Bradykinin‐stimulated prostaglandin synthesis in conscious rabbits

Warren, J. B.; Ritter, JM; Hickling, Nicola E.; Barrow, S.E.

doi:10.1111/j.1476-5381.1987.tb11395.x

Cited by 7 publications

(5 citation statements)

References 22 publications

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“…This pattern is similar to that produced by oral aspirin in man as regards serum TXB2 and bradykinin-stimulated 6-oxo-PGFic. (Heavey et al, 1985), but differs from the much slower recovery from intravenous aspirin of bradykininstimulated prostaglandin synthesis in the rabbit (Warren et al, 1987), indicating a species difference rather than one based on route of administration.…”

Section: Discussionmentioning

confidence: 81%

Differential effect of aspirin on thromboxane and prostaglandin biosynthesis in man.

Ritter

Cockcroft

Doktor

et al. 1989

Brit J Clinical Pharma

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1 Effects of a single intravenous dose of aspirin (600 mg) on bradykinin-stimulated prostaglandin (PG) and on thromboxane (TX) biosynthesis were determined in nine healthy male volunteers. Plasma concentrations of 6-oxo-PGF,1ll and 13,14-dihydro-15-oxo-PGF2a were measured in samples obtained during repeated 10 min intravenous infusions of bradykinin before and up to 6 h after the dose of aspirin. TXB2 was measured in serum from blood allowed to clot at 370 C. 2 Aspirin inhibited bradykinin stimulated PG and platelet TX biosynthesis 0.5 h after the dose. Serum TXB2 remained low, whereas PG synthesis recovered within 6 h. 3 Effects of intravenous sodium salicylate (600 mg) were studied identically in eight subjects. Prostanoid biosynthesis was not inhibited. 4 Biosynthesis of prostacyclin and TXA2 under basal conditions was studied in eight subjects by measuring 2,3-dinor-6-oxo-PGF1,, and 2,3-dinor-TXB2 in hourly urine samples obtained during and after intravenous infusion of aspirin and, on a separate occasion, of vehicle.5 Aspirin infusion reduced urinary excretion of both metabolites > 90%, but excretion of 2,3-dinor-6-oxo-PGF1a recovered more rapidly than did that of 2,3-dinor-TXB2. 6 We conclude that cyclo-oxygenase is rapidly synthesised in bradykinin-responsive tissues in vivo and that this reflects similarly rapid enzyme biosynthesis in tissues that produce PGI2 under basal conditions. Keywords thromboxane A2 prostacyclin prostaglandin metabolites bradykinin aspirin

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Section: Discussionmentioning

confidence: 81%

Differential effect of aspirin on thromboxane and prostaglandin biosynthesis in man.

Ritter

Cockcroft

Doktor

et al. 1989

Brit J Clinical Pharma

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“…Thus it is likely that in the isolated perfused heart the overall action of bradykinin will be the resultant not only of the stimulation of sensory nerve endings but also of a direct effect on its own receptor(s) on the coronary vasculature (Toda, 1977;Regoli & Barab&, 1980;Beny et al, 1987), and release of prostaglandin (Goldberg et al, 1976;Warren et al, 1987) and/or histamine (Johnson & Erdos, 1973). It is important to emphasize that, to obtain detectable release of sensory neuropeptides we used a high concentration of bradykinin.…”

Section: Discussionmentioning

confidence: 99%

A comparison of bradykinin‐ and capsaicin‐induced myocardial and coronary effects in isolated perfused heart of guinea‐pig: involvement of substance P and calcitonin gene‐related peptide release

Manzini

Perretti

Benedetti

et al. 1989

British J Pharmacology

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1 Bradykinin and capsaicin were compared for their ability to elicit functional effects and to release sensory neuropeptides from guinea-pig isolated perfused hearts. 2 Both bradykinin (1O/M) and capsaicin (1 pM) produced a marked increase in coronary flow, a large positive chronotropic effect and a significant reduction in contractile strength. These actions were associated with a marked release of substance P-like immunoreactivity (SP-LI) and calcitonin gene-related-like immunoreactivity (CGRP-LI). The percentage of the tissue content of SP-LI and CGRP-LI released by each agent was similar, although bradykinin was less effective than capsaicin. The ratio of SP-LI/CGRP-LI released by both agents was similar to that present in cardiac tissue. 3 Neuropeptide release could be evoked only once with capsaicin but at least four times with bradykinin. Also, functional responses to capsaicin underwent desensitization. After either in vitro or systemic capsaicin pretreatment, the release of SP-LI and CGRP-LI by bradykinin was reduced and the positive chronotropic effect of bradykinin was significantly reduced, while the increase in coronary flow and negative inotropic responses remained unchanged. 4 Pretreatment with indomethacin (10/M) strongly antagonized the release of SP-LI and CGRP-LI by bradykinin and reduced the increase in heart rate. 5 These findings suggest that activation by bradykinin (probably through indirect mechanisms) of capsaicin-sensitive sensory nerves in the heart, leads to a local release of sensory neuropeptides. These neuropeptides, in turn, could participate in determining the complex functional effects of this kinin on cardiac performance.

