Effects of hCGRP I and II on gastric blood flow and acid secretion in anesthetized rabbits

1989 ◽  
Vol 256 (1) ◽  
pp. G145-G149 ◽  
Author(s):  
P. Bauerfeind ◽  
R. Hof ◽  
A. Hof ◽  
M. Cucala ◽  
S. Siegrist ◽  
...  
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Regional Blood Flow ◽  
Gastric Blood Flow ◽  
Human Calcitonin ◽  
Inverse Effect

Effects of intravenously administered human calcitonin gene-related peptides (hCGRP) I and II on regional blood flow and gastric acid secretion were examined in barbiturate-anesthetized rabbits. Blood flow was measured by injection of radioactively labeled microspheres at 0, 10, 20, 30, and 60 min. hCGRP I and II and vehicle were infused intravenously in five rabbits in rising doses of 0.01 (0-10th min), 0.03 (11-20th min), and 0.1 microgram.kg-1.min-1 (21-30th min). hCGRP I and II increased gastric blood flow dose dependently. Moreover, hCGRP I raised regional conductance (inverse of vascular resistance) in the stomach, duodenum, heart, brain, and skeletal muscle. As a result of the increased total peripheral conductance the mean arterial pressure was reduced, but the cardiac output remained unchanged. hCGRP II increased blood flow and conductance selectively in the stomach and the pancreas. The total peripheral conductance and mean arterial pressure remained unchanged. Apparently, hCGRP II exerts a more localized effect on the stomach than hCGRP I. hCGRP I and II did not affect basal gastric acid secretion. Pentagastrin-stimulated acid secretion was increased by 28% with hCGRP I (0.025 micrograms.kg-1.min-1) and decreased by 27% with hCGRP II (0.025 micrograms.kg-1.min-1). The inverse effect of hCGRP I and II and the parallel stimulation of blood flow brought about with hCGRP I and II indicate a different mode of action of the peptides on gastric blood flow and gastric acid secretion.

CRF initiates biological actions within the brain that are observed in response to stress

1987 ◽  
Vol 252 (1) ◽  
pp. R34-R39 ◽  
Author(s):  
H. J. Lenz ◽  
A. Raedler ◽  
H. Greten ◽  
M. R. Brown
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Plasma Catecholamine ◽  
Biological Actions

Corticotropin-releasing factor (CRF) is thought to be an endogenous mediator of adrenocorticotropic hormone release following stress. We examined if CRF initiates further biological actions that are observed in response to stressful events. Male beagle dogs (10–12 kg) were fitted with a chronic intracerebroventricular cannula, intra-arterial and intravenous catheters, as well as a gastric fistula. Synthetic human CRF was microinjected into the third cerebral ventricle in conscious animals. CRF (0.1–1.0 nmol/kg) significantly (P less than 0.01) increased plasma concentrations of epinephrine, norepinephrine, glucagon, and glucose and elevated mean arterial pressure and heart rate. Pretreatment of the animals with the ganglionic blocking agent chlorisondamine completely abolished the increases in plasma catecholamine and glucose concentrations as well as the elevations in blood pressure and heart rate. CRF significantly (P less than 0.01) inhibited gastric acid secretion, but not plasma gastrin concentrations stimulated by an 8% liquid peptone meal. The gastric inhibitory action of CRF was completely prevented by chlorisondamine and, in part, by naloxone and a vasopressin antagonist. In contrast, bilateral truncal vagotomy did not affect the gastric inhibitory action of CRF. The results of this study indicate that CRF acts within the central nervous system to increase plasma glucose and glucagon concentrations, mean arterial pressure, and heart rate by activation of the autonomic nervous system. CRF inhibits meal-stimulated gastric acid secretion by activation of the sympathetic nervous system and, in part, by opiate and vasopressin-dependent pathways and not by inhibition of gastrin release.(ABSTRACT TRUNCATED AT 250 WORDS)

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

Effect of xenopsin on blood flow, hormone release, and acid secretion

1982 ◽  
Vol 243 (3) ◽  
pp. G195-G199 ◽  
Author(s):  
M. J. Zinner ◽  
F. Kasher ◽  
I. M. Modlin ◽  
B. M. Jaffe
Keyword(s):  
Blood Flow ◽  
Acid Secretion ◽  
Gastric Acid ◽  
Regional Blood Flow ◽  
Acid Output ◽  
Significant Inhibition ◽  
Organ Blood Flow ◽  
Hormone Release ◽  
Change In Mean ◽  
Specific Influence

We investigated the effects of the neurotensin analogue xenopsin on regional blood flow, central hemodynamics, and stimulated acid secretion in awake conscious dogs. Organ blood flow, estimated using the radioactive microsphere technique, was significantly increased during the xenopsin infusion to the adrenals, pancreas, and ileum. There was no change in mean arterial pressure or cardiac output (measured by thermodilution). Along with changes in blood flow, there was a significant increase in the hormone output from the pancreas. These included rises in plasma pancreatic polypeptide, insulin, and glucagon. There also was a rise in plasma cortisol levels during the infusion. Substance P levels rose slowly but significantly during the xenospin infusion. There was no change in plasma gastrin levels. Xenopsin produced a significant inhibition of tetragastrin-stimulated gastric acid output. Thus, xenopsin appears to have region-specific influence on blood flow that correlates with region-specific hormonal secretion. In addition, xenopsin, like its mammalian analogue neurotensin, is an inhibitor of stimulated gastric acid secretion. A mammalian xenopsinlike peptide may well be involved in the modulation of gastrointestinal function.

Role of gastric acid secretion and blood flow in the development of vagal stimulation induced gastric mucosal damage

1993 ◽  
Vol 71 (10-11) ◽  
pp. 829-834 ◽  
Author(s):  
Lynn E. Hierlihy ◽  
John L. Wallace ◽  
Alastair V. Ferguson
Keyword(s):  
Blood Flow ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Vagal Stimulation ◽  
Mucosal Damage ◽  
Secretory Rate ◽  
The Mean ◽  
Gastric Mucosal Erosions

Vagal stimulation has been shown to result in the development of gastric mucosal erosions in the rat, although the mechanisms underlying the development of such erosions are not known. The effects of vagal stimulation on gastric acid secretion and mucosal blood flow were examined in urethane-anesthetized male Sprague–Dawley rats to determine whether changes in these factors correlate with the mucosal damage in response to vagal stimulation. Electrical stimulation (5 Hz, 5 V, 1 ms for 60 min) of afferent or efferent components of the vagi was not found to induce any significant increase in the mean acid secretory rate compared with control animals (p > 0.05). In contrast, stimulation of intact vagus nerves induced a significant increase in the mean acid secretory rate compared with control and efferent- and afferent-stimulated groups (p < 0.01). Measurement of gastric blood flow with laser-Doppler flowmetry demonstrated intact vagal stimulation to have no significant effect on gastric blood flow. These data suggest that such vagal stimulation induced increases in acid secretion in urethane-anesthetized animals may represent a part of the integrated physiological response to such stimulation which leads to the development of gastric mucosal erosions within 60 min. Pretreatment with antisecretory agents such as cimetidine and inter-leukin-1β significantly reduce the gastric mucosal injury compared with untreated animals (p < 0.05), emphasizing the important role of acid secretion in the development of vagal-induced gastric damage.Key words: vagus, acid secretion, blood flow, gastric.

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