vasoactive-intestinal-peptide and Fever

The neural elements of the rostral diencephalon in the mammal have been implicated in the regulation of body temperature. Moreover, it may be the neural elements within this region of the brain which activate the febrile mechanisms in response to pyrogen. Is it possible that the neuropeptides located within this area of the brain serve as neurochemical intermediaries involved in temperature regulation, fever, and (or) antipyresis? Central administration of several neuropeptides can elicit marked changes in the core temperature of an animal. Although most of these purative neuroregulators exert only a very minor influence on thermoregulation, a small number of the neuropeptides have been shown to have a profound effect on the system controlling this basic vegetative function. One of these peptides, arginine vasopressin (AVP) may play a role as an endogenous antipyretic. The neuroanatomical localization of this peptide, as well as its axonal projections, are consistent with such a role for this neurohypophyseal peptide in the mediation of antipyresis. In addition, current evidence suggests that AVP does function as a neurotransmitter. Examination of the febrile response to pyrogen in both the periparturient animal and the neonate indicates that an elevation in plasma levels of AVP is closely correlated with the diminution in the febrile response. Also, when AVP is perfused into punctate regions of the brain, a pyrogen-induced fever may be markedly suppressed AVP appears to act primarily within the septal area, 2- to 3-mm rostral to the anterior commissure. During the development of fever, the release of AVP is altered within these same loci. As body temperature decreases during the febrile state, there is a concomitant increase in the amount of AVP released into the extracellular fluid of these septal sites. Very recent findings suggest that AVP may have additional central neurochemical functions. For example, this peptide may be involved in the etiology of some forms of convulsive disorders. The precise manner in which body temperature is regulated by the central nervous system normally and during fever is not well understood.(ABSTRACT TRUNCATED AT 400 WORDS)

Topics: Adrenocorticotropic Hormone; Angiotensin II; Animals; Arginine Vasopressin; Body Temperature Regulation; Bombesin; Diencephalon; Epilepsy; Fever; Nerve Tissue Proteins; Thyrotropin-Releasing Hormone; Vasoactive Intestinal Peptide

An amphetamine (AMPH) regimen that does not produce a prominent blood-brain barrier breakdown was shown to significantly alter the expression of genes regulating vascular tone, immune function, and angiogenesis in vasculature associated with arachnoid and pia membranes of the forebrain. Adult-male Sprague-Dawley rats were given either saline injections during environmentally-induced hyperthermia (EIH) or four doses of AMPH with 2 h between each dose (5, 7.5, 10, and 10 mg/kg d-AMPH, s.c.) that produced hyperthermia. Rats were sacrificed either 3 h or 1 day after dosing, and total RNA and protein was isolated from the meninges, arachnoid and pia membranes, and associated vasculature (MAV) that surround the forebrain. Vip, eNos, Drd1a, and Edn1 (genes regulating vascular tone) were increased by either EIH or AMPH to varying degrees in MAV, indicating that EIH and AMPH produce differential responses to enhance vasodilatation. AMPH, and EIH to a lesser extent, elicited a significant inflammatory response at 3 h as indicated by an increased MAV expression of cytokines Il1b, Il6, Ccl-2, Cxcl1, and Cxcl2. Also, genes related to heat shock/stress and disruption of vascular homeostasis such as Icam1 and Hsp72 were also observed. The increased expression of Ctgf and Timp1 and the decreased expression of Akt1, Anpep, and Mmp2 and Tek (genes involved in stimulating angiogenesis) from AMPH exposure suggest that angiogenesis was arrested or disrupted in MAV to a greater extent by AMPH compared to EIH. Alterations in vascular-related gene expression in the parietal cortex and striatum after AMPH were less in magnitude than in MAV, indicating less of a disruption of vascular homeostasis in these two regions. Changes in the levels of insulin-like growth factor binding proteins Igfbp1, 2, and 5 in MAV, compared to those in striatum and parietal cortex, imply an interaction between these regions to regulate the levels of insulin-like growth factor after AMPH damage. Thus, the vasculature and meninges surrounding the surface of the forebrain may be an important region in which AMPHs can disrupt vascular homeostasis.

Topics: Amphetamine; Animals; Blood Vessels; Body Temperature; Brain; Central Nervous System Stimulants; Connective Tissue Growth Factor; Cytokines; Dose-Response Relationship, Drug; Environment; Fever; Gene Expression Profiling; Gene Expression Regulation; HSP72 Heat-Shock Proteins; Male; Meninges; Neovascularization, Physiologic; Oligonucleotide Array Sequence Analysis; Rats; Rats, Sprague-Dawley; Time Factors; Vasoactive Intestinal Peptide

The release of brain-gut peptides during sauna bathing was studied in seven women. All women underwent a 20 min sauna bath. Their sublingual temperature rose from 36.9 +/- 0.1 degrees C to 38.6 +/- 0.2 degrees C (mean +/- SEM). A significant increase in circulating plasma vasoactive intestinal polypeptide (VIP) was observed during heat exposure, whereas plasma pancreatic polypeptide (PP), motilin and blood glucose rose and stayed significantly elevated first during the ensuing 60 min (P less than 0.05 in all cases). A similar increase in plasma insulin failed to reach statistical significance, whereas the plasma levels of somatostatin and cholecystokinin (CCK) remained unchanged. It is suggested that the plasma VIP levels are related to compensatory mechanisms during heat exposure with vasodilatation and heat loss.

Topics: Adult; Blood Glucose; Body Weight; Brain; Female; Fever; Gastrointestinal Hormones; Hemodynamics; Humans; Insulin; Middle Aged; Motilin; Pancreatic Polypeptide; Somatostatin; Steam Bath; Vasoactive Intestinal Peptide