Arginine vasotocin relaxation of gar (Lepisosteous spp.) hepatic vein in vitro

Daniel J. Conklin, Nathan W. Mick, Kenneth Olson

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The effects of arginine vasotocin (AVT) were examined in isolated gar arteries (afferent branchial, ABA; conus arteriosus, CA; ventral aorta, VA) and veins (hepatic, HV; intestinal; ovarian). AVT (10-11-10-7 M) had no effect in CA, produced contraction in ABA and VA and stimulated relaxation in veins. In precontracted HV, AVT relaxation was dose-dependent, long-lived (>30 min) and reduced total tension by 49.0 ± 10.7%. EC50s for AVT, arginine vasopressin, oxytocin, desmopressin, and isotocin in gar HV were 1.4 ± 0.3, 3.6 ± 0.2, 5.3 ± 1.7, 11.0 ± 6.5, and 19.0 ± 0.4 nM, respectively. AVT was more potent compared with isotocin. Strength of relaxation (percentage decrease in total tension) of AVT and structural analogs was similar (range = 32.5 to 55%). Endothelium removal did not alter percentage relaxation or sensitivity to AVT in HV. AVT relaxation was not inhibited by nitric oxide synthase inhibitors or propranolol or reversed by addition of methylene blue but it was significantly enhanced by indomethacin (10-5 M). Arginine vasopressin-receptor antagonists (V1- or V2-type selectivity; 10-6 M) were equally effective inhibitors, each blocked 99% of AVT relaxation. Forskolin (10-6 M) and papaverine (10-4 M) relaxed precontracted gar arteries and veins. The adenylyl cyclase inhibitors SQ 22536 and MDL 12,330A (10-5 M) produced transient contraction and stable relaxation, respectively, but did not inhibit AVT-induced relaxation in HV. Atrial natriuretic peptide (3 x 10-8 M) and sodium nitroprusside (10-4 M) had no effect in precontracted HV. AVT acts directly on gar venous smooth muscle cells via a nonclassical AVP receptor, possibly by increasing [cAMP]. AVT is a potent vasoconstrictor in vertebrate vasculature but produces a novel relaxation in gar veins.

Original languageEnglish (US)
Pages (from-to)52-60
Number of pages9
JournalGeneral and Comparative Endocrinology
Volume104
Issue number1
DOIs
StatePublished - Oct 1996

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Lepisosteidae
arginine vasotocin
Vasotocin
Hepatic Veins
liver
arginine vasopressin
Veins
arteries
In Vitro Techniques
abscisic acid
papaverine
Arteries
atrial natriuretic peptide
vasoconstrictor agents
propranolol
forskolin
adenylate cyclase
Deamino Arginine Vasopressin
Vasopressin Receptors
indomethacin

ASJC Scopus subject areas

  • Endocrinology

Cite this

Arginine vasotocin relaxation of gar (Lepisosteous spp.) hepatic vein in vitro. / Conklin, Daniel J.; Mick, Nathan W.; Olson, Kenneth.

In: General and Comparative Endocrinology, Vol. 104, No. 1, 10.1996, p. 52-60.

Research output: Contribution to journalArticle

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abstract = "The effects of arginine vasotocin (AVT) were examined in isolated gar arteries (afferent branchial, ABA; conus arteriosus, CA; ventral aorta, VA) and veins (hepatic, HV; intestinal; ovarian). AVT (10-11-10-7 M) had no effect in CA, produced contraction in ABA and VA and stimulated relaxation in veins. In precontracted HV, AVT relaxation was dose-dependent, long-lived (>30 min) and reduced total tension by 49.0 ± 10.7{\%}. EC50s for AVT, arginine vasopressin, oxytocin, desmopressin, and isotocin in gar HV were 1.4 ± 0.3, 3.6 ± 0.2, 5.3 ± 1.7, 11.0 ± 6.5, and 19.0 ± 0.4 nM, respectively. AVT was more potent compared with isotocin. Strength of relaxation (percentage decrease in total tension) of AVT and structural analogs was similar (range = 32.5 to 55{\%}). Endothelium removal did not alter percentage relaxation or sensitivity to AVT in HV. AVT relaxation was not inhibited by nitric oxide synthase inhibitors or propranolol or reversed by addition of methylene blue but it was significantly enhanced by indomethacin (10-5 M). Arginine vasopressin-receptor antagonists (V1- or V2-type selectivity; 10-6 M) were equally effective inhibitors, each blocked 99{\%} of AVT relaxation. Forskolin (10-6 M) and papaverine (10-4 M) relaxed precontracted gar arteries and veins. The adenylyl cyclase inhibitors SQ 22536 and MDL 12,330A (10-5 M) produced transient contraction and stable relaxation, respectively, but did not inhibit AVT-induced relaxation in HV. Atrial natriuretic peptide (3 x 10-8 M) and sodium nitroprusside (10-4 M) had no effect in precontracted HV. AVT acts directly on gar venous smooth muscle cells via a nonclassical AVP receptor, possibly by increasing [cAMP]. AVT is a potent vasoconstrictor in vertebrate vasculature but produces a novel relaxation in gar veins.",
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