title: ANG II prolongs splanchnic nerve-mediated inhibition of duodenal mucosal alkaline secretion in the rat.
abstract: Hypovolemia inhibits duodenal mucosal alkaline (HCO-3) secretion by activation of sympathoadrenergic nerves. A possible involvement of the renin-angiotensin system was investigated. Experiments were performed on chloralose-anesthetized rats. The mucosal alkaline output by a duodenal segment was measured using in situ pH-stat titration equipment. A modest hypovolemia was induced by bleeding the animals approximately 10% of the total blood volume. This procedure decreased duodenal mucosal alkaline secretion to a sustained level of approximately 50% of baseline and reduced mean arterial pressure by approximately 20 mmHg. Intravenous pretreatment with the angiotensin-converting enzyme (ACE) inhibitor enalaprilate (0.7 mg/kg) or the angiotensin II-receptor antagonist losartan (10 mg/kg) altered the response to hypovolemia to a transient one, and alkaline secretion returned to the control level within 40-50 min. When exogenous angiotensin II was administered intravenously (0.25 and 0.75 microgram.kg-1.h-1), a hypovolemia-induced sustained depression of the secretion was observed even during ACE inhibition. Direct electrical stimulation (3 Hz, 5 V, 5 ms, bilaterally) of the peripheral splanchnic nerves decreased duodenal mucosal alkaline secretion to approximately 60% of the control level and increased mean arterial pressure by approximately 20 mmHg. However, in enalaprilate-pretreated animals, the inhibition of alkaline secretion due to splanchnic nerve stimulation was transient, a response that became sustained on angiotensin II substitution. These results suggest that the renin-angiotensin system prolongs the sympathoadrenergic inhibition of duodenal mucosal alkaline secretion and that angiotensin II, in this regard, acts mainly on the peripheral sympathetic efferents.
authors.affiliation: Department of Physiology, Göteborg University, Sweden.
authors.forename: B
authors.initials: B
authors.lastname: Johansson
authors.forename: M
authors.initials: M
authors.lastname: Holm
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.forename: A
authors.initials: A
authors.lastname: Pettersson
authors.forename: C
authors.initials: C
authors.lastname: Jönson
authors.forename: L
authors.initials: L
authors.lastname: Fändriks
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D001713:Biphenyl Compounds / Q000494:pharmacology; D004386:Duodenum; D004558:Electric Stimulation; D004656:Enalapril / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D007093:Imidazoles / Q000494:pharmacology; D066298:In Vitro Techniques; D007413:Intestinal Mucosa / Q000294:innervation / Q000502:physiology*; D019808:Losartan; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System; D013153:Splanchnic Nerves / Q000187:drug effects / Q000502:physiology*; D013777:Tetrazoles / Q000494:pharmacology; D013997:Time Factors
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D001639:Bicarbonates; D001713:Biphenyl Compounds; D007093:Imidazoles; D013777:Tetrazoles; D000804:Angiotensin II; D004656:Enalapril; D019808:Losartan