DEPRESSOR EFFECT OF INTRAVENTRICULAR ADMINISTRATION OF CALCIUM ON SPONTANEOUSLY HYPERTENSIVE RATS

Citation
S. Kusano et al., DEPRESSOR EFFECT OF INTRAVENTRICULAR ADMINISTRATION OF CALCIUM ON SPONTANEOUSLY HYPERTENSIVE RATS, Brain research, 618(1), 1993, pp. 63-70
Citations number
40
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
618
Issue
1
Year of publication
1993
Pages
63 - 70
Database
ISI
SICI code
0006-8993(1993)618:1<63:DEOIAO>2.0.ZU;2-M
Abstract
The role of central Ca2+ in the regulation of blood pressure (BP) was investigated in conscious spontaneously hypertensive (SHR) and Wistar- Kyoto rats (WKY). Ten mul of a high Ca2+ solution (Ca2+: 32.6 mM) admi nistered intracerebroventricularly (i.c.v.) decreased the mean arteria l pressure (MAP) for more than 20 min in SHR (n = 7, P < 0.005), while no change of MAP was observed in the WKY (n = 6). This depressor resp onse to Ca2+ i.c.v. was dose-dependent at Ca2+ concentrations between 16.3 and 65.2 mM. We also investigated the effect of high Ca2+ i.c.v. in SHR after pretreatment with Ca2+ channel blockers, diltiazem (60 mu g/10 mul) or nisoldipine (4, 8, 16 and 32 mug/10 mul), administered i. c.v., the autonomic ganglion blocker, hexamethonium (50 mg/kg), admini stered i.v. and alpha-methyl-p-tyrosine (100 and 400 mug/10 mul) deliv ered i.c.v. Pretreatment with i.c.v. diltiazem (n = 8) or nisoldipine (n = 5 for 8 mug, n = 6 for 4, 16, 32 mug) abolished and/or blunted th e decrease of MAP due to high Ca2+. Hexamethonium administered i.v. (n = 6) also canceled the depressor action of i.c.v. Ca2+. Pretreatment with 100 mug of i.c.v. alpha-methyl-p-tyrosine could not prevent the d epressor action of i.c.v. Ca2+; however, 400 mug of alpha-methyl-p-tyr osine administered i.c.v. abolished the effect of i.c.v. Ca2+. Further more Ca2+ channel blockers administered i.c.v. in themselves increased MAP in SHR (P < 0.05). These results suggest that central Ca2+ is inv olved in the central regulation of BP in SHR. This effect may be media ted through changes in sympathetic activity.