PubMed · 17022550
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Miyuki Ishibashi, Tohru Yamaji. 2006-09-28. [Ectopic ADH-producing tumor].. https://pubmed.ncbi.nlm.nih.gov/17022550/
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UNLABELLED: Successful therapy of vasodilatory shock in adults and children with arginine-vasopressin (AVP) has been reported previously. Data on the use of vasopressin in neonates is limited. This retrospective study reports the effects of AVP-treatment in neonates with catecholamine-resistant systemic vasodilatation after cardiopulmonary bypass. From March 2003 through December 2005, 172 neonates underwent open-heart surgery, 17 developed vasopressor-resistant hypotension and were treated with AVP. Thirteen patients had a stage I palliation of single ventricle, two had a Ross-operation and two had an arterial switch operation. All patients received multiple traditional inotropes and vasopressors prior to administration of AVP. AVP was started at median 0.0001 U x kg(-1) x min(-1) (range 0.00005-0.0002) and titrated up to a maximum of median 0.0003 U x kg(-1) x min(-1) (range 0.0001-0.001). AVP led to a significant increase in blood pressure (from 49+/-8 mmHg to 69+/-7 mmHg) and the requirement of traditional vasopressors decreased significantly. No peripheral vasoconstriction or ischemia was observed. Four of 13 patients, all with single ventricle palliation, died. In two patients death occurred due to additional complications 6 days after AVP was discontinued. One patient, who was still on AVP, died 42 hours postoperatively after prolonged hypoxemia not responding to inhaled nitric oxide. One patient arrested on the third postoperative day when AVP was almost weaned. CONCLUSION: In neonates with vasodilatory shock after cardiopulmonary bypass AVP is a potent agent to increase blood pressure when traditional vasopressors are failing.
The molecular identity of receptor-operated, nonselective cation channels (ROCs) of vascular smooth muscle (VSM) cells is not known for certain. Mammalian homologues of the Drosophila canonical transient receptor potential channels (TRPCs) are possible candidates. This study tested the hypothesis that heteromultimeric TRPC channels contribute to ROC current of A7r5 VSM cells activated by [Arg(8)]-vasopressin. A7r5 cells expressed transcripts encoding TRPC1, TRPC4beta, TRPC6, and TRPC7. TRPC4, TRPC6, and TRPC7 protein expression was confirmed by immunoblotting and association of TRPC6 with TRPC7, but not TRPC4beta, was detected by coimmunoprecipitation. The amplitude of arginine vasopressin (AVP)-induced ROC current was suppressed by dominant-negative mutant TRPC6 (TRPC6(DN)) but not TRPC5 (TRPC5(DN)) mutant subunit expression. These data indicate a role for TRPC6- and/or TRPC7-containing channels and rule a more complex subunit composition including TRPC1 and TRPC4. Increasing extracellular Ca(2+) concentration ([Ca(2+)](o)) from 0.05 to 1 mmol/L suppressed currents owing to native, TRPC7, and heteromultimeric TRPC6-TRPC7 channels, but not TRPC6 current, which was slightly enhanced. The relative changes in native and heteromultimeric TRPC6-TRPC7 current amplitudes for [Ca(2+)](o) between approximately 0.01 and 1 mmol/L were identical, but the changes in homomultimeric TRPC6 and TRPC7 currents were significantly less and greater, respectively, compared with the native channels. Taken together, the data provide biochemical and functional evidence supporting the view that heteromultimeric TRPC6-TRPC7 channels contribute to receptor-activated, nonselective cation channels of A7r5 VSM cells.
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