PMID- 1877671
OWN - NLM
STAT- MEDLINE
DCOM- 19910923
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 261
IP  - 2 Pt 2
DP  - 1991 Aug
TI  - Activation of brain adenosine receptors evokes vasodilation in skin arterioles.
PG  - H457-62
AB  - Metabolically stable adenosine (ADO) agonists were infused into cannulas 
      chronically implanted in the lateral cerebral ventricle intracerebroventricularly 
      (icv) while responses in skin microcirculation of pentobarbital-anesthetized 
      hamsters were observed with intravital microscopy. Cyclohexyladenosine (CHA; 
      A1-receptor selective; 0.0001-1 pmol) and N-ethylcarboxoamidoadenosine (NECA; 
      A2-receptor selective; 0.01-0.05 pmol) were delivered in 10 microliters of 
      bicarbonate-buffered Ringer vehicle. Mean systemic arterial blood pressure, heart 
      rate, skin arteriolar diameter, and red blood cell velocity were continuously 
      monitored. Blood flow was calculated from measurements of arteriolar diameter 
      (20-40 microns) and red blood cell velocity. CHA icv caused dose-related 
      decreases in blood pressure and heart rate, as well as increases in cutaneous 
      perfusion. Comparable amounts of CHA administered intravenously evoked no 
      response. Pretreatment with an A1-selective antagonist xanthine amine congener 
      (XAC, 5 pmol icv or 1 mg/kg iv) had no effect on the depressor response but 
      antagonized the bradycardia. In contrast, a nonselective antagonist 
      8-phenyltheophylline (8pTHEO, 5 pmol icv or 0.3 mg/kg iv) had no effect on the 
      bradycardia but attenuated the depressor response. By either route, both 
      antagonists prevented the cutaneous microcirculatory responses evoked by icv CHA. 
      NECA icv produced hypotension but no change in the skin, and the depressor 
      response was not altered by icv XAC. These observations provide direct evidence 
      that chemical stimulation of central nervous system (CNS) ADO receptors is linked 
      to a cutaneous vascular response that can be dissociated from other 
      cardiorespiratory depressant actions of CNS ADO.
FAU - Proctor, K G
AU  - Proctor KG
AD  - Department of Physiology, University of Tennessee Health Science Center, Memphis 
      38163.
FAU - Stojanov, I
AU  - Stojanov I
FAU - Bealer, S L
AU  - Bealer SL
LA  - eng
GR  - HL-25877/HL/NHLBI NIH HHS/United States
GR  - HL-30663/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  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Receptors, Purinergic)
RN  - 0 (Vasodilator Agents)
RN  - 0 (Xanthines)
RN  - 35920-39-9 (Adenosine-5'-(N-ethylcarboxamide))
RN  - 36396-99-3 (N(6)-cyclohexyladenosine)
RN  - 96865-92-8 
      (8-(4-((2-aminoethyl)aminocarbonylmethyloxy)phenyl)-1,3-dipropylxanthine)
RN  - C137DTR5RG (Theophylline)
RN  - E6M543P3BL (8-phenyltheophylline)
RN  - K72T3FS567 (Adenosine)
SB  - IM
MH  - Adenosine/analogs & derivatives/pharmacology
MH  - Adenosine-5'-(N-ethylcarboxamide)
MH  - Animals
MH  - Arterioles/physiology
MH  - Brain/*metabolism
MH  - Cricetinae
MH  - Injections, Intraventricular
MH  - Male
MH  - Mesocricetus
MH  - Receptors, Purinergic/*physiology
MH  - Skin/*blood supply
MH  - Theophylline/analogs & derivatives/pharmacology
MH  - Vasodilation/*physiology
MH  - Vasodilator Agents/pharmacology
MH  - Xanthines/pharmacology
EDAT- 1991/08/01 00:00
MHDA- 1991/08/01 00:01
CRDT- 1991/08/01 00:00
PHST- 1991/08/01 00:00 [pubmed]
PHST- 1991/08/01 00:01 [medline]
PHST- 1991/08/01 00:00 [entrez]
AID - 10.1152/ajpheart.1991.261.2.H457 [doi]
PST - ppublish
SO  - Am J Physiol. 1991 Aug;261(2 Pt 2):H457-62. doi: 
      10.1152/ajpheart.1991.261.2.H457.