VISCERAL VASODILATATION AND SOMATIC VASOCONSTRICTION EVOKED BY ACID CHALLENGE OF THE RAT GASTRIC-MUCOSA - DIVERSITY OF MECHANISMS

1. Acid back-diffusion through a disrupted gastric mucosal barrier inc reases blood flow to the stomach without any change in systemic blood pressure. This study was undertaken to examine the gastric acid-evoked changes in blood flow in a number of visceral and somatic arterial be ds and to elucidate the mechanisms which lead to the regionally divers e haemodynamic responses. 2. The gastric mucosa of urethane-anaestheti zed rats was challenged with acid by perfusing the stomach with ethano l (15%, to disrupt the gastric mucosal barrier) in 0.15 M HCl. Blood f low was estimated by laser Doppler flowmetry, the hydrogen clearance m ethod or the ultrasonic transit time shift technique. 3. Gastric acid challenge increased blood flow in the gastric mucosa and left gastric artery while blood flow in the femoral artery and skin declined. 4. Af ferent nerve stimulation by intragastric administration of capsaicin e nhanced blood flow in the left gastric artery but did not diminish blo od flow in the femoral artery when compared with the vehicle. 5. The g astric acid-evoked dilatation of the left gastric artery was depressed by acute extrinsic denervation of the stomach, capsaicin-induced abla tion of afferent neurones or hexamethonium-induced blockade of autonom ic ganglionic transmission. 6. The gastric acid-induced constriction o f the femoral artery was attenuated by acute extrinsic denervation of the stomach but left unaltered by capsaicin, hexamethonium, guanethidi ne, indomethacin, telmisartan (an angiotensin II antagonist), [d(CH2)( 5)(1), Tyr(Me)(2), Arg(8)]-vasopressin (a vasopressin antagonist), bos entan (an endothelin antagonist) and acute ligation of the Mood vessel s to the adrenal glands. 7. These data show that acid challenge of the gastric mucosa elicits visceral vasodilatation and somatic vasoconstr iction via divergent mechanisms. The gastric hyperaemia is brought abo ut by extrinsic vasodilator nerves, whereas the reduction of somatic b lood flow seems to be mediated by non-neural, probably humoral, vasoco nstrictor messengers that remain to be identified.