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 sympathetic and parasympathetic nerves. The purpose of our experiments was 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 bolus) and NPY (12 or 1.7 nmol/kg body wt iv infusion; 4 min) were administered to anesthetized male rats (250-300 g) either alone or together, 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 as thyroid vascular conductance (TVC). NE or NPY at both doses decreased TVC relative to that in control saline-infused rats (P < 0.05). No potentiation of the NE effect by NPY was observed when the first dose of 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 low 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 but not that of NPY. Stimulation of the cervical sympathetic trunks decreased TVC (P < 0.01 vs. sham), and this effect was completely blocked by phentolamine.(ABSTRACT TRUNCATED AT 250 WORDS)