CENTRAL EFFECTS OF SOMATOSTATIN AND ATRIAL-NATRIURETIC-PEPTIDE ON TRACHEAL TONE

Citation
Ma. Haxhiu et al., CENTRAL EFFECTS OF SOMATOSTATIN AND ATRIAL-NATRIURETIC-PEPTIDE ON TRACHEAL TONE, Journal of applied physiology, 75(6), 1993, pp. 2353-2359
Citations number
30
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
75
Issue
6
Year of publication
1993
Pages
2353 - 2359
Database
ISI
SICI code
8750-7587(1993)75:6<2353:CEOSAA>2.0.ZU;2-P
Abstract
The effects of somatostatin and atrial natriuretic peptide applied top ically to the ventral surface of the medulla (VMS) on tracheal tone an d phrenic nerve activity (Phr) were studied in chloralose-anesthetized and paralyzed cats artificially ventilated with 7% CO2 in O-2. Surfac e application of drugs to the chemosensitive areas of the VMS signific antly decreased tracheal tension measured by changes in pressure in a balloon placed in a bypassed segment of the trachea (Ptseg). Applicati on of somatostatin (9 cats) caused a mean decrease in Ptseg from 17.3 +/- 1.8 (SE) to 4.3 +/- 1.4 cmH(2)O (P < 0.01) and a reduction in Phr from 24.9 +/- 3.4 to 10.3 +/- 3.4 units P < 0.05). Like somatostatin, application of atrial natriuretic peptide to the VMS (5 cats) produced tracheal relaxation (Ptseg decreased from 19.3 +/- 2.6 to 9.9 +/- 1.3 cmH(2)O(2) P < 0.01), but in contrast there was an insignificant redu ction in Phr (from 18.5 +/- 3.6 to 16.1 +/- 3.8 units, P > 0.05). When parasympathetic activity was abolished by atropine methylnitrate and tracheal tone was restored with 5-hydroxytryptamine somatostatin and a trial natriuretic peptide applied on the VMS had no effect on tracheal pressure, suggesting that observed changes were not caused by direct action of peptides on tracheal smooth muscle via the bloodstream or by facilitation of inhibitory pathways. Both somatostatin and atrial nat riuretic peptide applications were associated with a slight but signif icant decrease in arterial blood pressure. These data suggest that som atostatin and atrial natriuretic peptide acting on the chemosensitive structure of the VMS may play significant roles in modulating para sym pathetic outflow to airway smooth muscle.