AIMS: In the present study we investigated the intervention of nitric oxide and prostacyclin in the responses to vasopressin of isolated thyroid arteries obtained from multi-organ donors. MAIN METHODS: Paired artery rings from glandular branches of the superior thyroid artery, one normal and the other deendothelised, were mounted in organ baths for isometric recording of tension. Concentration-response curves to vasopressin were determined in the absence and in the presence of either the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP (10(-8)M), the nitric oxide synthase inhibitor N(G)-monomethyl-l-arginine (L-NMMA, 10(-4)M), or the inhibitor of prostaglandins indomethacin (10(-6)M). KEY FINDINGS: In artery rings under resting tension, vasopressin produced concentration-dependent, endothelium-independent contractions. The vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP (10(-8)M) displaced the control curve to vasopressin 19-fold to the right in a parallel manner. The contractile response to vasopressin was unaffected by L-NMMA or by indomethacin. SIGNIFICANCE: Vasopressin causes constriction of human thyroid arteries by stimulation of V1 vasopressin receptors located on smooth muscle cells. These effects are not linked to the presence of an intact endothelium or to the release of nitric oxide or prostaglandins. The constriction of thyroid arteries may be particularly relevant in certain pathophysiological circumstances in which vasopressin is released in amounts that could interfere with the blood supply to the thyroid gland.
AIMS: In the present study we investigated the intervention of nitric oxide and prostacyclin in the responses to vasopressin of isolated thyroid arteries obtained from multi-organ donors. MAIN METHODS: Paired artery rings from glandular branches of the superior thyroid artery, one normal and the other deendothelised, were mounted in organ baths for isometric recording of tension. Concentration-response curves to vasopressin were determined in the absence and in the presence of either the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP (10(-8)M), the nitric oxide synthase inhibitor N(G)-monomethyl-l-arginine (L-NMMA, 10(-4)M), or the inhibitor of prostaglandins indomethacin (10(-6)M). KEY FINDINGS: In artery rings under resting tension, vasopressin produced concentration-dependent, endothelium-independent contractions. The vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP (10(-8)M) displaced the control curve to vasopressin 19-fold to the right in a parallel manner. The contractile response to vasopressin was unaffected by L-NMMA or by indomethacin. SIGNIFICANCE: Vasopressin causes constriction of human thyroid arteries by stimulation of V1 vasopressin receptors located on smooth muscle cells. These effects are not linked to the presence of an intact endothelium or to the release of nitric oxide or prostaglandins. The constriction of thyroid arteries may be particularly relevant in certain pathophysiological circumstances in which vasopressin is released in amounts that could interfere with the blood supply to the thyroid gland.
Authors: Jeremy A Sandgren; Guorui Deng; Danny W Linggonegoro; Sabrina M Scroggins; Katherine J Perschbacher; Anand R Nair; Taryn E Nishimura; Shao Yang Zhang; Larry N Agbor; Jing Wu; Henry L Keen; Meghan C Naber; Nicole A Pearson; Kathy A Zimmerman; Robert M Weiss; Noelle C Bowdler; Yuriy M Usachev; Donna A Santillan; Matthew J Potthoff; Gary L Pierce; Katherine N Gibson-Corley; Curt D Sigmund; Mark K Santillan; Justin L Grobe Journal: JCI Insight Date: 2018-10-04