VASCULAR EFFECTS OF ARGININE VASOTOCIN IN TOAD SKIN

Authors
Citation
Gm. Malvin, VASCULAR EFFECTS OF ARGININE VASOTOCIN IN TOAD SKIN, The American journal of physiology, 265(2), 1993, pp. 180000426-180000432
Citations number
40
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
265
Issue
2
Year of publication
1993
Part
2
Pages
180000426 - 180000432
Database
ISI
SICI code
0002-9513(1993)265:2<180000426:VEOAVI>2.0.ZU;2-5
Abstract
Fluid balance in amphibians is regulated, in large part, by arginine v asotocin (AVT). One important action of this hormone is to facilitate water uptake by increasing the water permeability of the skin. Cutaneo us blood flow also affects water uptake, but the effects of AVT on ski n perfusion are unknown. This study tested the hypothesis that AVT fac ilitates water uptake, not only by increasing cutaneous water permeabi lity, but also by promoting cutaneous blood flow. The effects of AVT o n blood flow through the ventral pelvic skin, a region specialized for water uptake, were assessed in Bufo marinus by determining the conduc tance of the skin to acetylene (G(s)Ac), an index of cutaneous blood f low. A pump-perfused skin preparation was used to study the effects of AVT on the cutaneous vascular resistance (CVR) of the ventral pelvic skin and the dorsal skin (a region not normally involved in water upta ke). Bolus AVT injections (iv) of 10 pmol/kg and below had no signific ant effect on G(s)Ac (P > 0.45). However, 100 and 300 pmol/kg of AVT d ecreased G(s)Ac by 39 +/- 7 (P < 0.001) and 63 +/- 6% (P < 0.001), res pectively. The higher AVT doses increased mean arterial pressure. AVT increased CVR in both pump-perfused preparations. The lowest concentra tion of AVT tested that significantly raised CVR was 1 x 10(-10) M for the dorsal skin (P = 0.006) and 3 x 10(-10) M for the ventral pelvic skin (P = 0.038). AVT never decreased CVR, even after CVR was increase d by epinephrine (EPI). There was no significant difference in the 50% effective dose (ED50) (P = 0.46) or the maximal %increase in CVR betw een the two skin regions (P = 0.98). Both the V1-vasopressinergic anta gonist, d[(CH2)5Tyr(Me)]AVP (10(-7) M), and the V1V2-vasopressinergic antagonist, d[(CH2)5D-Tyr(Et)]VAVP (3 x 10(-7) M), increased the ED50 to AVT (P < 0.0004). The dose-response relationship to EPI was unaffec ted by these antagonists. These results indicate that AVT can decrease cutaneous blood flow by increasing CVR via stimulation of a vascular receptor similar to the mammalian V1-vasopressinergic receptor. The se nsitivity of the cutaneous vasculature to AVT suggests that cutaneous blood flow will not be affected by AVT under normal conditions. Plasma concentration of AVT, [AVT], during dehydration, hemorrhage, and salt loading as reported by others may be high enough to reduce cutaneous blood flow. Such a reduction in blood flow should oppose increases in cutaneous water uptake caused by AVT's effect on cutaneous water perme ability.