The Effect of Angiotensin on the Peristaltic Reflex of the Isolated Guinea‐pig Ileum

Beleslin, D.B.

doi:10.1111/j.1476-5381.1968.tb00458.x

Cited by 14 publications

(18 citation statements)

References 14 publications

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“…[4][5][6] Today, the RAS is regarded not only as an endocrine system, but can also be locally expressed and involve several bioactive angiotensinogen fragments. However, Ang II is still regarded to be the most prominent mediator, and presence of its receptors in a tissue can be used as an indicator of potential physiological actions.…”

Section: Introductionmentioning

confidence: 99%

The angiotensin II type 2 receptor and the gastrointestinal tract

Fändriks

2009

J Renin Angiotensin Aldosterone Syst

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The renin-angiotensin system (RAS) is well known for its vital involvement in body fluid homeostasis and circulation. However, very little research has been devoted to the impact of this regulatory system on the gastrointestinal (GI) system. This is surprising because the GI tract is fundamental for the intake and excretion of fluid and electrolytes (and nutrients), and it accommodates a large proportion of bodily haemodynamics and host defence systems. The RAS is well expressed and active in the GI tract, although the exact roles for the key mediator angiotensin II (Ang II) and its receptors in general, and the type 2 (AT 2 ) receptor in particular, are not completely settled. There are several reports showing Ang II regulation of intestinal fluid and electrolyte transport. For example, mucosaprotective duodenal bicarbonate-rich secretion is inhibited by Ang II via type 1 (AT 1 ) receptor-mediated facilitation of sympathoadrenergic activity, but this secretory process can also be stimulated by Ang II via AT 2 receptors. Novel data from human oesophagus and jejunum suggest that the AT 1 receptor mediates muscular contractions and that the AT 2 receptor regulates epithelial functions. Data are accumulating suggesting involvement of AT 1 and AT 2 receptors in GI inflammation and carcinogenesis. The picture of the RAS and AT 2 receptor in the GI tract is, however, far from complete. Much more basic research is needed with regard to GI pathophysiology before concluding clinical significance and potential applicability of pharmacological interferences with the RAS.

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Section: Introductionmentioning

confidence: 99%

The angiotensin II type 2 receptor and the gastrointestinal tract

Fändriks

2009

J Renin Angiotensin Aldosterone Syst

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“…Many pharmacological findings suggest that catecholamines interfere with synaptic transmission both in sympathetic and parasympathetic ganglia, including those of gastrointestinal tract (Marrazzi, 1939a, b Biilbring & Burn, 1942Marrazzi & Marrazzi, 1947;Kewitz & Reinert, 1952Lundberg, 1952McDougal & West, 1954;Matthews, 1956;Trendelenburg, 1956;Kosterlitz & Robinson, 1957;Costa, Revzin, Kuntzman & Brodie, 1961 ;Eccles & Libet. 1961 ;Pardo, Cato, Gijon & Alonso-de-Florida, 1963;Beleslin & VaragiC 1964;Elliot, 1965).…”

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confidence: 99%

The effect of catecholamines and sympathetic stimulation on the release of acetylcholine from the guinea‐pig colon

Beani

Bianchi

Crema

1969

British J Pharmacology

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1. In isolated guinea-pig terminal colon, the effect of sympathetic stimulation on contraction and acetylcholine release elicited by pelvic and transmural stimulation was investigated. 2. Sympathetic stimulation reduced the nerve-mediated contractile responses more than those produced by added acetylcholine. 3. Sympathetic stimulation also reduced the acetylcholine released during pelvic and transmural stimulation at low frequency. The inhibitory effect on acetylcholine released from resting colons is concealed by the simultaneous release of acetylcholine in considerable amounts from stimulated periarterial nerves which probably contain parasympathetic fibres. 4. The inhibitory effect of endogenous and exogenous catecholamines prevails when cholinergic neurones fire at low rates. It was confirmed that adrenaline is more active than noradrenaline. 5. The release of acetylcholine from unstimulated colons was for the most part maintained by nerve-conducted activity, because tetrodotoxin was able to reduce it to about one-tenth. 6. It is suggested that the sympathetic control of gastrointestinal tone and motility is exerted through two different routes: inhibition of intramural cholinergic plexuses and direct relaxation of smooth muscle cells. 7. The possible site and mechanism of action of catecholamines on intramural cholinergic structures is briefly discussed.The possible modulation of ganglionic transmission by the sympathetic system is still an open question and a matter of discussion. From careful investigations carried out on the gastrointestinal tract of rabbits and guinea-pigs, Gershon (1967) drew the conclusion that the sympathetic system exerts a direct inhibitory action on the smooth muscle without interfering with intramural ganglionic transmission of the parasympathetic outflow. Jansson & Martinson (1966) and Kewenter (1965), however, reached the opposite conclusion by examining the effect of the direct and reflex stimulation of the sympathetic nerves on the vagal control of gastric activity in the cat. Indeed, many morphological and pharmacological observations support the hypothesis that there is a sympathetic control of ganglionic transmission.

