NPY IS NOT A PRIMARY MEDIATOR OF THE ACUTE THYROID BLOOD-FLOW RESPONSE TO SYMPATHETIC-NERVE STIMULATION

It has been suggested that thyroid blood flow is regulated by both sym pathetic and parasympathetic nerves. The purpose of our experiments wa s to study the role of neuropeptide Y (NPY) in the sympathetic neural control of thyroid blood flow. Sympathetic nerve fibers to the thyroid contain both norepinephrine (NE) and NPY. Therefore, NE (15 nmol iv b olus) and NPY (12 or 1.7 nmol/kg body wt iv infusion; 4 min) were admi nistered to anesthetized male rats (250-300 g) either alone or togethe r, with or without an alpha-adrenergic receptor blocker (phentolamine; 10 mg/kg body wt iv bolus). Experiments were also performed in which the cervical sympathetic trunks were stimulated (30 Hz, 10 V; 0.5 ms; 2 min) with or without phentolamine. Thyroid blood flow was monitored continuously by laser-Doppler blood flowmetry. Results are expressed a s thyroid vascular conductance (TVC). NE or NPY at both doses decrease d TVC relative to that in control saline-infused rats (P < 0.05). No p otentiation of the NE effect by NPY was observed when the first dose o f NE was injected 2 min after a high or low dose of NPY. However, the effect of a second dose of NE, injected 15 min after the end of the lo w dose of NPY, was prolonged compared with the effect of a second dose of NE in saline-infused rats. Phentolamine blocked the effect of NE b ut not that of NPY. Stimulation of the cervical sympathetic trunks dec reased TVC (P < 0.01 vs. sham), and this effect was completely blocked by phentolamine. These results suggest that NPY does not take part in the mediation of the acute thyroid blood flow response during sympath etic nerve stimulation. However, NPY may prevent adrenergic desensitiz ation after prolonged sympathetic activity. This is suggested by the o bservation that the TVC effect of a second dose of NE is prolonged in rats pretreated with NPY.