid and short-lasting rise in blood pressure associated with a first slight tachycardia followed by a second sustained and pronounced increase in heart rate. These effects occurred in a dose-related manner. Pretreatment with a converting-enzyme inhibitor (perindopril) did not modify the hrIL-1 beta-induced increase in blood pressure. Blockade of beta 1-adrenoceptors (atenolol) prevented the tachycardia, but did not significantly affect the pressor response to hrIL-1 beta. On the contrary, the hrIL-1 beta-induced increase in blood pressure was inhibited by an alpha 1-adrenoceptor antagonist (prazosin), whereas the tachycardia was untouched. Finally, pretreatment with a cyclooxygenase inhibitor (indomethacin) completely abolished the cardiovascular response to hrIL-1 beta. These results suggest that the hrIL-1 beta-induced pressor response and associated tachycardia require the synthesis of prostaglandins and involve a sympathetic nervous system activation but do not depend on the renin-angiotensin system.

Role of median preoptic area in vasopressin-mediated bradycardia

1988 ◽  
Vol 254 (6) ◽  
pp. H1172-H1178 ◽  
Author(s):  
K. P. Patel ◽  
P. G. Schmid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve Activity ◽  
Preoptic Area ◽  
Local Administration ◽  
Base Line ◽  
Preoptic Nucleus ◽  
Nerve Activity ◽  
Median Preoptic Nucleus

To determine whether neural traffic through the median preoptic nucleus (MnPO) is involved in arginine vasopressin (AVP)-mediated bradycardia and sympathoinhibition, we recorded reflex decreases in heart rate (HR) and lumbar sympathetic nerve activity, in response to increases in arterial pressure induced either by intravenous phenylephrine (PE) or AVP before, during, and after local administration of lidocaine (200 nl, 2%) in the MnPO of chloralose-anesthetized rabbits. Base-line blood pressure and HR did not change in response to administration of lidocaine into the MnPO. Blockade of neural traffic (by lidocaine) in the MnPO produced an attenuation of AVP-mediated bradycardia but not the baroreflex-mediated bradycardia caused by PE. Lidocaine in the MnPO did not alter the sympathoinhibition produced with AVP. These results indicate that part of the bradycardia produced by AVP is mediated via forebrain structures such as the MnPO and is selective for bradycardia. Additionally, this response was mimicked by administration of yohimbine, an alpha 2-antagonist, into the MnPO, which suggests that noradrenergic mechanisms are involved in the baroreflex-mediated facilitation of bradycardia by AVP at the level of the MnPO.

Functional identification of central pressor pathways originating in the subfornical organ

1991 ◽  
Vol 69 (7) ◽  
pp. 1035-1045 ◽  
Author(s):  
John Ciriello ◽  
Michael B. Gutman
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Paraventricular Nucleus ◽  
Supraoptic Nucleus ◽  
Subfornical Organ ◽  
Preoptic Nucleus ◽  
Thoracic Spinal Cord ◽  
Median Preoptic Nucleus ◽  
Pressor Responses ◽  
Stimulation Of

The functional projections from pressor sites in the subfornical organ (SFO) were identified using the 2-deoxyglucose (2-DG) autoradiographic method in urethane-anesthetized, sinoaortic-denervated rats. Autoradiographs of brain and spinal cord sections taken from rats whose SFO was continuously stimulated electrically for 45 min with stereotaxically placed monopolar electrodes (150 μA, 1.5-ms pulse duration, 15 Hz) following injection of tritiated 2-DG were compared with control rats that received intravenous infusions of pressor doses of phenylephrine to mimic the increase in arterial pressure observed during SFO stimulation. Comparisons were also made to autoradiographs from rats in which the ventral fornical commissure (CFV), just dorsal to the SFO, was electrically stimulated. The pressor responses during either electrical stimulation of the SFO or intravenous infusion of phenylephrine were similar in magnitude. On the other hand, stimulation of the CFV did not elicit a significant pressor response. Electrical stimulation of the SFO increased 2-DG uptake, in comparison to the phenylephrine-infused rats, in the nucleus triangularis, septofimbrial nucleus, lateral septal nucleus, nucleus accumbens, bed nucleus of the stria terminalis, dorsal and ventral nucleus medianus (median preoptic nucleus), paraventricular nucleus of the thalamus, hippocampus, supraoptic nucleus, suprachiasmatic nucleus, paraventricular nucleus of the hypothalamus, and the intermediolateral nucleus of and central autonomic area of the thoracic spinal cord. In contrast, in rats whose CFV was stimulated, these nuclei did not demonstrate changes in 2-DG uptake compared with control animals that received pressor doses of phenylephrine. These data have demonstrated some of the components of the neural circuitry likely involved in mediating the pressor responses to stimulation of the SFO and the corrective responses to activation of the SFO by disturbances to circulatory and fluid balance homeostasis.Key words: cardiovascular reflex pathways, drinking, median preoptic nucleus, osmoreceptors, paraventricular nucleus of the hypothalamus, supraoptic nucleus.

Sign in / Sign up

Export Citation Format

Share Document