J. Josko et al., ATRIAL-NATRIURETIC-PEPTIDE SECRETION FOLLOWING SUBARACHNOID HEMORRHAGE IN SPONTANEOUSLY HYPERTENSIVE RATS, Journal of Physiology and Pharmacology, 47(4), 1996, pp. 641-648
Atrial natriuretic peptide (ANP) is released excessively in spontaneou
sly hypertensive rats (SHR), and vasodepression is its main effect on
the blood vessels. The aim of the study was to investigate the changes
in ANP secretion in the cerebral vasospasm following subarachnoid hem
orrhage (SAH) in SHRs. The SAH was induced by the injection of 100 mu
l Of unheparinized, autologous blood into the cerebrospinal fluid (CSF
), via a canule formerly inserted into the cisterna magna (CM). In the
sham SAH group the SAH was imitated with 0.9% saline injection. The c
oncentrations of ANP in the blood samples obtained in the acute and ch
ronic stages of vasospasm were radioimmunoassayed with commercial RIA
kits (Peninsula RIK 9103). It was found that both SAH and sham SAH ind
uced a significant increase in plasma ANP in the chronic phase of vaso
spasm. No such changes were observed in the acute phase. This shows th
at the chronic cerebral vasopasm following SAH considerably enhances t
he ANP secretion in SHRs, probably through the increased endothelin re
lease. These compensatory and regulatory mechanisms help prevent the d
evelopment of brain oedema and the progression of vasopasm through sec
ondary vasodilation.