Bradykinin‐induced Relaxation of Renal and Pulmonary Arteries Is Dependent Upon Intact Endothelial Cells

Altura, Burton M.; Chand, N.

doi:10.1111/j.1476-5381.1981.tb09948.x

Cited by 70 publications

(27 citation statements)

References 5 publications

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“…Our results show that in the aorta of the pig, as with several isolated arterial and venous preparations from other species, bradykinin, ATP, acetylcholine and the calcium ionophore A23187 induce relaxation by an endothelium-dependent mechanism (Furchgott & Zawadzki, 1980a;Zawadzki, Cherry & Furchgott, 1980;Altura & Chand, 1981;De Mey & Vanhoutte, 1981;Cherry et al, 1982). The most likely explanation of these results is that endothelial cells respond to each of these agents by generating a signal which causes the smooth muscle cells of the vessel wall to relax, but measurements of endothelium-dependent relaxation per se cannot establish the nature of this signal, nor determine whether all the agents act via the same pathway.…”

Section: Discussionmentioning

confidence: 96%

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Gordon

Martin

1983

British J Pharmacology

162

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1 Bradykinin, adenosine triphosphate (ATP) and acetylcholine each relaxed histamine-contracted strips of pig aorta in a dose-dependent manner. These relaxations were abolished when the endothelium was removed. 2 Relaxation induced by ATP was mimicked by adenosine diphosphate (ADP) but adenosine monophosphate (AMP) and adenosine were about 120 times less potent. 3 Relaxation induced by acetylcholine was antagonized by atropine in a competitive manner, and carbachol induced the same degree of relaxation as acetylcholine, but was about 10 times less potent. 4 The calcium ionophore, A23 187, also induced a dose-dependent relaxation of pig aortic strips provided the endothelium was present, suggesting that a rise in the level of ionized calcium within the endothelial cells is one means by which vascular smooth muscle relaxation can be triggered. 5 Bradykinin, ATP, ADP, AMP, adenosine and A23 187 each induced a dose-dependent increase in 86Rb efflux from preloaded pig aortic endothelial cells. The dose-response curves for stimulation of 86Rb efflux and for endothelium-dependent relaxation were similar for each individual compound. ADP was equipotent with ATP, but AMP and adenosine were about 120 times less potent. 6 Neither acetylcholine nor carbachol, in concentrations that induce endothelium-dependent relaxation, had any effect on 86Rb efflux from isolated aortic endothelial cells. 7 Lanthanum, which blocks calcium influx, abolished the increases in 86Rb efflux induced by bradykinin and ATP, and the calcium ionophore A23187 was the most effective stimulant of 86Rb efflux, suggesting that the potassium transport induced by these agents is calcium-activated. 8 It is concluded that endothelial responses to bradykinin and ATP can be assessed by monitoring 86Rb efflux, which probably reflects a calcium-activated efflux of potassium associated with the endothelium-dependent vascular relaxation induced by these agents. This pathway is apparently not involved in endothelial responses to acetylcholine.

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Section: Discussionmentioning

confidence: 96%

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Gordon

Martin

1983

British J Pharmacology

162

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“…Bradykinin (BK) is a potent vasoactive agent which relaxes different vascular smooth muscle preparations via an endothelium-dependent mechanism (Altura & Chand, 1981;Cherry et al, 1982). Endothelium-dependent relaxation involves the release of an endothelium-derived relaxing factor (EDRF) (Furchgott & Zawadzki, 1980) which has been identified as nitric oxide (NO) (Palmer et al, 1987) with L-arginine as its physiological precursor (Palmer et al, 1988a,b;Schmidt et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Effects of bradykinin in the rat isolated perfused heart: role of kinin receptors and endothelium‐derived relaxing factor

Baydoun

Woodward

1991

British J Pharmacology

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1 The effects of bradykinin (BK) in the microcirculation of the isolated perfused heart of the rat were examined. The kinin receptors mediating the effects of BK were characterized and the role of endothelium-derived relaxation factor (EDRF) and prostacyclin investigated. Gossypol (1-15pM), a presumed inhibitor of EDRF biosynthesis, caused a marked drop in perfusion pressure followed by vasoconstriction. These changes in coronary tone were accompanied by an irreversible depression of cardiac contractility and heart rate. Over the same concentration range gossypol abolished the vasodilator action of BK (1.Onmol), however it also blocked the endothelium-independent vasodilator response to sodium nitroprusside (30nmol) and the vasoconstrictor effect of endothelin-1 (1Opmol) which suggests non-specific toxic actions of gossypol. 6 Bolus injections of BK (0.001-1.Onmol) failed to elevate basal levels of prostacyclin (PGI2) as shown by assaying for its stable metabolite 6-keto-PGF<,,. In addition, BK-induced vasodilatation was not blocked by flurbiprofen (2,pM) or BW755C (7.5 pM) which are inhibitors of the arachidonic acid pathway.When added with L-NOArg (100pM), flurbiprofen (10pM) did not potentiate the inhibitory action of L-NOArg on the BK response. 7 These results show that the vasodilator action of BK in the rat heart is dependent on the activation of the kinin B2 receptors but independent of PGI2 release. Although a conclusive role for EDRF could not be established, this study has questioned the suitability of several agents commonly used as inhibitors of EDRF-mediated responses.

