Vascular Reflex Responses Induced by an Intraarterial Injection of Azaazepinophenothiazine, Andromedotoxin, Veratridine, Bradykinin and Kallikrein and Blocking Action of Sodium Salicylate

Hashimoto, Koroku; Kumakura, Seiji; Taira, Norio

doi:10.2170/jjphysiol.14.299

Cited by 28 publications

(14 citation statements)

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“…It has been known that aspirin-like drugs suppress pseudo-affective reflexes (Hashimoto, Kumakura & Taira, 1964;Lim, Guzman, Rodgers, Goto, Braun, Dickerson and Engle, 1964;Ferreira, Moncada & Vane, 1973;Moncada, Ferreira & Vane, 1975) and also nociceptive unit discharges (Scott, 1968). Bradykinin activates release of prostaglandins in various tissues (McGiff, Terragno, Malik & Lonigro, 1972;Ferreira et al 1973;Moncada et al 1975;Lembeck et al 1976) and prostaglandins enhance nociceptive reflexes .…”

Section: Discussionmentioning

confidence: 99%

Chemical responses of polymodal receptors of the scrotal contents in dogs.

Kumazawa¹,

Mizumura²

1980

The Journal of Physiology

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Section: Discussionmentioning

confidence: 99%

Chemical responses of polymodal receptors of the scrotal contents in dogs.

Kumazawa¹,

Mizumura²

1980

The Journal of Physiology

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“…Several long-acting coronary vasodilators (5,6,7,8,9,10,11) have been reported to enhance the coronary vascular response to adenosine, and the possible mechanism has been considered to he an inhibition of adenosine deaminase in the tissue (12), a blockade of the permeation of adenosine into erythrocytes (13) and vascular smooth muscle cells (14), and/or an inhibition of adenosine degradation in the lung (15).…”

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confidence: 99%

Enhancement of Coronary Vasodilating Action of Adenosine by Dilazep and Dipyridamole in the Dog

Sano

1974

Japanese Journal of Pharmacology

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Abstract-The mechanism of the augmentation of adenosine action by 1, 4-bis-[3 (3, 4, 5-trimethoxybenzoyl-oxy)-propyl] perhydro-1, 4-diazepine (dilazep I, N, N,) and dipyridamole on the coronary vessel was examined in the dog. Cororary blood flow was measured by applying a Morawitz cannula to the in vivo heart. It was found that the ratio of coronary vasodilating activity of adenosine administered into saphenous vein, right atrium, and left atrium was 1: 1.5: 30, and that coronary vaso dilating actions of adenosine administered into saphenous vein, right atrium, and left atrium after dilazep (10 μg/kg, i.v.) were 15.6, 10.8, and 3.3 times greater than those without dilazep, respectively. After dipyridamole coronary vasodilating actions of adenosine administered into saphenous vein, right atrium, and left atrium were 17.5, 14.3, and 5.4 times greater. These results indicate that augmentation of coronary vasodilating action of intravenously administered adenosine by dilazep or dipyrida mole was mainly exerted at the lung and myocardium, and slightly in the blood, and was due to inhibition of the disappearance of adenosine.It is well known that there is a close relationship between coronary blood flow and myocardial metabolism (1); either an augmentation of the myocardial metabolism or hypoxia of the myocardium results in an increased coronary blood flow.Berne (2) has hypothesized that the metabolic regulation of coronary circulation is mediated by adenosine, which produces a powerful coronary vasodilation. Adenosine is always released in a small amount from the myocardium, and the amount of this adeno sine release is increased in a hypoxic condition (3, 4).Several long-acting coronary vasodilators (5,6,7,8,9,10,11) have been reported to enhance the coronary vascular response to adenosine, and the possible mechanism has been considered to he an inhibition of adenosine deaminase in the tissue (12), a blockade of the permeation of adenosine into erythrocytes (13) and vascular smooth muscle cells (14), and/or an inhibition of adenosine degradation in the lung (15).The objective of this study was to clarify the mechanism of the potentiation of adeno sine by certain long-acting vasodilators. MATERIALS AND METHODSForty-six male dogs, weighing 10 to 13 kg, were used. One hr after s.c. administration of 3 mg/kg of morphine and I g/kg of urethane, these animals were anesthetized with 20 mg/kg ix. of sodium pentobarbital.An endotracheal tube was applied to each animal and

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“…Narcotic analgesics such as morphine produce their analgesic actions by a central mechanism (Jaffe & Martin, 1975). On the other hand, it has been re-LI;"., ported that anti-pyretic analgesics, such as aspirin, act peripherally (Guzman, Braun, Lim, Potter & Rodgers, 1964;Lim, Guzman, Rodgers, Goto, Braun, Dickerson & Engle, 1964;Hashimoto, Kumakura & Taira, 1964;Hirata, Tanaka, Taira & Hashimoto, 1966;Lim, 1968;Taira, Nakayama & Hashimoto, 1968). However, it is supposed that salicylates produce their analgesic actions partly by a central mechanism (Winder, 1959;Dubas & Parker, 1971) and some influences of aminopyrine on the electroencephalograph have also been reported (Ban, 1963;Sasa, Fukuda & Takaori, 1969).…”

Section: Discussionmentioning

confidence: 99%

Site of Analgesic Action of a Non‐steroidal, Antiinflammatory Drug, Tolmetin Sodium, in Rats

Nakamura

Shimizu

1981

British J Pharmacology

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1 The site of the analgesic action of tolmetin sodium was investigated by use of the acetic acid writhing test in rats. 2 Tolmetin sodium was administered to the rat between 15 and 60 min after an intraperitoneal injection of 1 ml of a 1 % acetic acid aqueous solution. Number of writhings was counted for 20 min beginning from 60 min after acetic acid injection. 3 When the rat was given tolmetin sodium 5 mg/kg orally, a relatively large quantity of tolmetin was found in the peritoneal exudate and there was a rough correlation between anti-writhing activity and the exudate tolmetin content.4 Anti-writhing ED50 of tolmetin sodium was 1.42 (0.82-2.91) and 92.0 (57.0-140) pg/kg when given intraperitoneally and intravenously, respectively, and the potency ratio of intraperitoneal to intravenous tolmetin sodium was 40.0 (18.5-80.2). This potency ratio for salicylic acid and morphine hydrochloride was 19.4 and 1.0, respectively. 5 When equipotent doses (5 pg/kg i.p.; 200 pg/kg i.v.) of tolmetin sodium were administered to the rat, the plasma tolmetin level after the intraperitoneal administration was less than one-fortieth that after the intravenous administration during the counting time of 20 min, while both the peritoneal exudate contents of tometin were nearly equal. 6 From these results, it is concluded that the site of anti-writhing action of tolmetin sodium is in the peritoneum and that tolmetin sodium produces its anti-writhing action mainly by a peripheral mechanism in the rat.

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Vascular Reflex Responses Induced by an Intraarterial Injection of Azaazepinophenothiazine, Andromedotoxin, Veratridine, Bradykinin and Kallikrein and Blocking Action of Sodium Salicylate

Cited by 28 publications

References 1 publication

Chemical responses of polymodal receptors of the scrotal contents in dogs.

Chemical responses of polymodal receptors of the scrotal contents in dogs.

Enhancement of Coronary Vasodilating Action of Adenosine by Dilazep and Dipyridamole in the Dog

Site of Analgesic Action of a Non‐steroidal, Antiinflammatory Drug, Tolmetin Sodium, in Rats

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