Vasodilatory effect of arginine vasopressin is mediated by nitric oxide in human forearm vessels

Tatsuya Tagawa, Tsutomu Imaizumi, Toyonari Endo, Masanari Shiramoto, Yoshitaka Hirooka, Shin Ichi Ando, Akira Takeshita

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Abstract

Arginine vasopressin (AVP) causes biphasic changes in vascular resistance in human forearms; vasoconstriction at lower doses and vasodilation at higher doses. Vasoconstriction is mediated by the V1 receptor. However, the mechanism of A VP-induced vasodilation is not known. We investigated whether AVP-induced vasodilation is mediated by nitric oxide (NO) in human forearms by examining the effects of L-arginine (a precursor of NO) and NG-monomethyl-L-arginine (L-NMMA, a blocker of NO synthase) on AVP-induced vasodilation. AVP was infused intraarterially at doses of 0.05, 0.1, 0.2, 0.5, and 1.0 ng/kg per min (n = 8). The lower doses of AVP (≤ 0.1 ng/kg per min) increased, whereas the higher doses of AVP (≥ 0.5 ng/kg per min) decreased forearm vascular resistance (FVR) (P < 0.01). Intraarterially infused L-arginine at 10 mg/min did not alter arterial pressure, baseline FVR, or heart rate. L-arginine did not alter the magnitude of AVP-induced vasoconstriction at the lower doses, but L-arginine augmented the magnitude of AVP-induced vasodilation at doses of 0.2 (P < 0.05), 0.5 (P < 0.01), and 1.0 (P < 0.05) ng/kg per min. In another group (n = 6), intraarterially infused L-NMMA (4 μmol/min for 5 min) increased baseline FVR without systemic effects, and inhibited acetylcholine-induced vasodilation (P < 0.01). L-NMMA at this dose inhibited AVP-induced vasodilation (P < 0.01) but did not affect vasoconstriction. L-arginine reversed the inhibitory effect of L-NMMA. Our results suggest that the vasodilatory effect of AVP may be mediated by NO in human forearms.

Original languageEnglish
Pages (from-to)1483-1490
Number of pages8
JournalJournal of Clinical Investigation
Volume92
Issue number3
DOIs
Publication statusPublished - Sep 1993

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Arginine Vasopressin
Forearm
Nitric Oxide
Vasodilation
omega-N-Methylarginine
Arginine
Vasoconstriction
Vascular Resistance
Vasopressin Receptors
Nitric Oxide Synthase
Acetylcholine
Arterial Pressure
Heart Rate

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Tagawa, T., Imaizumi, T., Endo, T., Shiramoto, M., Hirooka, Y., Ando, S. I., & Takeshita, A. (1993). Vasodilatory effect of arginine vasopressin is mediated by nitric oxide in human forearm vessels. Journal of Clinical Investigation, 92(3), 1483-1490. https://doi.org/10.1172/JCI116726

Vasodilatory effect of arginine vasopressin is mediated by nitric oxide in human forearm vessels. / Tagawa, Tatsuya; Imaizumi, Tsutomu; Endo, Toyonari; Shiramoto, Masanari; Hirooka, Yoshitaka; Ando, Shin Ichi; Takeshita, Akira.

In: Journal of Clinical Investigation, Vol. 92, No. 3, 09.1993, p. 1483-1490.

