1. The purpose of this study was to examine the contribution of the 
sympatho-adrenomedullary system to the blood pressure response to an intravenous 
bolus of thyrotropin-releasing hormone (TRH) in conscious medullectomized and 
sham-operated rats. 2. The peak pressor effect of 0.5 mg TRH was significantly 
increased in rats having no adrenal medulla (+24.2 +/- 1.6 mmHg, mean +/- 
s.e.m., P < 0.01) as compared to sham-operated animals (+12.2 +/- 3.0 mmHg). 3. 
Blockade of alpha-adrenergic receptors with phentolamine abolished the pressor 
effect of TRH in control rats (+2.1 +/- 1.9 mmHg) but did not attenuate the 
blood pressure response of medullectomized rats (+21.5 +/- 4.7 mmHg). In 
contrast, beta-blockade with propranolol blunted the blood pressure 
responsiveness of rats subjected to adrenal medullectomy (+12.4 +/- 2.6 mmHg) 
but did not modify the effect of TRH in sham-operated controls (+10.9 +/- 2.9 
mmHg). 4. The direct in vitro effect of TRH on isolated mesenteric rat arteries 
was also evaluated. TRH did not induce contractions of isolated arteries. 5. 
These results suggest that in rats with intact adrenals, the pressor effect of 
intravenous TRH is mediated primarily by a stimulation of alpha-adrenergic 
receptors. Adrenal medullectomy appears to enhance the blood pressure response 
to intravenous TRH. Activation of cardiac beta-adrenoceptors seems to contribute 
to the blood pressure increasing effect of intravenous TRH in medullectomized 
animals.