STUDY OBJECTIVE - The aim of the study was to develop a new procedure to produce abdominal aortocaval shunts in the rat without vascular microsurgery. PROCEDURE - The inferior vena cava and abdominal aorta were exposed by laparotomy. The aorta was punctured caudal to the left renal artery with an 18 gauge disposable needle which was advanced into the vessel, perforating the adjacent wall between aorta and vena cava and penetrating the latter. A bulldog vascular clamp was placed across the aorta cephalic to the puncture, the needle was withdrawn, and the aortic puncture point was sealed with a drop of cyanoacrylate glue. The clamp was removed 30 s later. Patency of the shunt was verified visually by swelling of the vena cava and admixture of arterial and venous blood. No local haemorrhages were seen. The laporatomy was then closed. The procedure takes less than 10 min. RESULTS - Of 11 rats which received this procedure, only one died within 24 h. All the other animals were killed 4 weeks after operation. Nine of these 10 animals had developed cardiac hypertrophy of about the same magnitude. There were no changes in sham operated controls. CONCLUSIONS - This is a reproducible, simple and rapid method of developing high output heart failure and cardiac hypertrophy in the rat which could be useful in many laboratories.

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Rats were injected either with synthetic 125I-Arg 101-Tyr 126 atrial natriuretic factor (ANF) or with 125I-ANF together with an excess of cold Arg 101-Tyr 126 ANF. Binding sites in various tissues were accepted depending on two criteria: displacement of radioactivity by cold ANF and absence of localization of silver grains on putative target cells in the presence of cold ANF. Binding sites were localized on zona glomerulosa cells and on adrenergic and noradrenergic cells of adrenal medulla, on hepatocytes, on the base of mature epithelial cells of villi in the small intestine, on smooth muscle cells of the muscularis layer of the colon and on the base of epithelial cells of the ciliary bodies. In addition, binding sites were localized in the vasculature of kidney, adrenal cortex, lung and liver. Binding sites were particularly numerous on renal glomerular endothelial cells. These results indicate that ANF may have important hemodynamic effects in kidney, lung, liver and adrenal cortex, may regulate water and ion transport in small intestine and ciliary bodies and may have metabolic effects in the liver. The presence of binding sites on the zona glomerulosa is in agreement with the important inhibitory effect of the peptide on aldosterone secretion.

Since atrial natriuretic factor (ANF) blocks the contractile effect of angiotensin II on vascular strips, we investigated the action of the synthetic 48-73 ANF (previously called 8-33 ANF) on another target tissue of angiotensin II, the adrenal glomerulosa. ANF did not affect basal aldosterone output by isolated rat adrenal glomerulosa cells. ANF inhibited aldosterone secretion stimulated by 10(-8)M angiotensin II with an IC50 of 1.3 X 10(-9)M. Aldosterone secretion stimulated by 2.9 X 10(-10)M ACTH and by 15 mM potassium was similarly inhibited by ANF. In vivo, ANF blocked the effect of angiotensin II infused iv on aldosterone secretion in conscious unrestrained rats. We conclude that ANF is a non-selective inhibitor of stimulated aldosterone output.