Research output: Contribution to journalArticle

Tagawa, T, Imaizumi, T, Endo, T, Shiramoto, M, Hirooka, Y, Ando, SI & Takeshita, A 1993, 'Vasodilatory effect of arginine vasopressin is mediated by nitric oxide in human forearm vessels', Journal of Clinical Investigation, vol. 92, no. 3, pp. 1483-1490. https://doi.org/10.1172/JCI116726
Tagawa, Tatsuya ; Imaizumi, Tsutomu ; Endo, Toyonari ; Shiramoto, Masanari ; Hirooka, Yoshitaka ; Ando, Shin Ichi ; Takeshita, Akira. / Vasodilatory effect of arginine vasopressin is mediated by nitric oxide in human forearm vessels. In: Journal of Clinical Investigation. 1993 ; Vol. 92, No. 3. pp. 1483-1490.
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abstract = "Arginine vasopressin (AVP) causes biphasic changes in vascular resistance in human forearms; vasoconstriction at lower doses and vasodilation at higher doses. Vasoconstriction is mediated by the V1 receptor. However, the mechanism of A VP-induced vasodilation is not known. We investigated whether AVP-induced vasodilation is mediated by nitric oxide (NO) in human forearms by examining the effects of L-arginine (a precursor of NO) and NG-monomethyl-L-arginine (L-NMMA, a blocker of NO synthase) on AVP-induced vasodilation. AVP was infused intraarterially at doses of 0.05, 0.1, 0.2, 0.5, and 1.0 ng/kg per min (n = 8). The lower doses of AVP (≤ 0.1 ng/kg per min) increased, whereas the higher doses of AVP (≥ 0.5 ng/kg per min) decreased forearm vascular resistance (FVR) (P < 0.01). Intraarterially infused L-arginine at 10 mg/min did not alter arterial pressure, baseline FVR, or heart rate. L-arginine did not alter the magnitude of AVP-induced vasoconstriction at the lower doses, but L-arginine augmented the magnitude of AVP-induced vasodilation at doses of 0.2 (P < 0.05), 0.5 (P < 0.01), and 1.0 (P < 0.05) ng/kg per min. In another group (n = 6), intraarterially infused L-NMMA (4 μmol/min for 5 min) increased baseline FVR without systemic effects, and inhibited acetylcholine-induced vasodilation (P < 0.01). L-NMMA at this dose inhibited AVP-induced vasodilation (P < 0.01) but did not affect vasoconstriction. L-arginine reversed the inhibitory effect of L-NMMA. Our results suggest that the vasodilatory effect of AVP may be mediated by NO in human forearms.",
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AU - Hirooka, Yoshitaka

AU - Ando, Shin Ichi

AU - Takeshita, Akira

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N2 - Arginine vasopressin (AVP) causes biphasic changes in vascular resistance in human forearms; vasoconstriction at lower doses and vasodilation at higher doses. Vasoconstriction is mediated by the V1 receptor. However, the mechanism of A VP-induced vasodilation is not known. We investigated whether AVP-induced vasodilation is mediated by nitric oxide (NO) in human forearms by examining the effects of L-arginine (a precursor of NO) and NG-monomethyl-L-arginine (L-NMMA, a blocker of NO synthase) on AVP-induced vasodilation. AVP was infused intraarterially at doses of 0.05, 0.1, 0.2, 0.5, and 1.0 ng/kg per min (n = 8). The lower doses of AVP (≤ 0.1 ng/kg per min) increased, whereas the higher doses of AVP (≥ 0.5 ng/kg per min) decreased forearm vascular resistance (FVR) (P < 0.01). Intraarterially infused L-arginine at 10 mg/min did not alter arterial pressure, baseline FVR, or heart rate. L-arginine did not alter the magnitude of AVP-induced vasoconstriction at the lower doses, but L-arginine augmented the magnitude of AVP-induced vasodilation at doses of 0.2 (P < 0.05), 0.5 (P < 0.01), and 1.0 (P < 0.05) ng/kg per min. In another group (n = 6), intraarterially infused L-NMMA (4 μmol/min for 5 min) increased baseline FVR without systemic effects, and inhibited acetylcholine-induced vasodilation (P < 0.01). L-NMMA at this dose inhibited AVP-induced vasodilation (P < 0.01) but did not affect vasoconstriction. L-arginine reversed the inhibitory effect of L-NMMA. Our results suggest that the vasodilatory effect of AVP may be mediated by NO in human forearms.

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