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This Article Full Text Full Text (PDF) All Versions of this Article: 294/3/R689    most recent 00453.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Matsumoto, I. Articles by Aikawa, T. PubMed PubMed Citation Articles by Matsumoto, I. Articles by Aikawa, T.

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Control Mechanisms of Renin Synthesis and Release: A 21st Century Perspective

Stimulation of brain mast cells by compound 48/80, a histamine liberator, evokes renin and vasopressin release in dogs

¹Department of Physiology, Nagasaki University School of Medicine, Nagasaki, Japan; and ²Department of Anatomy and Physiology, Faculty of Wellness, Kwassui Women's College, Nagasaki, Japan

Submitted 26 June 2007 ; accepted in final form 14 December 2007

Because degranulation of brain mast cells activates adrenocortical secretion (41, 42), we examined whether activation of such cells increases renin and vasopressin (antidiuretic hormone: ADH) secretion. For this, we administered compound 48/80 (C48/80), which liberates histamine from mast cells, to pentobarbital-anesthetized dogs. An infusion of 37.5 µg/kg C48/80 into the cerebral third ventricle evoked increases in plasma renin activity (PRA), and in plasma epinephrine (Epi) and ADH concentrations. Ketotifen (mast cell-stabilizing drug; given orally for 1 wk before the experiment) significantly reduced the C48/80-induced increases in PRA, Epi, and ADH. Resection of the bilateral splanchnic nerves (SPX) below the diaphragm completely prevented the C48/80-induced increases in PRA and Epi, but potentiated the C48/80-induced increase in ADH and elevated the plasma Epi level before and after C48/80 challenge. No significant changes in mean arterial blood pressure, heart rate, concentrations of plasma electrolytes (Na⁺, K⁺, and Cl^–), or plasma osmolality were observed after C48/80 challenge in dogs with or without SPX. Pyrilamine maleate (H₁ histaminergic-receptor antagonist) significantly reduced the C48/80-induced increase in PRA when given intracerebroventricularly, but not when given intravenously. In contrast, metiamide (H₂ histaminergic-receptor antagonist) given intracerebroventricularly significantly potentiated the C48/80-induced PRA increase. A small dose of histamine (5 µg/kg) administered intracerebroventricularly increased PRA twofold and ADH fourfold (vs. their basal level). These results suggest that in dogs, endogenous histamine liberated from brain mast cells may increase renin and Epi secretion (via the sympathetic outflow) and ADH secretion (via the central nervous system).

degranulation of brain mast cells; H₁-histaminergic antagonist; H₂-histaminergic antagonist; splanchnicectomy