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“…Vasodilators such as NO [13], prostacyclin [14], bradykinin [15], endothelium-derived hyperpolarizing factor (EDHF) [16], and vasoconstrictors such as endothelin (ET)-1 [17] and thromboxane [18] are important factors modulating pulmonary vascular tone. ET-1 plasma levels are higher at birth than at 3 days and in adults [19].…”

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confidence: 99%

Maturational changes of endothelial vasoactive factors and pulmonary vascular tone at birth

Lévy¹,

Souil²,

Sabry³

et al. 2000

Eur Respir J

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The aim of this study was to determine which endothelial factors were involved in the decrease of pulmonary vascular resistance at birth, and how they changed with maturation.Response of intrapulmonary artery rings precontracted with prostaglandin F 2a were studied from piglets aged <2 h, 2±3 day, 10 day and adult pigs for pharmacological responses to acetylcholine (ACh) and cromakalim (CMK) in the presence and the absence of the nitric oxide synthase (NOS) inhibitor, N v -nitro-L-arginine (L-NA), the adenosine triphosphate sensitive potassium (KATP) channel blocker, glibenclamide and the endothelin (ET)-A receptor antagonist, BQ123. In situ hybridization and immunochemistry studies were performed in lung tissues of the same animals in order to determine the expression of NOS and ET.There was a small contractile effect of ACh in the newborn. Relaxation to ACh, which was blocked by L-NA and reduced by glibenclamide, only appeared from the age of 3 days. The significantly greater relaxation to CMK in rings without endothelium (p<0.05) was abolished by BQ123 in the newborn, and then disappeared by 2 days of age. Glibenclamide had a greater inhibitory effect on relaxation induced by CMK at 10 days than in the newborn and 2 days old piglets. NOS expression was low in pulmonary arteries of the newborn and increased by 2 days of age whereas the converse was seen with ET expression.It is concluded that: 1) relaxant response to acetylcholine was absent at birth and appeared at 2 days; 2) the reduced relaxant response to cromakalin in rings with endothelium at birth could be blocked by BQ123; and 3) the expression of endothelin decreased whereas the expression of nitric oxide synthase increased from birth to 2 days of age. Eur Respir J 2000; 15: 158±165. Pulmonary arterial pressure and resistance are high at birth, and decrease rapidly thereafter due to structural [1±3] and functional [4,5] changes. The underlying mechanisms of these modifications are not fully understood, but nitric oxide (NO) is known to play a role. NO [6±8] is released from the lungs of foetal and newborn animals [5,9,10]. It reduces basal tone in utero and contributes to the postnatal fall in pulmonary vascular resistance. However, endothelium-dependent relaxation to various agonists is either absent [11] or very weak [12] until the third day after birth. Then it rapidly increases during the first week of life [11,12]. These observations suggest that immediately after birth the interactions between the endothelium and the underlying smooth muscle may be different from those in adult porcine pulmonary vasculature.Vasodilators such as NO [13], prostacyclin [14], bradykinin [15], endothelium-derived hyperpolarizing factor (EDHF) [16], and vasoconstrictors such as endothelin (ET)-1 [17] and thromboxane [18] are important factors modulating pulmonary vascular tone. ET-1 plasma levels are higher at birth than at 3 days and in adults [19]. Although endothelium-dependent relaxation to acetylcholine (ACh) is absent, the amount of cyclic guanosine...

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Bradykinin‐induced Relaxation of Renal and Pulmonary Arteries Is Dependent Upon Intact Endothelial Cells

Cited by 70 publications

References 5 publications

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Effects of bradykinin in the rat isolated perfused heart: role of kinin receptors and endothelium‐derived relaxing factor

Maturational changes of endothelial vasoactive factors and pulmonary vascular tone at birth

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Bradykinin‐induced Relaxation of Renal and Pulmonary Arteries Is Dependent Upon Intact Endothelial Cells

Cited by 70 publications

References 5 publications

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of 86Rb efflux from isolated endothelial cells

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of 86Rb efflux from isolated endothelial cells

Effects of bradykinin in the rat isolated perfused heart: role of kinin receptors and endothelium‐derived relaxing factor

Maturational changes of endothelial vasoactive factors and pulmonary vascular tone at birth

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Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells