Central Effects of Interleukin‐1 on Blood Pressure, Thermogenesis, and the Release of Vasopressin, ACTH, and Atrial Natriuretic Peptide

Abstract

To assess the central role of interleukin 1-beta (IL-1 beta) in the release of ACTH, vasopressin (AVP) and atrial natriuretic peptide (ANP) and in the regulation of blood pressure and thermogenesis, 3 ng (0.173 pM) x 100-1 x BW-1 (LIL), 30 ng (1.73 pM) x 100g-1 x BW-1 (MIL), and 150 ng (8.63 pM) x 100g-1 x BW-1 (HIL) of human IL-1 beta dissolved in sterile saline were injected intracerebroventricularly to conscious rats. In the control rats, saline alone (5 microliters) was administered. In three other groups, rats were pretreated with indomethacin, a cyclooxygenase inhibitor, given i.v. (1 mg x 100g-1 x BW-1); medium and high doses of IL-1 beta or its vehicle were given. In the LIL group, IL-1 beta increased blood pressure, body temperature and plasma AVP and ANP without any changes in heart rate (HR) and plasma ACTH. In the MIL group, plasma ACTH was increased, and changes in the other parameters were similar to those in the LIL group. In the HIL group, however, the pressor and thermogenetic responses were attenuated; plasma AVP, ACTH, and ANP were increased; and HR was unchanged. In the control (CON) group, none of these parameters was changed throughout the studies. Indomethacin abolished the AVP and ACTH responses to IL-1 beta, but potentiated the pressor and hypothermic responses and increased plasma ANP. These data suggest that the actions of IL-1 beta on AVP and ACTH release and thermogenesis, but not on blood pressure and the release of ANP, are modulated by the stimulated central production of prostaglandins.

Hyponatremia in a Patient with Chronic Inflammatory Disease.

“…It is knownthat immuneresponses are associated with a variety ofendocrine activities (4). Interleukin (IL)-l , IL-6, and tumor necrosis factor (TNF)-acan stimulate the synthesis and secretion of corticotropin-releasing hormoneand vasopressin directly in rats (5,6). Furthermore, it has been confirmed that intravenous administration of recombinant IL-6 stimulates AVPsecretion through a nonosmotic mechanism in man (7).…”

“…Plasma AVPlevels were also elevated, suggesting that IL-6 activated the magnocellular AVPsecreting neurons, and it may be involved in SIADH. Cytokines are known to exhibit a hormone-like action, and they stimulate the secretion of corticotropin-releasing hormoneand anti-diuretic hormone (ADH) (5,6). Accordingly, the immune system is considered to participate in regulating the homeostasis of body fluids by affecting neuroendocrine mechanisms.…”

Role of Atrial Natriuretic Peptide in Interleukin 1.BETA.-Induced Natriuresis in Conscious Rats.

“…This may be due to the formation of PGs, because this response was blocked by indomethacin (Kimura et al 1993;Yamamoto et al 1994). In the present study, the natriuresis and increased plasma ANP were not accompanied by a diuresis.…”

“…Moreover, pyrogen and cytokines have been reported neither to increase GFR nor to suppress the proximal and distal tubular Na reabsorption (Brandt et al 1956; Gombos et al 1967;Caverzasio et al 1987; Beasley et al 1988; Kohan et al 1989). Kimura et al (1993) and Yamamoto et al (1994) reported recently that central as well as peripheral administration of interleukin lfl (IL-1/l) increased the release of atrial natriuretic peptide (ANP), inducing a natriuresis and vasodilatation, of vasopressin (AVP) and of ACTH and a sympathetic activity in conscious rats. Therefore, it is likely that the formation of ANP in response to IL-1/3 plays an important role in the natriuresis after cytokine administration.…”

Using optogenetics to translate the “inflammatory dialogue” between heart and brain in the context of stress

“…Earlier studies revealed that central infusion of pro-inflammatory cytokines such as IL-1β and TNF-α leads to significant hemodynamic and neurohormonal responses (such as increased arterial blood pressure) that are typical of CVDs, sympathetic activity, and the synthesis of renin, aldosterone and vasopressin [65,66] . Recent studies further showed that myocardial infarction induces the production of cytokines in the hypothalamus, which modulate neurotransmission in the PVN during the subsequent process of heart failure, resulting in elevated sympathoexcitation [67][68][69] .…”