PMID- 3117464
OWN - NLM
STAT- MEDLINE
DCOM- 19871125
LR  - 20190824
IS  - 0305-1870 (Print)
IS  - 0305-1870 (Linking)
VI  - 14
IP  - 4
DP  - 1987 Apr
TI  - Sympathetic nervous system mediates urinary kallikrein excretion in conscious 
      rats.
PG  - 291-301
AB  - 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 less than 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-l-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 beta-adrenergic blockade 
      and peripheral sympathectomy led to the hypothesis that normal sympathetic tone 
      in the kidney inhibits the release of kallikrein into the urine.
FAU - Albertini, R
AU  - Albertini R
AD  - Laboratory of Physiology, Faculty of Biological Sciences, Pontificia Universidad 
      Catolica de Chile, Santiago.
FAU - Vargas, L
AU  - Vargas L
FAU - Oliveri, P
AU  - Oliveri P
FAU - Pardo, F
AU  - Pardo F
FAU - Paredes, M C
AU  - Paredes MC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - Clin Exp Pharmacol Physiol
JT  - Clinical and experimental pharmacology & physiology
JID - 0425076
RN  - 0 (Hydroxydopamines)
RN  - 8HW4YBZ748 (Oxidopamine)
RN  - 9Y8NXQ24VQ (Propranolol)
RN  - EC 3.4.21.- (Kallikreins)
SB  - IM
MH  - Adrenal Medulla/physiology
MH  - Animals
MH  - Blood Pressure
MH  - Female
MH  - Hydroxydopamines
MH  - Kallikreins/*urine
MH  - Oxidopamine
MH  - Propranolol/pharmacology
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Stress, Physiological/physiopathology/*urine
MH  - Sympathectomy, Chemical
MH  - Sympathetic Nervous System/*physiology
MH  - Urinary Catheterization
EDAT- 1987/04/01 00:00
MHDA- 1987/04/01 00:01
CRDT- 1987/04/01 00:00
PHST- 1987/04/01 00:00 [pubmed]
PHST- 1987/04/01 00:01 [medline]
PHST- 1987/04/01 00:00 [entrez]
AID - 10.1111/j.1440-1681.1987.tb00974.x [doi]
PST - ppublish
SO  - Clin Exp Pharmacol Physiol. 1987 Apr;14(4):291-301. doi: 
      10.1111/j.1440-1681.1987.tb00974.x.