Influence of angiotensin II on the concentration of arterial plasma electrolytes in anaesthetized sheep.

Angiotensin II and I significantly raised potassium and lowered sodium and chloride ion concentrations in arterial plasma, with peak changes occurring in the first 2 min of a 6-min infusion period. The octapeptide increased the arterial K+ level in a dose-dependent manner, but the response showed tachyphylaxis when multiple infusions of 6-min duration were administered after a recovery interval of only 5 min. Raising the arterial blood pressure by 20-33 mmHg with adrenaline and noradrenaline failed to account for the increase in arterial plasma K+ concentration produced by the two peptides. These findings, in particular the rise in K+ concentration, are discussed in relation to possible mechanisms by which angiotensin II affects arteriolar tone.

Radioimmunoassay of unprocessed sheep blood extracts to follow angiotensin metabolism.

The acceptability of radioimmunoassay to determine the levels of compounds antigenic to anti-angiotensin antibodies, in unprocessed methanolic blood extracts, was established for sheep blood. This approach was used to follow the clearance of antigenic compounds after administration of angiotensins I and II and fragments of angiotensin II in anesthetized sheep. The organs supplied by the systemic circulation and also the lungs effectively removed angiotensin I, but the removal of octapeptide occurred only in the peripheral tissues. The blood concentrations of compounds reacting with the anti-angiotensin II antibody always increased with passage of angiotensin I through the pulmonary circulation but not with passage of angiotensin II. The results indicate that factors other than efficiency of removal by the tissue is important in establishing blood levels. The sites of administration and of sampling were shown to be important in relation to ratios of the concentrations of antigenic material. There was a similar uptake of both hormones in the kidney; the relative inability of angiotensin I to reduce renal blood flow, therefore, does not result from a failure of uptake.