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“…It is known from our previous results that similar effects are produced by carbachol, pilocarpine, arecoline, anticholinesterases and angiotensin (Beleslin & Varagid, 1963;Beleslin, 1966). On the other hand, in the non-fatigued ileum, eledoisin has no effect on the normal peristaltic reflex elicited by raising the intraluminal pressure for short periods; indeed, when high concentrations are used, eledoisin depresses and sometimes abolishes the reflex.…”

Section: Discussionmentioning

confidence: 77%

“…This depression is probably a non-specific inhilbition similar to that observed by Kosterlitz & Robinson (1957) after high concentrations of carbachol. Angiotensin, which also produces contraction of the longitudinal muscle, has no effect on the normal peristaltic reflex except in high concentrations (Beleslin, 1968).…”

Section: Discussionmentioning

confidence: 94%

“…It has been found previously that other polypeptides-for example, suibstance P and angiotensin-restore the peristaltic reflex blocked by fatigue, 5-hydroxytryptamine, lowering of the temperature of the bath, ganglion-blocking substances, morphine, catecholamines or atropine 242-D. B. Beleslin (Beleslin & Varagic, 1958;Beleslin, 1968). On the other hand, bradykinin fails to restore the peristaltic reflex blocked by tetraethylammonium, methadone or atropine (Beleslin, Radmanovic & Rakic, 1966).…”

Section: Discussionmentioning

confidence: 99%

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The action of eledoisin on the peristaltic reflex of guinea‐pig isolated ileum

Beleslin

1969

British J Pharmacology

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. Low concentrations of eledoisin, acting from the serosal surface of the guinea‐pig isolated ileum, had no effect on the peristaltic reflex, whereas in high concentrations it depressed or sometimes abolished this reflex. . Eledoisin stimulated the peristaltic activity of the guinea‐pig ileum subjected to continuously raised intraluminal pressure. This stimulatory effect could be produced regularly when the interval between additions of eledoisin was at least 20 min. When added at shorter intervals, tachyphylaxis to eledoisin developed, but its ability to promote peristaltic activity was restored by the addition of an anticholinesterase to the bath fluid. During tachyphylaxis to eledoisin, nicotine and dimethylphenylpiperazinium were unable to restore peristalsis. . When the peristaltic reflex had been abolished by ganglion‐blocking agents, morphine and morphine‐like substances, or adrenaline, eledoisin restored the reflex. Eledoisin was much more effective in overcoming the blocking effect of hexamethonium, tetraethylammonium and azamethonium than that of nicotine or dimethylphenylpiperazinium. . Eledoisin did not antagonize the inhibitory effects of atropine, hyoscine and hyoscine butylbromide. . It is suggested that the stimulant effect of eledoisin may be due to a direct action on the smooth muscle and a release of acetylcholine from postganglionic nerve endings, but an effect on the intestinal ganglion cells cannot be excluded.

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The Effect of Angiotensin on the Peristaltic Reflex of the Isolated Guinea‐pig Ileum

Cited by 14 publications

References 14 publications

The angiotensin II type 2 receptor and the gastrointestinal tract

The angiotensin II type 2 receptor and the gastrointestinal tract

The effect of catecholamines and sympathetic stimulation on the release of acetylcholine from the guinea‐pig colon

The action of eledoisin on the peristaltic reflex of guinea‐pig isolated ileum

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