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Notes: 1. The influence of the sympathetic nervous system on urinary kallikrein excretion (UKal) was investigated in conscious rats during stress produced by inserting a silastic catheter through the urethra into the bladder. The effect of this stress on blood glucose (BG), mean arterial pressure (MAP), urinary volume (Uv), urinary sodium (UVNa), and glomerular filtration rate (GFR) was also studied.2. In intact animals stress of 120 min duration produced a non-significant increase of MAP, a significant increase of BG and a decrease of UNa (P 〈 0.001 t-test, 9 d.f.), but it did not affect Uv and GFR. In stressed rats UKal was considerably lower (52 milli Amidasic Units [mAU] per 100 g bodyweight, s.e.m. = 5, n= 6) than in control rats (170 mAU per 100 g, s.e.m. = 21, n= 5). The inhibitory effect on UKal was also observed when kallikrein was measured by the kininogenase method.3. Adrenal medullectomy, performed 1 week before the experiment, suppressed the stress hyperglycaemia but did not affect the reduction of urinary kallikrein or the anti-natriuresis.4. Intracerebroventricular (i.c.v.) injection of saline also had no effect in the control or in the stressed rats, while i.c.v. d-l-propranolol decreased MAP, suppressed the stress hyperglycaemia and the anti-natriuresis and stimulated UKal, without changes in Uv and GFR. Non-stressed control rats i.c.v. injected with saline excreted considerably less kallikrein than rats i.c.v. injected with d-1-propranolol (control saline: 162, s.e.m. = 14, n= 6; vs control d-l-propranolol: 559, s.e.m. = 20, n= 6). Even in stressed rats this difference was registered (stressed saline: 56, s.e.m. = 8, n= 6; vs stressed d-l-propranolol: 554 mAU per 100 g, s.e.m. = 33, n= 6).5. Peripheral sympathectomy with 6-hydroxydopamine (6-OHDA) did not suppress the hyperglycaemic response to stress, but it stimulated UKal. Kallikrein excretion was similar in 6-OHDA stressed (534 mAU per 100 g, s.e.m. = 30, n= 6) than in 6-OHDA control rats (491 mAU per 100 g, s.e.m. = 34, n= 6). No differences were observed on UNa and GFR between control 6-OHDA treated rats and stressed 6-OHDA treated rats.6. The present results suggest strongly that urinary kallikrein excretion is modulated by sympathetic activity. Results after central β-adrenergic blockade and peripheral sympathectomy led to the hypothesis that normal sympathetic tone in the kidney inhibits the release of kallikrein into the urine.