{'fraction_non_alphanumeric': 0.02157164869029276, 'fraction_numerical': 0.0015408320493066256, 'mean_word_length': 5.836842105263158, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Adrenalectomy inhibits noradrenergic, adrenergic, and vasopressor responses to angiotensin II in the Pekin duck (Anas platyrhynchos).

The iv injection of Asp1, Val5-angiotensin II(AII) was followed by increases in arterial plasma norepinephrine (NE) and epinephrine (E) concentrations and elevation of arterial blood pressure in the anesthetized Pekin duck. AII injection did not affect the concentration of unconjugated dopamine in arterial plasma. Adrenalectomy inhibited the increases in plasma NE and E concentrations elicited by AII. Pressor responses to AII also were diminished after adrenalectomy, whereas pressor responses to exogenous NE and tyramine were not measurably affected. The alpha-adrenergic blocking drug phenoxybenzamine diminished the pressor effect of AII in both shamoperated and adrenalectomized ducks. The blockade of alpha-adrenergic receptors by phenoxybenzamine was incomplete, since pressor responses to exogenous NE were lessened by not abolished. We conclude from these experiments that AII increases arterial blood pressure in the Pekin duck by mobilizing NE and E from both adrenal and extraadrenal stores. It remains unknown whether the residual pressor response to AII in phenoxybenzamine-treated, adrenalectomized ducks involves an alpha-adrenergic mechanism.