Sar1-Ala8 angiotensin II blocks renin-angiotensin but not beta-adrenergic dipsogenesis

Tang, Maisy; Falk, John L.

doi:10.1016/0091-3057(74)90087-2

Cited by 39 publications

(9 citation statements)

References 33 publications

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“…Furthermore, drinking of both solutions in response to either stimulus was inhibited by a single injection of saralasin acetate (P-113) given through the ventricular cannula suggesting that isoprenaline may activate a cerebral renin-angiotensin system. The effect of P-1 13 on beta adrenergicdrinking seen in the present experiment contradicts the results reported by Tang & Falk, 1974. The inhibitory effect of centrally injected SQ-20881 on isoprenalineevoked drinking is consistent with the inhibition of AII-evoked drinking by peripherally injected SQ-20881 reported previously (Chiaraviglio, 1976).…”

Section: Discussionsupporting

confidence: 85%

Drinking behaviour in rats treated with isoprenaline, angiotensin II or angiotensin antagonists

Chiaraviglio

1979

The Journal of Physiology

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SUMMARY1. Isoprenaline hydrochloride injected subcutaneously in rats given a choice test of 1-8 % NaCi 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 jug/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 isoprenalineinduced NaCl and water intake, while the alpha-adrenoceptor antagonist phenoxybenzamine abolished isoprenaline-induced NaCl intake and enhanced water intake.6. Saralasin acetate (P-1 13), 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.

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Section: Discussionsupporting

confidence: 85%

Drinking behaviour in rats treated with isoprenaline, angiotensin II or angiotensin antagonists

Chiaraviglio

1979

The Journal of Physiology

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“…The finding that renin release is not a prerequisite for the dipsogenic action of isoprenaline is compatible with the presence of a significant drinking response to s.c. renin after depletion of the renal renin store by treatment with desoxycortone and salt in rats (Lehr, Goldman & Casner, 1973), as well as a number of pharmacological observations (Lehr et al 1973; Lehr, 1974;Tang & Falk, 1974) which argue against a major role of renin release in isoprenaline-induced drinking.…”

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confidence: 99%

The role of circulating renin in drinking in response to isoprenaline

Atkinson

Kaesermann

Lambelet

et al. 1979

The Journal of Physiology

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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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“…On the other hand, blockade o f angiotensin receptors suggested that endogenous angiotensin is in volved in several hypertensive states (16). Angiotensin (or renin) caused drinking when administered intravenously, intracerebroventricularly (IVT), or by direct injection into specific brain areas (7,22,23). Pretreatment o f animals with angiotensin receptor blocking drugs reduced drinking when angiotensin was sub-' Partly supported by NIH Grant HL19320.…”

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confidence: 99%

“…Angiotensin (or renin) caused drinking when administered intravenously, intracerebroventricularly (IVT), or by direct injection into specific brain areas (7,22,23). Pretreatment o f animals with angiotensin receptor blocking drugs reduced drinking when angiotensin was sub-sequently injected by the same route (7,22,23). However, i.v.…”

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confidence: 99%

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Drinking Behavior in Water Deprived Rats after Angiotensin Receptor Blockade

Severs¹,

Kapsha²,

Klase³

et al. 1977

Pharmacology

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Angiotensin II is a peptide normally present in the bloodstream and central nervous system. Exogenous angiotensin induces drinking which is inhibited by saralasin, a specific receptor antagonist. Administration of saralasin does not reduce endogenously stimulated drinking. Angiotensin is dipsogenic after intravenous or intracerebroventricular infusion, raising the possibility of multiple access routes to the brain. Water deprived rats were given saralasin by both routes simultaneously to block the access of endogenous angiotensin to receptors reached from blood and ventricular cerebrospinal fluid (CSF). Water deprivation increased plasma (Na⁺), hematocrit, vasopressin content and renin activity but saralasin treatment did not reduce water intake after 30 or 60 min. Therefore, blood or CSF-borne angiotensin does not appear to be an absolute requirement for water deprivation drinking behavior.

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Sar1-Ala8 angiotensin II blocks renin-angiotensin but not beta-adrenergic dipsogenesis

Cited by 39 publications

References 33 publications

Drinking behaviour in rats treated with isoprenaline, angiotensin II or angiotensin antagonists

Drinking behaviour in rats treated with isoprenaline, angiotensin II or angiotensin antagonists

The role of circulating renin in drinking in response to isoprenaline

Drinking Behavior in Water Deprived Rats after Angiotensin Receptor Blockade

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