PMID- 2693290
OWN - NLM
STAT- MEDLINE
DCOM- 19900312
LR  - 20191022
IS  - 0767-3981 (Print)
IS  - 0767-3981 (Linking)
VI  - 3 Suppl
DP  - 1989
TI  - Central cardiovascular effects of dihydropyridines in spontaneously hypertensive 
      rats.
PG  - 47s-56s
AB  - Intracerebroventricular (i.c.v.) injections of dihydropyridine derivatives 
      calcium channel agonist (BAY K8644) and antagonist (nifedipine, nicardipine, PN 
      200-110) induced opposite long-lasting changes in blood pressure (BP) in 
      pentobarbital anesthetized spontaneously hypertensive rats (SMR). I.c.v. 
      nifedipine (NIF), nicardipine (NIC), and PN 200-110 decreased mean blood pressure 
      dose-dependently and stereoselectively, (+) NIC and (+) PN being 8 and 3 times 
      more potent than their (-) isomers, respectively. The decrease in BP was due to a 
      withdrawal of the sympathetic tone, since NIF- and NIC-induced falls in BP were 
      suppressed after either hexamethonium (HXM), 6 OHDA or bilateral adrenalectomy. 
      I.c.v. BAY K8644 increased BP dose-dependently. The i.c.v. BAY K8644-induced 
      hypertensive effect was inhibited: a), by NIF and (+) PN but not by (-) PN, 
      therefore probably occurring at central DHP sites; b), by HXM and reserpine, thus 
      probably mediated by an increase in sympathetic tone; c) by i.c.v. methylatropine 
      (MA) while i.v. MA and i.c.v. HXM had no inhibitory effect, thus probably 
      involving central muscarinic sites. In SHR, NIC did not after the K(+)-evoked ACh 
      release but suppressed the BAY K8644-induced increase in ACh release. In 
      anesthetized normotensive control rats (WKY), neither i.c.v. NIF, NIC or BAY 
      increased BP and HR while, in conscious SHR it decreased BP without any change in 
      HR. These data increased BP and HR while, in conscious SHR it decreased BP 
      without any change in HR. These data suggest that central DHP sites may be 
      involved in the cholinergic transmission and may participate in genetic 
      hypertension via sympathetic tone.
FAU - Laurent, S
AU  - Laurent S
AD  - Laboratoire de Neuropharmacologie Cardio-Vasculaire et INSERM U228, Paris, 
      France.
FAU - Brisac, A M
AU  - Brisac AM
FAU - Champeroux, P
AU  - Champeroux P
FAU - Lacolley, P
AU  - Lacolley P
FAU - Huguet, F
AU  - Huguet F
FAU - Legrand, M
AU  - Legrand M
FAU - Lucet, B
AU  - Lucet B
FAU - Tsoucaris, D
AU  - Tsoucaris D
FAU - Briand, V
AU  - Briand V
FAU - Schmitt, H
AU  - Schmitt H
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Fundam Clin Pharmacol
JT  - Fundamental & clinical pharmacology
JID - 8710411
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Dihydropyridines)
SB  - IM
MH  - Animals
MH  - Calcium Channel Blockers/*pharmacology
MH  - Dihydropyridines/*pharmacology
MH  - Hemodynamics/*drug effects
MH  - Hypertension/genetics/*physiopathology
MH  - Rats
MH  - Rats, Inbred SHR
RF  - 38
EDAT- 1989/01/01 00:00
MHDA- 1989/01/01 00:01
CRDT- 1989/01/01 00:00
PHST- 1989/01/01 00:00 [pubmed]
PHST- 1989/01/01 00:01 [medline]
PHST- 1989/01/01 00:00 [entrez]
AID - 10.1111/j.1472-8206.1989.tb00474.x [doi]
PST - ppublish
SO  - Fundam Clin Pharmacol. 1989;3 Suppl:47s-56s. doi: 
      10.1111/j.1472-8206.1989.tb00474.x.