Effects of vasopressin on the sympathetic contraction of rabbit ear artery during cooling

Abstract

In order to analyse the effects of arginine-vasopressin on the vascular contraction to sympathetic nerve stimulation during cooling, the isometric response of isolated, 2-mm segments of the rabbit central ear (cutaneous) artery to electrical field stimulation (1-8 Hz) was recorded at 37 and 30 degrees C. Electrical stimulation (37 degrees C) produced frequency-dependent arterial contraction, which was reduced at 30 degrees C and potentiated by vasopressin (10 pM, 100 pM and 1 nM). This potentiation was greater at 30 than at 37 degrees C and was abolished at both temperatures by the antagonist of vasopressin V1 receptors d(CH2)5 Tyr(Me)AVP (100 nM). Desmopressin (1 microM) did not affect the response to electrical stimulation. At 37 degrees C, the vasopressin-induced potentiation was abolished by the purinoceptor antagonist PPADS (30 microM), increased by phentolamine (1 microM) or prazosin (1 microM) and not modified by yohimbine (1 microM), whilst at 30 degrees C, the potentiation was reduced by phentolamine, yohimbine or PPADS, and was not modified by prazosin. The Ca2+-channel blockers, verapamil (10 microM) and NiCl2 (1 mM), abolished the potentiating effects of vasopressin at 37 degrees C whilst verapamil reduced and NiCl2 abolished this potentiation at 30 degrees C. The inhibitor of nitric oxide synthesis, L-NOARG (100 microM), or endothelium removal did not modify the potentiation by vasopressin at 37 and 30 degrees C. Vasopressin also increased the arterial contraction to the alpha2-adrenoceptor agonist BHT-920 (10 microM) and to ATP (2 mM) at 30 and 37 degrees C, but it did not modify the contraction to noradrenaline (1 microM) at either temperature. These results suggest that in cutaneous (ear) arteries, vasopressin potentiaties sympathetic vasoconstriction to a greater extent at 30 than at 37 degrees C by activating vasopressin V1 receptors and Ca2+ channels at both temperatures. At 37 degrees C, the potentiation appears related to activation of the purinoceptor component and, at 30 degrees C, to activation of both purinoceptor and alpha2-adrenoceptor components of the sympathetic response.

Figure 1

Contraction of rabbit ear arteries at 37 and 30°C to electrical field stimulation (1–8 Hz, 0.2 ms pulse duration, 70 V, for 5 s) in arteries: (a) in the absence (control) and in the presence of vasopressin (10 pM–1 nM); (b) pretreated with the antagonist of vasopressin V₁ receptors d(CH₂)₅ Tyr(Me)AVP (100 nM) in the absence (control) and in the presence of vasopressin (10 pM–1 nM); and (c) in the absence (control) and in the presence of desmopressin (1 μM). Points are means±s.e.mean. ^* Significantly different (P<0.01) from the control. n=number of animals.

Figure 2

Contraction of rabbit ear arteries at 37 and 30°C to electrical field stimulation (1–8 Hz, 0.2 ms pulse duration, 70 V, for 5 s) in the absence (control) and in the presence of: (a) phentolamine (1 μM); (b) prazosin (1 μM); and (c) yohimbine (1 μM). Points are means±s.e.mean. ^*, ^**, Significantly different from the control (^*P<0.05, ^**P<0.01). n=number of animals.

Figure 3

Contraction of rabbit ear arteries at 37 and 30°C to electrical field stimulation (1–8 Hz, 0.2 ms pulse duration, 70 V, for 5 s) in the absence (control) and in the presence of: (a) PPADS (30 μM); and (b) PPADS (30 μM) plus phentolamine (1 μM). Points are means±s.e.mean. ^*, ^**, Significantly different from the control (^*P<0.05, ^**P<0.01). n=number of animals.

Figure 4

Contraction of rabbit ear arteries at 37 and 30°C to electrical field stimulation (1–8 Hz, 0.2 ms pulse duration, 70 V, for 5 s) in the absence (control) and in the presence of vasopressin (10 pM–1 nM) in arteries pretreated with: (a) phentolamine (1 μM); (b) prazosin (1 μM); (c) yohimbine (1 μM); (d) PPADS (30 μM); and (e) PPADS (30 μM) plus phentolamine (1 μM). Points are means ±s.e.mean. ^*, ^**, Significantly different from the control (^*P<0.05, ^**P<0.01). n=number of animals.

Figure 5

Contraction of rabbit ear arteries at 37 and 30°C to electrical field stimulation (1–8 Hz, 0.2 ms pulse duration, 70 V, for 5 s) in arteries under control conditions and in arteries: (a) pretreated with verapamil (10 μM); (b) pretreated with NiCl₂ (1 mM); (c) without endothelium; and (d) pretreated with L-NOARG (100 μM). Points are means±s.e.mean. ^*, ^**, Significantly different from the control (^*P<0.05, ^**P<0.01). n=number of animals.

Figure 6

Contraction of rabbit ear arteries at 37 and 30°C to electrical field stimulation (1–8 Hz, 0.2 ms pulse duration, 70 V, for 5 s) in arteries in the absence (control) and in the presence of vasopressin (10 pM–1 nM): (a) pretreated with verapamil (10 μM); (b) pretreated with NiCl₂ (1 mM); (c) without endothelium; and (d) pretreated with L-NOARG (100 μM). Points are means±s.e.mean. ^*, ^**, Significantly different from the control (^*P<0.05, ^**P<0.01). n=number of animals.

Figure 7

Contraction of rabbit central ear arteries at 37 and 30°C, in the absence (control) and in the presence of vasopressin (10 pM–1 nM), in response to: (a) noradrenaline (1 μM); (b) BHT-920 (10 μM) in the presence of prazosin (1 μM); and (c) ATP (2 mM). Values are means±s.e.mean. ^*Significantly different from its control (^*P<0.01). n=number of animals.