Atrial natriuretic peptide (ANP) can be extracted from rat hearts, and is found to increase fluid excretion by the kidneys when injected into test animals. The mechanism of ANP action is still unclear. ANP may reduce sodium reabsorption in the renal tubules, but it is also known that it increases the rate of glomerular filtration in the kidney, and relaxes preparations of smooth muscle, including one made from arteries that supply the kidney. To clarify its mode of action, we have studied directly the effects of semi-purified and synthetic ANP on blood vessels in the kidney of anaesthetized rats. We found that ANP causes a vasodilatation of the blood vessels which supply the glomeruli and a vasoconstriction of the arterioles which drain them. This substantiates the finding that increased filtration pressure participates in the natriuretic response.

Positron emission tomography (PET) was used in the follow-up of patients with colorectal malignancies to differentiate between recurrent colorectal tumor and scar. Patients were examined with oxygen-15-labeled water and with fluorine-18-labeled deoxyglucose (FDG). FDG was injected intravenously to assess tumor metabolism. The tracer concentration was quantitatively evaluated by means of a region-of-interest technique and standardized for both injected dose and body volume. Of 29 patients, 21 had recurrent colorectal malignancy, and eight had a nonmalignant mass. All malignancies were seen on the PET cross sections. Nonmalignant lesions had a low FDG accumulation on images obtained 60 minutes after injection. While the tumor-soft tissue ratio was highest shortly after the intravenous injection of FDG, the tumor-scar ratio was highest 60 minutes after injection. It was possible to differentiate tumor from non-malignant tissue with FDG with the use of standardized concentration values and tumor-soft tissue ratios. Imaging with O-15-labeled water gave no additional information.

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Plasma renin levels are elevated in accelerated or malignant hypertension. To see if this increase of renin is a concurrent phenomenon or a pathogenetic factor in the increase of blood pressure, severe hypertension was produced in rats by occluding the aorta between the origins of the renal arteries. Eight days later, these animals had developed severe hypertension (mean blood pressure = 201 ± 3 mm Hg) and markedly elevated plasma renin levels (151 ± 35 ng angiotensin II/ml hr -1 ; normal range = 11 ± 0.6). When the kidney distal to the ligature was excised at the time of the coarctation, the animals developed only a moderate increase in blood pressure (mean = 120 ± 1.3 mm Hg) and their plasma renin levels remained in the normal range. When the nonnephrectomized animals with severe hypertension were injected with antibodies against angiotensin II, blood pressure decreased, reaching its lowest point (126 ± 12 mm Hg) 2 days later. This work demonstrates that the severe increase in blood pressure is not due to the mechanical increase in resistance caused by complete coarctation of the aorta; rather, it is due to a humoral factor produced by the kidney, and this factor is renin.