Visceral vasodilatation and somatic vasoconstriction evoked by acid challenge of the rat gastric mucosa: diversity of mechanisms.

Wachter, C; Heinemann, Ákos; Jocič, Milana; Holzer, Peter

doi:10.1113/jphysiol.1995.sp020829

Cited by 14 publications

(15 citation statements)

References 29 publications

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“…Blood flow, in ml min −1 , is calculated from the modification of the beam transit time, which is solely dependent on blood flow but independent from the vessel's diameter and largely insensitive to probe misalignment (Barnes et al , 1983; Burton & Gorewit, 1984). The 1 mm flow probe has been developed for measurements in small vessels and repeatedly used and validated in different arteries of the rat (Myers & Hernandez, 1992; Wachter et al , 1995; D'Almeida et al , 1995).…”

Section: Methodsmentioning

confidence: 99%

Dilatation by angiotensin II of the rat femoral arterial bed in vivo via pressure/flow‐induced release of nitric oxide and prostaglandins

Heinemann

Wachter

Peskar

et al. 1997

British J Pharmacology

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1 The haemodynamic e ects of angiotensin II (AII) and, for comparison, arginine vasopressin (AVP) in the femoral and superior mesenteric artery of urethane-anaesthetized rats were analysed with the ultrasonic transit time shift technique. 2 I.v. bolus injection of AII (0.1 ± 3 nmol kg 71 ) and AVP (0.03 ± 1 nmol kg 71 ) increased blood pressure which was accompanied by a decrease in blood¯ow through the superior mesenteric artery and an increase in femoral blood¯ow. The femoral hyperaemia was in part due to vasodilatation as indicated by a rise of femoral vascular conductance up to 200% relative to baseline. The femoral vasodilatation caused by AVP, but not AII, was followed by vasoconstriction. 3 Blockade of angiotensin AT 1 receptors by telmisartan (0.2 ± 20 mmol kg 71 ) prevented all haemodynamic responses to AII. 4 The femoral dilator responses to AII and AVP depended on the increase in vascular perfusion pressure since vasodilatation was reversed to vasoconstriction when blood pressure was maintained constant by means of a gravity reservoir. However, the AII-evoked femoral vasodilatation was not due to an autonomic or neuroendocrine re¯ex because it was not depressed by hexamethonium (75 mmol kg 71 ), prazosin (0.25 mmol kg 71 ) or propranolol (3 mmol kg 71 ). 5 The AII-induced femoral vasodilatation was suppressed by blockade of nitric oxide (NO) synthesis with N G -nitro-L-arginine methyl ester (L-NAME, 40 mmol kg 71 ) and reversed to vasoconstriction when L-NAME was combined with indomethacin (30 mmol kg 71 ), but was left unaltered by antagonism of endothelin ET A/B receptors with bosentan (37 mmol kg 71 ). 6 These results demonstrate that the e ect of AII to increase systemic blood pressure and the resulting rise of perfusion pressure in the femoral artery stimulates the formation of NO and prostaglandins and thereby dilates the femoral arterial bed. This local vasodilator mechanism is su cient to mask the direct vasoconstrictor response to AII.

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Section: Methodsmentioning

confidence: 99%

Dilatation by angiotensin II of the rat femoral arterial bed in vivo via pressure/flow‐induced release of nitric oxide and prostaglandins

Heinemann

Wachter

Peskar

et al. 1997

British J Pharmacology

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“…81 Blood pressure has been measured in a few cases. 14,35,37,62,63,67,78,82,215 Ulcers have been examined macroscopically, 38,[84][85][86][87][88][89]91 by light microscopy 31,37,38,61,85,87 and scanning electron microscopy (SEM). 37,38,61,85,86 Ulcers have been followed histologically 34,[61][62][63]84,86,90,92,93 histochemically 65,88 immuno histochemically, 65 by an independent observer grading histologically 34,161 and by biochemical index.…”

Section: Methodsmentioning

confidence: 99%

“…23 Gastric alkali has also been measured at pH 7 using a pH-stat method in the chambered stomach or proximal duodenum in the presence of omeprazole to inhibit acid secretion. 28 Gmbf has been measured by aminopyrene clearance, 14 14 C aniline clearance as an indirect method, 37 hydrogen gas clearance technique 61−71 by laser doppler flowmetry (LDF) 25,[31][32][33][34]41,67,72,75,76,83,176,215 and by pulsed flow-metry. 77 Arterial blood flow has been measured with ultrasonic transit time shift technique 67,69 using microspheres injected with radioactive labels 58 and by transit-time flowmetry in the portal vein and celiac artery.…”

Section: Methodsmentioning

confidence: 99%

“…264 Gastric blood flow and acid secretion by capsaicin increasing in a parallel manner but not the other way and direct stimulation of the pareital cell causing increase in blood flow were noted. 14 Capsaicin 0.16-6.55 µM/kg administered into the lumen via gastric fistula, 14 i.g., 35,37,54,61,67,130,165,166 topically, 35,75,120,166,265 parenterally, 130 or on perfusion (10-640 µM) of the stomach in anesthetized rats 63 induces hyperemia. The increase in blood flow by capsaicin 1.6 × 10 −4M is the same whether administered i.g.…”

