Vagal nerve stimulation releases vasoactive intestinal peptide which significantly increases coronary artery blood flow

Feliciano, Lillybeth; Henning, Robert J.

doi:10.1016/s0008-6363(98)00122-9

Cited by 41 publications

(40 citation statements)

References 39 publications

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“…Additional evidence for peptide involvement in the relaxation at this frequency of TNS is provided by the augmentation of the response by phosphoramidon. These findings agree with previous reports showing that VIP release occurs after high-frequency (16-20 Hz) stimulation rather than low-frequency (1-8 Hz) stimulation (Lundberg et al, 1981;Goadsby and Shelley, 1990;Feliciano and Henning, 1998;Mule and Serio, 2003).…”

Section: Discussionsupporting

confidence: 93%

Location and Function of VPAC₁, VPAC₂ and NPR-C Receptors in VIP-Induced Vasodilation of Porcine Basilar Arteries

Grant

Lutz

McPhaden

et al. 2005

J Cereb Blood Flow Metab

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Vasoactive intestinal peptide (VIP) is a vasodilator peptide present in cerebrovascular nerves. Vasoactive intestinal peptide can activate VPAC 1 , VPAC 2 and the NPR-C receptor. This study sought to determine the receptors involved in VIP-induced vasodilation of porcine basilar arteries. Porcine basilar arteries contained the messenger ribonucleic acid of all three receptors. Immunocytochemical analysis of porcine basilar arteries revealed that the VPAC 1 receptor is expressed on the endothelium, VPAC 2 on the outer layers of the media and the NPR-C receptor throughout the artery, including nerves. Vasodilator responses to all receptor agonists showed that the receptors are functional. The vasodilator response to the VPAC 1 receptor agonist was inhibited by L-NAME and abolished by endothelial denudation. Vasodilation induced by Ro-25-1553, the VPAC 2 agonist, was unaffected by NOS inhibition or removal of the endothelium. Activation of the NPR-C receptor produced a vasodilation, which was susceptible to NOS inhibition and independent of endothelium. The vasodilator response to electrical stimulation at 20 Hz was attenuated by PG-99-465, the VPAC 2 antagonist. This study shows that all known VIP receptors are involved in VIP-mediated vasodilation of porcine basilar arteries. The VPAC 1 receptor is located on the endothelium and elicits vasodilation by generating nitric oxide (NO). The VPAC 2 receptor is mainly expressed in the outer layers of the smooth muscle and induces vasodilation independently of NO in response to VIP released from intramural nerves. The NPR-C receptor produces NO-dependent vasodilation independently of the endothelium by stimulation of nNOS in intramural nerves.

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Section: Discussionsupporting

confidence: 93%

Location and Function of VPAC₁, VPAC₂ and NPR-C Receptors in VIP-Induced Vasodilation of Porcine Basilar Arteries

Grant

Lutz

McPhaden

et al. 2005

J Cereb Blood Flow Metab

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“…This makes it an important modulator of physiological cardiovascular function [27][28][29]. An upregulation in the expression of its receptor VIPR1 in coronary artery SMCs induced by nebivolol administration might thus increase coronary artery blood flow.…”

Section: Discussionmentioning

confidence: 99%

Major differences in gene expression in human coronary smooth muscle cells after nebivolol or metoprolol treatment

Wolf

Sauter

Jobst

et al. 2008

International Journal of Cardiology

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“…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%

An Evaluation of the Efficacy of Vasoactive Intestinal Polypeptide Antagonists in vivo in the Anaesthetized Dog

Markos

Hennessy²,

Fitzpatrick³

et al. 2002

Pharmacology

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The effectiveness of competitive peptide vasoactive intestinal polypeptide (VIP) receptor antagonists was evaluated on heart rate in the anaesthetized dog. Two specific antagonists, VIP (6–28) and [D-p-Cl-Phe⁶, Leu¹⁷]-VIP, and a nonspecific antagonist, pituitary adenylate cyclase activating peptide fragment (6–27) (PACAP), were studied. VIP (6–28) and [D-p-Cl-Phe⁶, Leu¹⁷]-VIP (100 µg i.c.) increased the heart rate, whereas PACAP (100 µg i.c.) reduced the baseline heart rate. All three shifted the VIP dose-response curve to the right by two- to threefold for 30 min. In conclusion, PACAP, VIP (6–28), and [D-p-Cl-Phe⁶, Leu¹⁷]-VIP have a direct effect on the heart rate, are equally effective, and the effects last approximately 30 min in vivo.

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Vagal nerve stimulation releases vasoactive intestinal peptide which significantly increases coronary artery blood flow

Abstract: The present experiments suggest that VNS releases VIP which directly dilates coronary arteries and significantly increases coronary artery blood flow.

Cited by 41 publications

References 39 publications

Location and Function of VPAC₁, VPAC₂ and NPR-C Receptors in VIP-Induced Vasodilation of Porcine Basilar Arteries

Location and Function of VPAC₁, VPAC₂ and NPR-C Receptors in VIP-Induced Vasodilation of Porcine Basilar Arteries

Major differences in gene expression in human coronary smooth muscle cells after nebivolol or metoprolol treatment

An Evaluation of the Efficacy of Vasoactive Intestinal Polypeptide Antagonists in vivo in the Anaesthetized Dog

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Vagal nerve stimulation releases vasoactive intestinal peptide which significantly increases coronary artery blood flow

Abstract: The present experiments suggest that VNS releases VIP which directly dilates coronary arteries and significantly increases coronary artery blood flow.

Cited by 41 publications

References 39 publications

Location and Function of VPAC1, VPAC2 and NPR-C Receptors in VIP-Induced Vasodilation of Porcine Basilar Arteries

Location and Function of VPAC1, VPAC2 and NPR-C Receptors in VIP-Induced Vasodilation of Porcine Basilar Arteries

Major differences in gene expression in human coronary smooth muscle cells after nebivolol or metoprolol treatment

An Evaluation of the Efficacy of Vasoactive Intestinal Polypeptide Antagonists in vivo in the Anaesthetized Dog

Contact Info

Product

Resources

About

Location and Function of VPAC₁, VPAC₂ and NPR-C Receptors in VIP-Induced Vasodilation of Porcine Basilar Arteries

Location and Function of VPAC₁, VPAC₂ and NPR-C Receptors in VIP-Induced Vasodilation of Porcine Basilar Arteries