{'fraction_non_alphanumeric': 0.01903114186851211, 'fraction_numerical': 0.004325259515570935, 'mean_word_length': 5.254054054054054, '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}}
Role of renal nerves in sodium depletion-induced salt appetite.

The ingestion of water and 0.3 M NaCl solution and the secretion of key hormones were studied in groups of intact and bilaterally renal-denervated rats after extracellular fluid depletion. Hypovolemia with mild hypotension was produced by subcutaneous injections of the diuretic furosemide (10 mg/kg) followed by injections of the angiotensin-converting enzyme inhibitor captopril (5 mg/kg s.c.). Denervated rats drank significantly less of a concentrated saline solution in response to depletion than intact control rats did, but drank similar amounts of water. Denervated rats finished testing in significantly greater negative water and sodium balance compared with controls. Renal denervation did not impair the secretion of renin and aldosterone or the formation of angiotensin I. The diminished sodium intake of denervated rats is not attributable to reduced water and sodium excretion in response to the hypovolemic protocol. These results indicate that the integrity of the renal nerves is important for the normal elaboration of salt appetite in response to hypovolemia/hypotension.