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Drinking behaviour in rats treated with isoprenaline, angiotensin II or angiotensin antagonists
Author(s) -
Chiaraviglio Emma
Publication year - 1979
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1979.sp012999
Subject(s) - isoprenaline , angiotensin ii , thirst , chemistry , endocrinology , medicine , saralasin , propranolol , saline , stimulation , blood pressure
1. Isoprenaline hydrochloride injected subcutaneously in rats given a choice test of 1·8% NaCl and water, first induced saline intake which started immediately and was almost concluded in 15 min, followed by a copious water intake. When either saline or water were given in a separate test, saline intake surpassed the water intake in the first 15 min. 2. The delay of 15, 30 or 60 min after injection of isoprenaline, 100 μg/kg, before drinking was allowed, significantly reduced saline intake but did not modify the amount of water subsequently drunk. 3. Isoprenaline caused a sudden drop in arterial blood pressure, the extent and duration depending on the dose. The time of maximum drop 3‐4 min after injection coincided with the time the rat drank salt. 4. Isoprenaline‐induced saline drinking was significantly reduced after bilateral nephrectomy but water intake was unaffected. 5. The beta‐adrenoceptor blocking agent, propranolol, inhibited isoprenaline‐induced NaCl and water intake, while the alpha‐adrenoceptor antagonist phenoxybenzamine abolished isoprenaline‐induced NaCl intake and enhanced water intake. 6. Saralasin acetate (P‐113), a competitive inhibitor of angiotensin II, given into the third brain ventricle, prevented the isoprenaline‐induced NaCl and water intake as well as angiotensin II‐induced drinking. The angiotensin converting enzyme inhibitor SQ‐20881 reduced the isoprenaline‐induced NaCl and water intake. 7. In conclusion, hypotension might be a component of salt drinking evoked by isoprenaline although the dipsogenic action of beta‐stimulation is mainly due to endogenous renin‐angiotensin activation.