In a normal male mouse, which had been kept isolated for some time, confrontation with another male mouse, resulted in aggressive behaviour, including fighting. The aggressive behaviour resulted in secretion of a few microlitre of saliva with vast renin concentration. The renin concentration in saliva reached values of 6000Goldblatt units \m=x\ml \m=-\1, corresponding to 15 mg/ml of renin. This concentration is 6 orders of magnitude higher than normal plasma renin concentrations. The secretory pattern could be mimicked by ip injection of pharmacological doses (2\p=n-\18mg/kg) of the \g=a\-adrenergic agonist phenylephrine. This is probably the first demonstration of a physiological secretion of renin to saliva which may be of importance since renin most likely is injected into the opponent or prey through bites.

\g=a\-adrenergic stimulation with phenylephrine causes release of vast amounts of mouse submaxillary gland renin to saliva. The amount released is about 100-fold higher than that released after \g=b\-adrenergic stimulation with isoproterenol and about 1000-fold higher than the amount released after cholinergic stimulation with pilocarpine. \g=a\-blockadewith phenoxybenzamine before phenylephrine stimulation strongly inhibits the renin release. However, phenoxybenzamine or \ g = b \ \ x = r e q -\ blockade with propranolol before isoproterenol stimulation have no effect on the amount of renin released.Thus, the release of submaxillary mouse renin to saliva is triggered mainly by activation of \g=a\-adrenergicreceptors. Renin in cholinergic and \g=a\-and \g=b\-adrenergic stimulated saliva has the same molecular weight and the same specific enzymatic activity as renin in the submaxillary gland. This indicates that renin is secreted to saliva, and probably also to the blood, in its fully enzymically active 40000 mol. wt. form regardless of the stimulus used. The vast amounts of renin released to saliva (up to 600 Goldblatt Units) demonstrate that submaxillary mouse renin is secreted predominantly to saliva and much less to the blood. The mouse submaxillary gland therefore seems to have an exocrine rather than an endocrine role for release of renin.

1 The source of renin was found to be the submaxillary gland and the kidneys; however, other sources were also demonstrated but not identified.

ABSTRACT. The present report describes a case of potassium‐wasting nephropathy with the physiological and endocrinological findings that are typical for Bartter's syndrome (BS). However, the renal juxtaglomerular apparatus shawed no hyperplasia at two renal biopsies two years apart. The short‐term (9 days) effect of indomethacin in combination with spironolactone was a suppression of hyperreninemia and hyperaldosteronism and an increase in vascular sensitivity to angiotensin II associated with potassium and sodium retention. Subsequently, on indomethacin alone, potassium balance was obtained on a lower level with persistent hypokalemia and persistent renal potassium leakage. Hypokalemia persisted during long‐term (9 months) treatment with indomethacin despite normalization of the activity of the renin‐aldosterone system. The results indicate that indomethacin as long‐term treatment may be ineffective in maintaining a normal potassium balance in BS.

1. In male mice without kidneys and submaxillary, as well as sublingual, glands aggressive behaviour causes a vast release of renin [J. Bing & K. Poulsen (1979) Acta Physiologica Scandinavica, 107, 251-256]. 2. This resulted in about an 800-fold increase in plasma renin concentration from the control level of 0.52 (range 0.15-0.8) Goldblatt unit (G.U.) x 10(-3)/ml to 430 (range 300-500) G.U. x 10(-3)/ml after aggression. 3. The aggression-provoked renin fulfil all the criteria so far studied for being active renin, identical with normal mouse plasma renin and pure submaxillary mouse renin. 4. It generates angiotensin I with renin substrate and Km (1.2 mumol/l) is the same. It is neutralized by pepstatin but not by inhibitors of metallo-, thiol and serine proteinases, indicating that it is an aspartate proteinase (acidic proteinase). 5. It is a 40 000-mol.wt. renin, which has full enzymatic activity with a specific enzymatic activity of 0.32 G.U./micrograms, identical with that of normal plasma renin. 6. Its enzymatic activity is neutralized by a specific antibody against pure submaxillary renin. It is measureable in the direct renin radioimmunoassay with a dilution curve which parallels that of the standards. It demonstrates complete antigenic identity with pure submaxillary renin in crossed immunoelectrophoresis. 7. Its origin is unknown.