PMID- 10622216
OWN - NLM
STAT- MEDLINE
DCOM- 20000127
LR  - 20190725
IS  - 0021-5198 (Print)
IS  - 0021-5198 (Linking)
VI  - 81
IP  - 3
DP  - 1999 Nov
TI  - Centrally produced neuronal nitric oxide in the control of baroreceptor reflex 
      sensitivity and blood pressure in normotensive and spontaneously hypertensive 
      rats.
PG  - 279-85
AB  - We studied the effect of chronic nitric oxide synthase (NOS) blockade in the 
      brain on mean arterial pressure [MAP (mmHg)], heart rate [HR (bpm)] and 
      baroreceptor reflex sensitivity [BRS (mean slope: bpm/mmHg)] in Wistar-Kyoto 
      (WKY) and spontaneously hypertensive rats (SHR). Intracerebroventricular (i.c.v.) 
      infusion of the nonselective NOS inhibitor N-Nitro-L-arginine-methylester 
      (L-NAME) (50 microg/kg per day, 11-12 days) increased MAP in WKY and SHR 
      (125+/-2.1 vs 118+/-1.1 controls, P<0.01 and 179+/-3.59 vs 156+/-4.0 controls, 
      P<0.001, respectively) without affecting HR. In L-NAME-treated WKY, BRS to 
      bradycardia was suppressed (-0.79+/-0.09 vs -1.76+/-0.17 controls, P=0.001), 
      whereas in SHR, L-NAME did not affect BRS to bradycardia. BRS to tachycardia 
      remained unaffected in either strain. In WKY, 7-nitroindazole (7-NI x Na+) (34 
      microg i.c.v./kg per day, 11-12 days), a selective nNOS inhibitor, did not affect 
      MAP or HR, but BRS to bradycardia and tachycardia was decreased (-0.37+/-0.20 vs 
      -0.97+/-0.41 controls, P<0.01 and -1.78+/-0.20 vs -2.52+/-0.40 controls, P=0.05, 
      respectively). In SHR, the same dose of 7-NI x Na+ increased resting MAP 
      (171+/-5.00 vs 150+/-7.00 controls, P<0.05) without affecting HR or BRS to 
      bradycardia or tachycardia. Thus in WKY, BRS to acute changes in systemic blood 
      pressure (BP) is regulated by NO produced by nNOS in the brain, serving as a 
      neurotransmitter in sympathetic and parasympathetic efferent pathways. In SHR, 
      systemic BP is regulated in part by NO released by the type I NOS isoenzyme in 
      the brain.
FAU - Qadri, F
AU  - Qadri F
AD  - Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, MI 
      48202-2689, USA.
FAU - Carretero, O A
AU  - Carretero OA
FAU - Scicli, A G
AU  - Scicli AG
LA  - eng
GR  - HL 28982-15/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Japan
TA  - Jpn J Pharmacol
JT  - Japanese journal of pharmacology
JID - 2983305R
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Indazoles)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type I)
RN  - EC 1.14.13.39 (Nos1 protein, rat)
RN  - UX0N37CMVH (7-nitroindazole)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
SB  - IM
MH  - Animals
MH  - Baroreflex/drug effects/physiology
MH  - Blood Pressure/drug effects/*physiology
MH  - Brain/drug effects/enzymology
MH  - Enzyme Inhibitors/administration & dosage/pharmacology
MH  - Heart Rate/drug effects
MH  - Indazoles/administration & dosage/pharmacology
MH  - Injections, Intraventricular
MH  - NG-Nitroarginine Methyl Ester/administration & dosage/pharmacology
MH  - Nitric Oxide Synthase/antagonists & inhibitors/biosynthesis/*physiology
MH  - Nitric Oxide Synthase Type I
MH  - Pressoreceptors/*physiology
MH  - Rats
MH  - Rats, Inbred SHR
EDAT- 2000/01/06 00:00
MHDA- 2000/01/06 00:01
CRDT- 2000/01/06 00:00
PHST- 2000/01/06 00:00 [pubmed]
PHST- 2000/01/06 00:01 [medline]
PHST- 2000/01/06 00:00 [entrez]
AID - 10.1254/jjp.81.279 [doi]
PST - ppublish
SO  - Jpn J Pharmacol. 1999 Nov;81(3):279-85. doi: 10.1254/jjp.81.279.