Influence of cyclooxygenase blockade on responses to isoproterenol, bradykinin and nitroglycerin in the feline pulmonary vascular bed

Lippton, Howard; Nandiwada, P. A.; Hyman, Albert L.; Kadowitz, Philip J.

doi:10.1016/0090-6980(84)90061-3

Cited by 17 publications

(6 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Under basal conditions, bradykinin minimally constricted the pulmonary vascular bed of the rabbit (250), but reduced P PA in isolated perfused dog lung (350). Vasodilation became evident, however, when the vasculature was precontracted (183,359).…”

Section: Bradykininmentioning

confidence: 93%

Lung Circulation

Suresh

Shimoda

2016

Comprehensive Physiology

111

View full text Add to dashboard Cite

The circulation of the lung is unique both in volume and function. For example, it is the only organ with two circulations: the pulmonary circulation, the main function of which is gas exchange, and the bronchial circulation, a systemic vascular supply that provides oxygenated blood to the walls of the conducting airways, pulmonary arteries and veins. The pulmonary circulation accommodates the entire cardiac output, maintaining high blood flow at low intravascular arterial pressure. As compared with the systemic circulation, pulmonary arteries have thinner walls with much less vascular smooth muscle and a relative lack of basal tone. Factors controlling pulmonary blood flow include vascular structure, gravity, mechanical effects of breathing, and the influence of neural and humoral factors. Pulmonary vascular tone is also altered by hypoxia, which causes pulmonary vasoconstriction. If the hypoxic stimulus persists for a prolonged period, contraction is accompanied by remodeling of the vasculature, resulting in pulmonary hypertension. In addition, genetic and environmental factors can also confer susceptibility to development of pulmonary hypertension. Under normal conditions, the endothelium forms a tight barrier, actively regulating interstitial fluid homeostasis. Infection and inflammation compromise normal barrier homeostasis, resulting in increased permeability and edema formation. This article focuses on reviewing the basics of the lung circulation (pulmonary and bronchial), normal development and transition at birth and vasoregulation. Mechanisms contributing to pathological conditions in the pulmonary circulation, in particular when barrier function is disrupted and during development of pulmonary hypertension, will also be discussed.

show abstract

Section: Bradykininmentioning

confidence: 93%

Lung Circulation

Suresh

Shimoda

2016

Comprehensive Physiology

111

View full text Add to dashboard Cite

show abstract

“…Uberraschend war der Befund, dab auch Indometacin ohne Einflu8 auf die bradykinininduzierte Vasodilatation blieb. An der an/isthesierten Katze hingegen land schliel3lich eine andere Gruppe, dab unter Bradykinin der Pulmonalarteriendruck deutlich abfiel [19]. Unsere Befunde schliegen allerdings einen solchen Wirkmechanismus als prim/iren Mechanismus ffir die Vasodilatation aus.…”

Section: Ergebnisseunclassified

“…In pharmakologischen Versuchen an verschiedenen Tierspezies besaB Bradykinin eine natriuretische, diuretische sowie eine ausgeprfigte vasodilatierende und bluckdrucksenkende Eigenschaft [17,32]. Bezfiglich der pulmonalen Effekte von Bradykinin waren die Ergebnisse widersprfichlich, und es fanden sich sowohl Blutdruckanstiege als auch Blutdruckabffille nach Bradykinin [3,11,12,19,27,29]. Untersuchungen am Menschen waren bisher nur von zwei Arbeitsgruppen durchgefiihrt worden, wobei sowohl Blutdruckanstiege [3,12], keine Verfinderungen im Pulmonalarteriendruck [11] oder gar Druckabfalle im Lungenkreislauf [3] beobachtet wurden.…”

Section: Introductionunclassified

Einflüsse von Bradykinin auf die systemische und die pulmonale Hämodynamik am Menschen

et al. 1989

View full text Add to dashboard Cite

In our studies we investigated the vasodepressor effects of bradykinin in vivo in normotensive and hypertensive subjects. Bradykinin was injected intravenously and intraarterially (40-6050 pM/kg) respectively was infused intraarterially (40-6050 pM/kg/min). The investigations were performed in 21 normotensives and 15 hypertensives. Bradykinin injections were performed after the following pharmacological interventions: salt restriction (10 mmol Na/d), salt loading (300 mmol Na/d), captopril (50 mg), ramipril (5 mg), lisinopril (20 mg), ketotifen (2 x 1 mg), indomethacin (2 x 50 mg), and propranolol (80 mg). The results show that bradykinin lowers blood pressure dose related by marked reduction in peripheral vascular resistance. The blood pressure reduction was strongly correlated with the increase in kinin concentration. This effect of bradykinin appears to be independent of changes in sodium metabolism, of beta adrenoceptors, of histamine-1 receptors, and of prostaglandins. ACE-inhibitors potentiate the blood pressure lowering effect of bradykinin about 20- to 50-fold. In case of an intraarterial injection of bradykinin in only 2-5% o the intravenously used dose of bradykinin are needed to produce an identical fall in blood pressure. From this experiments a pulmonary clearance rate of bradykinin over 95% can be calculated. In the pulmonary arteries bradykinin has no effect on the vascular resistance. In patients suffering from primary or renovascular hypertension the blood pressure response to bradykinin was enhanced. The bradykinin potentiating effect of the ACE-inhibitors was not altered in the hypertensives. In patients suffering from bradykinin hypertension or primary hyperaldosteronism bradykinin developed the same blood pressure lowering effect as in the normotensives.

show abstract

“…However, there is no unequivocal evidence that prostaglandins mediate the vasorelaxant effect of NTG. Indeed, several in vitro and in vivo studies have been unable to show such a mediating role for prostaglandins (Lippton et al 1984, Rehr et al 1984, McGregor & Kelinstein 1984, Bennet et al 1983, DeCaterina et al 1985.…”

Section: Effects Mediated Via Prostaglandinsmentioning

confidence: 99%

Biological effects of organic nitroesters and their mechanism of action

Ahlner

Axelsson

Bornfeldt

1986

Acta Pharmacologica et Toxicologica

View full text Add to dashboard Cite

Organic nitroesters e.g. glyceryltrinitrate (NTG) are of great clinical importance in the treatment of angina pectoris. The most important of their biological effects is vasodilatation of peripheral arteries, peripheral veins and coronary arteries. Other biological effects, of unknown clinical relevance, are effects on myocardial metabolism and on platelet aggregation. In recent years evidences have accumulated that the vasodilating effects of organic nitroesters are mediated via the cGMP‐system, although the exact mechnism of activation of the cGMP‐producing enzyme guanylate cyclase is still obscure. Further research about this may elucidate the mechanism behind the development of tolerance. Another theory concerning the mechanism behind the vasodilating properties of NTG is that arachidonic acid metabolites are involved. However no clearcut evidences have been presented to support this theory. We show in this paper results indicating that arachidonic acid metabolites are of no importance for the vasodilating effects of NTG, at least not in vitro. NTG has also been shown to decrease the intracellular Ca2+‐concentration, an effect probably mediated via cGMP but the exact underlying mechanism is not yet fully understood.

show abstract

Influence of cyclooxygenase blockade on responses to isoproterenol, bradykinin and nitroglycerin in the feline pulmonary vascular bed

Cited by 17 publications

References 32 publications

Lung Circulation

Lung Circulation

Einflüsse von Bradykinin auf die systemische und die pulmonale Hämodynamik am Menschen

Biological effects of organic nitroesters and their mechanism of action

Contact Info

Product

Resources

About