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This Article Full Text Full Text (PDF) All Versions of this Article: 289/6/E1058    most recent 00162.2005v1 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 Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Zhang, D. X. Articles by Campbell, W. B. Search for Related Content PubMed PubMed Citation Articles by Zhang, D. X. Articles by Campbell, W. B.

Mechanisms of histamine-induced relaxation in bovine small adrenal cortical arteries

Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin

Submitted 12 April 2005 ; accepted in final form 25 July 2005

Adrenal steroidogenesis is closely correlated with increases in adrenal blood flow. Many reports have studied the regulation of adrenal blood flow in vivo and in perfused glands, but until recently few studies have been conducted on isolated adrenal arteries. The present study examined vasomotor responses of isolated bovine small adrenal cortical arteries to histamine, an endogenous vasoactive compound, and its mechanism of action. In U-46619-precontracted arteries, histamine (10^–9-5 x 10^–6 M) elicited concentration-dependent relaxations. The relaxations were blocked by the H₁ receptor antagonists diphenhydramine (10 µM) or mepyramine (1 µM) (maximal relaxations of 18 ± 6 and 22 ± 6%, respectively, vs. 55 ± 5% of control) but only partially inhibited by the H₂ receptor antagonist cimetidine (10 µM) and the H₃ receptor antagonist thioperamide (1 µM). Histamine-induced relaxations were also blocked by the nitric oxide synthase inhibitor N-nitro-L-arginine (L-NA, 30 µM; maximal relaxation of 13 ± 7%) and eliminated by endothelial removal or L-NA combined with the cyclooxgenase inhibitor indomethacin (10 µM). In the presence of adrenal zona glomerulosa (ZG) cells, histamine did not induce further relaxations compared with histamine alone. Histamine (10^–7-10^–5 M) concentration-dependently increased aldosterone production by adrenal ZG cells. Compound 48/80 (10 µg/ml), a mast cell degranulator, induced significant relaxations (93 ± 0.6%), which were blocked by L-NA plus indomethacin or endothelium removal, partially inhibited by the combination of the H₁, H₂, and H₃ receptor antagonists, but not affected by the mast cell stabilizer sodium cromoglycate (1 mM). These results demonstrate that histamine causes direct relaxation of small adrenal cortical arteries, which is largely mediated by endothelial NO and prostaglandins via H₁ receptors. The potential role of histamine in linking adrenal vascular events and steroid secretion requires further investigation.

endothelium; nitric oxide; prostacyclin; aldosterone

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