I.v. injection of 40 mg/kg or 65 mg/kg streptozotocin reliably induced diabetes in female Sprague-Dawley rats, but failed to induced hypertension within the following 42 days. In most animals injected with the higher dose and in some animals injected with the lower dose the tail blood flow was permanently impaired so that no blood pressure signals could be obtained by tail plethysmography. This phenomenon occurred also when the drug was injected into the jugular vein and thus was not due to a local effect of streptozotocin. 15 days after 65 mg/kg streptozotocin, the mean arterial pressure of the rats was similar to that of controls, when measured inthe awake state (carotid cannula) or under ether anaesthesia. 42 days after streptozotocin, under pentobarbital anaesthesia, the blood pressure was again normal in the animals given 40 mg/kg of the drug and depressed in the animals given 65 mg/kg of the drug 42 days previously. The increase of blood pressure induced by 1 microgram/kg (-)-noradrenaline i.v. was similar in the latter group of animals and in controls. The renal cortical renin concentration was much lower than in controls 42 days after either dose of streptozotocin, while the plasma renin activity was normal (40 mg/kg) or increased 65 mg/kg). The low renal renin content may have been due to the diabetic state, rather than to the drug itself. Adrenal medullary dopamine-beta-hydroxylase activity was increased 42 days after the higher dose of streptozotocin.
SUMMARY1. In nephrectomized rats, s.c. (0*12 mg.kg body wt.-') or intracerebroventricular (i.c.v.: 0-03 mg. kg-'), 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-' isoprenaline s.c. in intact or sham-operated rats.3. Isoprenaline (0.12 mg.kg body wt.-', 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.
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