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THE EFFECT OF ANGIOTENSIN II INFUSION, RENAL HYPERTENSION AND NEPHRECTOMY ON SALT APPETITE OF SODIUM‐DEFICIENT SHEEP
Author(s) -
Bott Elspeth,
Denton DA,
Weller Sigrid
Publication year - 1967
Publication title -
australian journal of experimental biology and medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0004-945X
DOI - 10.1038/icb.1967.61
Subject(s) - appetite , medicine , endocrinology , natriuresis , furosemide , renin–angiotensin system , blood pressure , nephrectomy , sodium , angiotensin ii , renal artery , kidney , chemistry , organic chemistry
Summary The sodium appetite of sodium deficient sheep with permanent unilateral parotid fistulae was studied under the following conditions: (i) Intravenous infusions of pressor amounts of angiotensin II; (ii) experimental renal hypertension involving the partial occlusion of one renal artery with the other left untouched. In two sheep the contralateral renal artery was clamped at a later date; (iii) intravenous infusion of angiotensin II in hypertensive sheep; (iv) following nephrectomy. It was observed that intravenous angiotensin II infusion (60–120 μg./hr.) caused a small, but statistically significant, reduction of salt appetite evoked by salt deficiency. In three hypertensive sheep angiotensin II infusion did not cause a significant change in sodium appetite. The induction of renal hypertension did not modify salt appetite in response to sodium deficiency. The early phase of hypertension was associated with reduction of salivary volume and in some animals, with a large natriuresis, similar to that seen in animals without parotid fistulae. Salt appetite varied with the overall effect on sodium balance. In three of six sheep studied nephrectomy did not eliminate salt appetite. This was tested 3–6 or 24 hr. post‐operatively, at which time renin would have been at a much reduced level or absent from the blood.