AJP - Endocrinology and Metabolism, Vol 265, Issue 1 E24-E30, Copyright © 1993 by American Physiological Society
NPY is not a primary mediator of the acute thyroid blood flow response to sympathetic nerve stimulation
M. Dey, M. Michalkiewicz, L. Huffman and G. A. Hedge
Department of Physiology, West Virginia University Health Sciences Center, Morgantown 26506.
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)
