1998
DOI: 10.1016/s0165-1838(97)00109-4
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Vagal nerve stimulation during muscarinic and beta-adrenergic blockade causes significant coronary artery dilation

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Cited by 16 publications
(7 citation statements)
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“…While previous studies have shown a positive inotropic effect of VIP in the electrically driven auricle of the human right atrium [17], as well as in isolated trabeculae from the human right ventricle [18], this is to our knowledge the first study to demonstrate a direct positive inotropic effect of VIP in the human left ventricle in vitro. The role of VIP as a potential positive inotropic agent in the left ventricle has been questioned, however, since vagal stimulation of dogs, probably via endogenously released VIP, caused increased contractility of the right atrium and the right ventricle, but not the left ventricle [4][5][6][7]. The role of VIP as a potential positive inotropic agent in the left ventricle has been questioned, however, since vagal stimulation of dogs, probably via endogenously released VIP, caused increased contractility of the right atrium and the right ventricle, but not the left ventricle [4][5][6][7].…”
Section: Discussionmentioning
confidence: 99%
“…While previous studies have shown a positive inotropic effect of VIP in the electrically driven auricle of the human right atrium [17], as well as in isolated trabeculae from the human right ventricle [18], this is to our knowledge the first study to demonstrate a direct positive inotropic effect of VIP in the human left ventricle in vitro. The role of VIP as a potential positive inotropic agent in the left ventricle has been questioned, however, since vagal stimulation of dogs, probably via endogenously released VIP, caused increased contractility of the right atrium and the right ventricle, but not the left ventricle [4][5][6][7]. The role of VIP as a potential positive inotropic agent in the left ventricle has been questioned, however, since vagal stimulation of dogs, probably via endogenously released VIP, caused increased contractility of the right atrium and the right ventricle, but not the left ventricle [4][5][6][7].…”
Section: Discussionmentioning
confidence: 99%
“…The dose of VIP receptor antagonists used in the present study, 100 Ìg i.c. given to dogs with an average weight of 19.5 kg, was effectively just above 5 mg kg -1 , a concentration which is generally larger than that used by other investigators [10][11][12][15][16][17].…”
Section: Discussionmentioning
confidence: 73%
“…In laboratory animals, using various experimental settings, a direct positive inotropic effect of VIP on myocardial tissue from different parts of the heart, including the left ventricle, has been demonstrated, and this effect seems to be mediated through increased production of cAMP [8,[12][13][14][15][16]. The role of VIP as a potential positive inotropic agent in the left ventricle has been questioned, however, since vagal stimulation of dogs, probably via endogenously released VIP, caused increased contractility of the right atrium and the right ventricle, but not the left ventricle [4][5][6][7]. These differences might be explained by the sparse innervation of VIP-immunoreactive nerve fibres in the left ventricle compared with the atria and the right ventricle of canine hearts [8,26].…”
Section: Discussionmentioning
confidence: 99%
“…Cardiac vagal nerve stimulation in dogs during muscarinic and β-adrenergic receptor blockade, caused increased contractile force in the right atrium [4] and the right ventricle [5,6], whereas no significant [5][6][7]. It was also shown that intracoronary infusion of the VIP antagonist [4Cl-D-Phe',Leu"(]VIP could significantly reduce the vagal-induced increases in right atrial\right ventricular contractility, suggesting that VIP was the mediator of this positive inotropic effect in the right atrium and ventricle [4,6,8].…”
Section: Introductionmentioning
confidence: 99%