The role of circulating renin in drinking in response to isoprenaline

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Abstract
1. In nephrectomized rats, S.C. (0·12 mg. kg body wt.−1) or intracerebroventricular ( I.C.V.: 0·03 mg. kg−1), isoprenaline failed to elicit drinking. However, when preceded (5‐20 min) by a non‐dipsogenic dose of I.V. pig renin, S.C. isoprenaline induced a marked, and I.C.V. isoprenaline a smaller drinking response. 2 hr after I.V. renin, S.C. isoprenaline no longer caused drinking. 2. Pig renin did not enhance drinking in response to 0·12 mg. kg−1 isoprenaline S.C. in intact or sham‐operated rats. 3. Isoprenaline (0·12 mg. kg body wt.−1, S.C.) caused a larger fall of blood pressure in unanaesthetized nephrectomized than in intact unanaesthetized rats, but it was not the resulting hypotension that interfered with the nephrectomized rats’ ability to drink, since intact rats with similar falls in blood pressure drank avidly in response to large doses of isoprenaline. 4. Since the rate of inactivation of pig renin in nephrectomized rats was not modified by isoprenaline, drinking in nephrectomized animals in response to renin+isoprenaline was not attributable to increased plasma renin levels. 5. Since isoprenaline induces drinking in the presence of circulating renin, but in the absence of renin release from kidneys, renin plays a permissive role in isoprenaline‐induced drinking. Angiotensin and isoprenaline may interact at the level of intracranial receptors.