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Comparative Study
. 2013;50(6):478-85.
doi: 10.1159/000355265. Epub 2013 Oct 29.

Vasopressin-induced constriction of the isolated rat occipital artery is segment dependent

Stephen P Chelko  1 , Chad W Schmiedt, Tristan H Lewis, Stephen J Lewis, Tom P Robertson
Affiliations
Comparative Study

Vasopressin-induced constriction of the isolated rat occipital artery is segment dependent

Stephen P Chelko et al. J Vasc Res. 2013.

Abstract

Background: Circulating factors delivered to the nodose ganglion (NG) by the occipital artery (OA) have been shown to affect vagal afferent activity, and thus the contractile state of the OA may influence blood flow to the NG.

Methods: OA were isolated and bisected into proximal and distal segments relative to the external carotid artery.

Results: Bisection highlighted stark differences between maximal contractile responses and OA sensitivity. Specifically, maximum responses to vasopressin and the V1 receptor agonist were significantly higher in distal than proximal segments. Distal segments were significantly more sensitive to 5-hydroxytryptamine (5-HT) and the 5-HT2 receptor agonist than proximal segments. Angiotensin II (AT)2, V2 and 5-HT(1B/1D) receptor agonists did not elicit vascular responses. Additionally, AT1 receptor agonists elicited mild, yet not significantly different maximal responses between segments.

Conclusion: The results of this study are consistent with contractile properties of rat OA being mediated via AT1, V1 and 5-HT2 receptors and dependent upon the OA segment. Furthermore, vasopressin-induced constriction of the OA, regardless of a bolus dose or a first and second concentration-response curve, retained this unique segmental difference. We hypothesize that these segmental differences may be important in the regulation of blood flow through the OA in health and disease.

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Figures

Figure 1
Figure 1
Mean ± SEM responses of proximal (■) and distal (▲) segments of the OA to A. AT, B. vasopressin and C. 5-HT. *P < 0.05.
See this image and copyright information in PMC

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