PMID- 2538181
OWN - NLM
STAT- MEDLINE
DCOM- 19890425
LR  - 20190510
IS  - 0007-1188 (Print)
IS  - 0007-1188 (Linking)
VI  - 96
IP  - 1
DP  - 1989 Jan
TI  - Decreased arterial responsiveness to multiple cyclic AMP-generating receptor 
      agonists in spontaneously hypertensive rats.
PG  - 227-35
AB  - 1. Arterial relaxant responses via beta-adrenoceptors are decreased in 
      spontaneously hypertensive rats (SHR) when compared with normotensive 
      Wistar-Kyoto rats (WKY). Recent studies from this laboratory proposed that a 
      reduced function of stimulatory guanosine 5'-triphosphate (GTP)-binding protein 
      (Gs) is responsible for the decreased beta-adrenoceptor responsiveness in the SHR 
      femoral artery. Since the Gs is common to all tissues, as opposed to receptors, 
      which are tissue specific, the reduced function of Gs should lead to resistance 
      to multiple receptors that act by activating adenylate cyclase (AC). To test this 
      hypothesis, relaxant responses via beta-adrenoceptors, A2-adenosine, H2-histamine 
      and D1-dopamine receptors were compared between arterial strips from 13 week-old 
      WKY and age-matched SHR. 2. The relaxant responses to noradrenaline (NA) via 
      beta-adrenoceptors in femoral, mesenteric, renal and carotid arteries were 
      significantly decreased in the SHR, when compared with the respective arteries 
      from WKY. 3. However, under the same conditions arterial relaxant responses to 
      forskolin, an activator of AC, were not significantly different between the WKY 
      and SHR. 4. The relaxant responses due to activation of A2-adenosine. 
      H2-histamine and D1-dopamine receptors were significantly decreased in the SHR 
      arteries. 5. Nitroprusside and nifedipine, agents which are independent of the 
      Gs.AC system, produced similar arterial relaxations in the WKY and SHR. 6. These 
      results support the hypothesis that a reduced function of Gs in the SHR is 
      responsible for the decreased arterial responsiveness to a variety of receptor 
      agonists whose mechanism of action involves AC activation.
FAU - Masuzawa, K
AU  - Masuzawa K
AD  - Department of Pharmacology, Nagoya City University Medical School, Japan.
FAU - Matsuda, T
AU  - Matsuda T
FAU - Asano, M
AU  - Asano M
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br J Pharmacol
JT  - British journal of pharmacology
JID - 7502536
RN  - 0 (Receptors, Adrenergic, beta)
RN  - 0 (Receptors, Dopamine)
RN  - 0 (Receptors, Dopamine D1)
RN  - 0 (Receptors, Histamine H2)
RN  - 0 (Receptors, Purinergic)
RN  - 169D1260KM (Nitroprusside)
RN  - 1F7A44V6OU (Colforsin)
RN  - E0399OZS9N (Cyclic AMP)
RN  - I9ZF7L6G2L (Nifedipine)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Animals
MH  - Carotid Arteries/drug effects
MH  - Colforsin/pharmacology
MH  - Cyclic AMP/*biosynthesis
MH  - Femoral Artery/drug effects
MH  - In Vitro Techniques
MH  - Male
MH  - Mesenteric Arteries/drug effects
MH  - Nifedipine/pharmacology
MH  - Nitroprusside/pharmacology
MH  - Norepinephrine/pharmacology
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Receptors, Adrenergic, beta/*drug effects
MH  - Receptors, Dopamine/drug effects
MH  - Receptors, Dopamine D1
MH  - Receptors, Histamine H2/drug effects
MH  - Receptors, Purinergic/drug effects
MH  - Renal Artery/drug effects
PMC - PMC1854328
EDAT- 1989/01/01 00:00
MHDA- 1989/01/01 00:01
PMCR- 1990/01/01
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]
PHST- 1990/01/01 00:00 [pmc-release]
AID - 10.1111/j.1476-5381.1989.tb11804.x [doi]
PST - ppublish
SO  - Br J Pharmacol. 1989 Jan;96(1):227-35. doi: 10.1111/j.1476-5381.1989.tb11804.x.