EFFECT OF CONVERTING ENZYME BLOCKADE ON ISOPRENALINE‐ AND ANGIOTENSIN I‐INDUCED DRINKING

Article date: November 1974

By: G. HERTTING, D.K. MEYER in Volume 52, Issue 3, pages 381-386

Intravenous infusion of 0.072 μmol kg−1 h−1 (1‐Asp, 5‐Ile) angiotensin I, 0.116 μmol kg−1 h−1 of (1‐Asp β‐amid, 5‐Val) angiotensin II or of (1‐Asp, 5‐Ile) angiotensin II, caused food‐deprived and water‐satiated rats to drink about 3.0 ml of water per animal. This indicates that angiotensin I has a 1.6 times stronger dipsogenic effect than the angiotensin II preparations when infused intravenously.

The converting‐enzyme‐inhibitor SQ 20881 (Pyr‐Trp‐Pro‐Arg‐Pro‐Gln‐Ile‐Pro‐Pro) (1.0 mg/kg i.v.) had no intrinsic dipsogenic effect.

SQ 20881 given in combination with angiotensin I or angiotensin II potentiated the dipsogenic effect of angiotensin I, but not that of the two angiotensin II preparations.

The drinking induced by isoprenaline (100 μg/kg, i.m.) was potentiated by SQ 20881 to the same extent as drinking produced by angiotensin I infusion.

Angiotensin I plasma levels were determined after angiotensin I infusion and isoprenaline application. Both were significantly raised by SQ 20881.

It is concluded that one of the mechanisms which mediate the dipsogenic effect of isoprenaline is stimulation of the renin‐angiotensin system and that increased plasma levels of angiotensin I may play a substantial role in this type of drinking.

Intravenous infusion of 0.072 μmol kg−1 h−1 (1‐Asp, 5‐Ile) angiotensin I, 0.116 μmol kg−1 h−1 of (1‐Asp β‐amid, 5‐Val) angiotensin II or of (1‐Asp, 5‐Ile) angiotensin II, caused food‐deprived and water‐satiated rats to drink about 3.0 ml of water per animal. This indicates that angiotensin I has a 1.6 times stronger dipsogenic effect than the angiotensin II preparations when infused intravenously.

The converting‐enzyme‐inhibitor SQ 20881 (Pyr‐Trp‐Pro‐Arg‐Pro‐Gln‐Ile‐Pro‐Pro) (1.0 mg/kg i.v.) had no intrinsic dipsogenic effect.

SQ 20881 given in combination with angiotensin I or angiotensin II potentiated the dipsogenic effect of angiotensin I, but not that of the two angiotensin II preparations.

The drinking induced by isoprenaline (100 μg/kg, i.m.) was potentiated by SQ 20881 to the same extent as drinking produced by angiotensin I infusion.

Angiotensin I plasma levels were determined after angiotensin I infusion and isoprenaline application. Both were significantly raised by SQ 20881.

It is concluded that one of the mechanisms which mediate the dipsogenic effect of isoprenaline is stimulation of the renin‐angiotensin system and that increased plasma levels of angiotensin I may play a substantial role in this type of drinking.

DOI: 10.1111/j.1476-5381.1974.tb08606.x

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