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“…It is interesting to note that besides the hindquarters vasodilator effects of BK, none of the other cardiovascular responses were significantly affected by the neonatal treatment with capsaicin. Thus, it is likely that in vehicle-treated rats, the overall action of BK would be the resultant not only of the stimulation of capsaicin-sensitive sensory nerve endings, but also of direct effects, as well as indirect effects via the release of other mediators (such as histamine, prostaglandins and nitric oxide) (Johnson & Erdos, 1973;Goldberg et al, 1976;Warren et al, 1987;Gardiner et al, 1990c).…”

Section: Haemodynamic Effects Of Bradykininmentioning

confidence: 99%

Involvement of capsaicin‐sensitive neurones in the haemodynamic effects of exogenous vasoactive peptides: studies in conscious, adult Long Evans rats treated neonatally with capsaicin

Bachelard

Gardiner

Kemp

et al. 1992

British J Pharmacology

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1 The regional haemodynamic effects of i.v. bolus injections of bradykinin (0.05 or 0.5 nmol), cholecystokinin (0.175 or 1.75 nmol), substance P (0.01 or 0.1 nmol) and calcitonin gene-related peptide (0.05 or 0.5 nmol) were assessed in conscious, adult Long Evans rats that had been treated neonatally with either capsaicin (50 mg kg'-, s.c.) or vehicle. 2 In vehicle-treated rats, both doses of bradykinin were without effect on blood pressure, but caused tachycardia and hindquarters vasodilatation. Moreover, after the higher dose there were dilatations in the renal and superior mesenteric vascular beds. In capsaicin-treated rats the hindquarters vasodilator effects elicited by both doses of bradykinin were significantly reduced, while the tachycardia and responses in the renal and superior mesenteric vascular beds were unchanged. 3 In vehicle-treated rats, cholecystokinin caused dose-dependent increases in blood pressure accompanied by renal, superior mesenteric and hindquarters vasoconstriction followed, after the higher dose, by a hindquarters vasodilatation. The lower dose produced a tachycardia, while there was a bradycardia followed by a tachycardia after the higher dose. In capsaicin-treated rats, the pressor response, as well as the renal vasoconstrictor effects of cholecystokinin, were greater than in vehicle-treated rats, while the heart rate, superior mesenteric or hindquarters responses were not different. 4 In vehicle-treated rats, substance P produced a dose-dependent depressor response and tachycardia accompanied by dilatations in the renal and hindquarters vascular beds and constriction in the superior mesenteric vascular bed. In capsaicin-treated rats, the responses to the lower dose of substance P were not different from those in vehicle-treated rats, while the depressor response to the higher dose of substance P was slightly less than in vehicle-treated rats and the renal vasodilatation was absent. 5 In vehicle-treated rats, calcitonin gene-related peptide caused dose-dependent hypotensive and tachycardic effects associated with dilatations in renal and hindquarters vascular beds and a constriction in the superior mesenteric vascular bed. After the higher dose, the renal vasodilatation was followed by a modest vasoconstriction. In capsaicin-treated rats, the depressor responses to both doses of calcitonin generelated peptide were slightly more prolonged than in vehicle-treated animals, whereas the heart rate and renal and mesenteric vascular conductance changes were not significantly different. However, there was a more sustained hindquarters vasodilator response to the higher dose of calcitonin gene-related peptide in the capsaicin-treated rats. 6 The results suggest that peripheral, capsaicin-sensitive neurones are involved in the cardiovascular responses to exogenous bradykinin and cholecystokinin in conscious rats. It does not appear that the extent of involvement of these neurones is underestimated on account of development of marked supersensitivity to the peptides they normally release, si...

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Bradykinin‐stimulated prostaglandin synthesis in conscious rabbits

Cited by 7 publications

References 22 publications

Differential effect of aspirin on thromboxane and prostaglandin biosynthesis in man.

Differential effect of aspirin on thromboxane and prostaglandin biosynthesis in man.

A comparison of bradykinin‐ and capsaicin‐induced myocardial and coronary effects in isolated perfused heart of guinea‐pig: involvement of substance P and calcitonin gene‐related peptide release

Involvement of capsaicin‐sensitive neurones in the haemodynamic effects of exogenous vasoactive peptides: studies in conscious, adult Long Evans rats treated neonatally with capsaicin

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