Section: Stimulation Of Gastric Mucosal Blood Flow (Gmbf)mentioning

confidence: 99%

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Capsaicin and Gastric Ulcers

2006

Critical Reviews in Food Science and Nutrition

108

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In recent years, infection of the stomach with the organism Helicobacter Pylori has been found to be the main cause of gastric ulcers, one of the common ailments afflicting humans. Excessive acid secretion in the stomach, reduction in gastric mucosal blood flow, constant intake of non-steroid anti-inflammatory drugs (NSAIDS), ethanol, smoking, stress etc. are also considered responsible for ulcer formation. The prevalent notion among sections of population in this country and perhaps in others is that "red pepper" popularly known as "Chilli," a common spice consumed in excessive amounts leads to "gastric ulcers" in view of its irritant and likely acid secreting nature. Persons with ulcers are advised either to limit or avoid its use. However, investigations carried out in recent years have revealed that chilli or its active principle "capsaicin" is not the cause for ulcer formation but a "benefactor." Capsaicin does not stimulate but inhibits acid secretion, stimulates alkali, mucus secretions and particularly gastric mucosal blood flow which help in prevention and healing of ulcers. Capsaicin acts by stimulating afferent neurons in the stomach and signals for protection against injury causing agents. Epidemiologic surveys in Singapore have shown that gastric ulcers are three times more common in the "Chinese" than among Malaysians and Indians who are in the habit of consuming more chillis. Ulcers are common among people who are in the habit of taking NSAIDS and are infected with the organism "Helicobacter Pylori," responsible for excessive acid secretion and erosion of the mucosal layer. Eradication of the bacteria by antibiotic treatment and avoiding the NSAIDS eliminates ulcers and restores normal acid secretion.

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“…In lowering the excitability of sympathetic post‐ganglionic neurons, hexamethonium could have also interfered with axonal reflexes originating from spinal sensory neurons that pass through pre‐vertebral ganglia and synapse with sympathetic post‐ganglionic neurons on their way from the stomach 10,46 . In this context, it needs to be considered that the gastric vasodilator response to mucosal acid backdiffusion is attenuated by hexamethonium and blocked by coeliac ganglionectomy 47,48 . It seems, therefore, that sympathetic and/or enteric pathways play a role in the acid‐evoked gastric vasodilation, which, in addition, involves NO 49,50 .…”

Section: Role Of Nicotinic Transmission In the Activation Of Myenterimentioning

confidence: 99%

Capsaicin‐sensitive extrinsic afferents are involved in acid‐induced activation of distinct myenteric neurons in the rat stomach

Schicho¹,

Schemann²,

Pabst³

et al. 2003

Neurogastroenterology Motil

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Challenge of the rat gastric mucosa with 0.5 mol L(-1) HCl activates nitrergic neurons in the myenteric plexus as visualized by c-Fos immunohistochemistry. In the present study, we characterized the activated neurons more extensively by their chemical coding and investigated whether a neural pathway that involves capsaicin-sensitive extrinsic afferents and/or cholinergic neurons transmitting via nicotinic receptors contributes to the activation of myenteric neurons. In multiple labelling experiments, c-Fos was examined for co-localization with nitric oxide synthase (NOS), vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), enkephalin (ENK), gastrin-releasing peptide (GRP), substance P (SP), calbindin D-28k (CALB) and neurofilament 145 (NF 145). All c-Fos-positive neurons were immunoreactive for NOS, VIP, NPY and NF 145, but not for SP, ENK, GRP and CALB. Nerve fibres co-expressing NOS, VIP and NPY were predominantly found in the external muscle layer and in the muscularis mucosae but rarely in the mucosa. Pre-treatment with capsaicin or hexamethonium or a combination of both pre-treatments reduced HCl-induced c-Fos expression by 54, 66 and 63%, respectively. Acid challenge of the stomach, therefore, leads to activation of presumably inhibitory motor neurons responsible for muscle relaxation. Activation of these neurons is partly mediated by capsaicin-sensitive afferents and involves ganglionic transmission via nicotinic receptors.

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Visceral vasodilatation and somatic vasoconstriction evoked by acid challenge of the rat gastric mucosa: diversity of mechanisms.

Cited by 14 publications

References 29 publications

Dilatation by angiotensin II of the rat femoral arterial bed in vivo via pressure/flow‐induced release of nitric oxide and prostaglandins

Dilatation by angiotensin II of the rat femoral arterial bed in vivo via pressure/flow‐induced release of nitric oxide and prostaglandins

Capsaicin and Gastric Ulcers

Capsaicin‐sensitive extrinsic afferents are involved in acid‐induced activation of distinct myenteric neurons in the rat stomach

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