| Research Abstract |
1. Central effects of interleukin-1beta on blood pressure, thermogenesis and the release of vasopressin, ACTH and atrial natriuretic peptide. Interleukin 1-beta (IL-1beta) increased plasma vasopressin (AVP), ACTH and atrial natriuretic peptide (ANP). IL-1beta in the low dose (3-30 ng ・ 100g^<-1> ・ BW) increased body temperature (BT) and blood pressure (BP), but its high dose (150 ng ・ 100g^<-1> ・ BW) depressed them. Indomethacin, a cycloxygenase inhibitor, prevented the responses to IL-1beta except for increases in ANP release.
2. Peripheral Effects of interleukin-1beta on blood pressure, themoregulation and the release of vasopressin, ACTH and atrial natriuretichormones. IL-1beta given iv stimulated the release of AVP, ACTH, and ANP and increased or decreased blood pressure and thermogenesis. Indomethacin attenuatted all these responses to IL-1beta except for increases in ANP.
3. Effects of a nitric oxide synthase inhibitor (LNAME) on vasopressin and atrial natriuretic hormone releaase, thermogenesis and cardiovascular function in response to interleukin-1beta in rats. LNAME stimulted the release of AVP and ANP and body temperature and blood pressure. NO formed by IL-1beta may not have direct effects on the release of these hormones, and the regulation of body temperature, but decreased transiently blood pressure.
4. Roles of atrial natriuretic peptide in an interleukin-1beta-induced natriuresis in conscious rats. IL-1beta brought about a natriuresis in accordance with increased plasma ANP and the specific ANP receptor antagonist "HS 142-1" prevented the natriuresis induced by IL-1beta, despite increased plasma ANP.
|
