Effects of Bradykinin, Eledoisin, and Physalaemin on Cardiovascular Dynamics

Nakano, Jiro

doi:10.1007/978-1-4684-3198-8_21

Cited by 11 publications

(3 citation statements)

References 29 publications

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“…Since proteolytic enzymes are ubiquitous in the body, all tissues presumably are capable of releasing bradykinin from plasma (1). Bradykinin has repeatedly been demonstrated to be one of the most potent coronary dilators in isolated perfused mammalian hearts (2) as well as in intact animals (3)(4)(5). Indeed, there is evidence to suggest that bradykinin is involved in the local humoral control of coronary blood flow.…”

mentioning

confidence: 99%

Mechanism and modification of bradykinin-induced coronary vasodilation.

Needleman¹,

Key²,

Denny³

et al. 1975

Proc. Natl. Acad. Sci. U.S.A.

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In isolated perfused rabbit hearts, bradykinin produced a concentration-dependent decrease in coronary resistance directly associated with biosynthesis and release of prostaglandin-E-like substance. An inhibitor of bradykinin destruction (the nonapeptide SQ-20881) markedly enhanced both the coronary vasodilation and release of prostaglandin-E-like substance produced by cardiac injection of bradykinin. Indomethacin inhibited both the myocardial prostaglandin biosynthesis and the decrease in coronary resistance induced by bradykinin. The demonstration that bradykinin is a potent stimulator of prostaglandin biosynthesis in the heart has implications as to the cause of the afferent cardiovascular reflexes and pain in myocardial infarction and angina pectoris.Bradykinin is generated by the action of a proteolytic enzyme upon plasma alpha-2-globulin. Since proteolytic enzymes are ubiquitous in the body, all tissues presumably are capable of releasing bradykinin from plasma (1). Bradykinin has repeatedly been demonstrated to be one of the most potent coronary dilators in isolated perfused mammalian hearts (2) as well as in intact animals (3-5). Indeed, there is evidence to suggest that bradykinin is involved in the local humoral control of coronary blood flow. The bradykinin-induced coronary vasodilation could be the result of either a direct relaxation of coronary vascular smooth muscle or an indirect action by means of an endogenous substance. As to the second possibility, the action of bradykinin on coronary resistance does not appear to be the result of the elaboration of histamine, catecholamines, acetylcholine, or serotonin (2, 3).To establish that an endogenous substance mediates a physiologic event requires temporal and quantitative correlation between changes in concentration of the putative mediator with changes in functional status of the organ. The concentration of the mediator substance should be proportional to the stimulus (bradykinin in this case) and, in addition, abolition of the synthesis of the mediator should abolish the physiologic action of the stimulus. In view of the previous demonstration that the heart readily synthesizes and releases prostaglandins (6-8), we have investigated the possible involvement of endogenously synthesized prostaglandins in mediating the coronary vasodilation produced by bradykinin in isolated perfused rabbit hearts. METHODSIsolated rabbit (New Zealand) hearts were perfused through the aorta with Krebs-Henseleit medium (in an atmosphere of 95% 02 and 5% C02) at a constant flow of 30 ml/min. Abbreviation: PG, prostaglandin.Changes in perfusion pressure (Statham transducer, Brush recorder) were indicative of alterations in coronary resistance. Ventricular pressure and rate were recorded from a fluidfilled balloon tied into the left ventricle (isovolumic heart).The coronary venous effluent was continuously and immediately assayed for the presence of vasoactive substances. This was achieved by continuously superfusing a series of isolated assay tissues with the coro...

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mentioning

confidence: 99%

Mechanism and modification of bradykinin-induced coronary vasodilation.

Needleman¹,

Key²,

Denny³

et al. 1975

Proc. Natl. Acad. Sci. U.S.A.

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“…Recent studies, however, have shown that captopril also has a venodilating effect, which cannot be explained solely by the inhibition of angiotensin II (Awan et al, 1981). The venodilatory effect may be due to local accumulation of bradykinin, which is a potent vasodilator of both arteriolar and venous beds (Nakano, 1970). The slight but significant reduction in total heart volume in our patients was probably also due to the venodilating effect of captopril.…”

Section: Discussionmentioning

confidence: 53%

Short and long‐term effects of treatment with low dose captopril in patients with severe congestive heart failure.

Dahlström¹,

Karlberg²

1982

Brit J Clinical Pharma

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1 In an open study the clinical short‐term and long‐term effects of low‐ dose captopril (mean daily dose 45 +/‐ 15 mg) were evaluated in 20 patients with severe congestive heart failure refractory to conventional treatment with digitalis and diuretics. 2 After two weeks' treatment 16 out of 20 patients showed an improvement in New York Heart Association functional class, followed by a significant reduction in body weight and heart volume. The ratio between urinary sodium and potassium excretion was significantly increased and the urinary aldosterone excretion was significantly decrease. In 10 of the patients the initial effects were sustained during long‐term treatment (6 +/‐ 2 months). 3 In conclusion, captopril may be a useful therapeutic adjunct for the long‐term treatment of patients with severe heart failure or when conventional treatment has failed.

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“…A brief statement about the cardiovascular effects of tachykinins seems appropriate because they are much more potent than the bradykinins. Comparative studies have not been done in man but, in the dog, the hypotensive threshold dose of physalaemin is 0.25 ngjkg while eledoisin and bradykinin were 25 and 0.5% as potent, respectively (NAKANO, 1970). Substance P is as potent or slightly more potent than physalaemin .…”

Section: B Tachykininsmentioning

confidence: 98%

Kinins in Nature

Pisano¹

1979

Bradykinin, Kallidin and Kallikrein

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Effects of Bradykinin, Eledoisin, and Physalaemin on Cardiovascular Dynamics

Cited by 11 publications

References 29 publications

Mechanism and modification of bradykinin-induced coronary vasodilation.

Mechanism and modification of bradykinin-induced coronary vasodilation.

Short and long‐term effects of treatment with low dose captopril in patients with severe congestive heart failure.

Kinins in Nature

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