Effect of Partial Gastric Devascularization on Mucosal Blood Flow and Acid Secretion in Cats

1979 ◽  
Vol 11 (1) ◽  
pp. 15-26 ◽  
Author(s):  
I.E. Varhaug ◽  
K. Svanes ◽  
O.. Søreide ◽  
A. Skarstein
Keyword(s):  
Blood Flow ◽  
Acid Secretion ◽  
Mucosal Blood Flow

Gastric Mucosal Blood Flow Response to Stimulation and Inhibition of Gastric Acid Secretion

1988 ◽  
Vol 95 (3) ◽  
pp. 642-650 ◽  
Author(s):  
Josep M. Pique ◽  
Felix W. Leung ◽  
Heck W. Tan ◽  
Edward Livingston ◽  
Oscar U. Scremin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Blood Flow Response ◽  
Flow Response

Tachykinin-induced increase in gastric mucosal resistance: role of primary afferent neurons, CGRP, and NO

1996 ◽  
Vol 271 (6) ◽  
pp. G1017-G1027
Author(s):  
T. Stroff ◽  
S. Plate ◽  
J. S. Ebrahim ◽  
K. H. Ehrlich ◽  
M. Respondek ◽  
...  
Keyword(s):  
Blood Flow ◽  
Acid Secretion ◽  
Mucosal Blood Flow ◽  
Afferent Nerve ◽  
Receptor Blockade ◽  
Afferent Neurons ◽  
Primary Afferent Neurons ◽  
Primary Afferent ◽  
Nk2 Receptor ◽  
Primary Afferent Nerve

The tachykinins [Ala5,beta-Ala8]neurokinin A-(4-10) -[Ala5,beta-Ala8]NKA-(4-10) inverted question mark and NKA-(4-10) dose dependently protected against ethanol-induced gastric mucosal damage in rats (half-maximal inhibitory dose, 46 and 48 nmol/kg, respectively). These effects were abolished by primary afferent nerve denervation, calcitonin gene-related peptide (CGRP) immunoneutralization, the CGRP receptor antagonist human (h) hCGRP-(8-37), and inhibition of nitric oxide (NO) biosynthesis by NG-nitro-L-arginine methyl ester. Tachykinin-induced protection occurred despite marked depression of gastric mucosal blood flow and was not associated with increased acid secretion. NK2-receptor blockade antagonized the protective effects of [Ala5,beta-Ala8]NKA-(4-10) and NKA-(4-10), whereas NK1-receptor blockade was ineffective. Blockade of NK2 but not NK1 receptors prevented by 65% the protection evoked by topical capsaicin without affecting capsaicin-induced hyperemia. We conclude that the increase in gastric mucosal resistance evoked by tachykinins is NK2 receptor-mediated and involves primary afferent neurons, CGRP, and NO. Gastric mucosal hyperemia and increased acid secretion do not participate in the effect. Tachykinins activating NK2 receptors contribute to the increase in gastric mucosal resistance but not the increment in mucosal blood flow after primary afferent nerve stimulation by capsaicin.

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