PMID- 8735636
OWN - NLM
STAT- MEDLINE
DCOM- 19961016
LR  - 20190512
IS  - 0007-1188 (Print)
IS  - 0007-1188 (Linking)
VI  - 118
IP  - 2
DP  - 1996 May
TI  - The mechanism of relaxation induced by atrial natriuretic peptide in the porcine 
      renal artery.
PG  - 343-51
AB  - 1. The mechanisms underlying the relaxation of the porcine renal artery induced 
      by atrial natriuretic peptide (ANP) were investigated, using front-surface 
      fluorimetry with fura-2 and receptor-coupled permeabilization by alpha-toxin. 2. 
      ANP decreased the cytosolic Ca2+ concentration ([Ca2+]i) and tension during the 
      contraction induced by a high external K+ solution, in a concentration-dependent 
      manner. This ANP-induced decrease in [Ca2+]i during the contraction induced by 
      high K+ solution was composed of two phases, an initial rapid phase, followed by 
      a maintenance phase. The initial rapid decrease in [Ca2+]i, but not the 
      maintained decrease in [Ca2+]i, was inhibited when the tissue was treated with 
      thapsigargin, a selective Ca2+ pump inhibitor of the sarcoplasmic reticulum. When 
      the tissues were treated with thapsigargin and external Ca2+ was replaced by 
      Ba2+, which cannot be transported by the Ca2+ pump, ANP did not induce a decrease 
      in [Ba2+]i, even though the elevation of tension induced by Ba2+ was strongly 
      inhibited. 3. In the absence of extracellular Ca2+, ANP inhibited the release of 
      Ca2+ from the intracellular store induced by noradrenaline (NA). 4. The [Ca2+]i 
      (abscissa scale)-tension (ordinate scale) relationship observed during the 
      contraction induced by various concentrations of high external K+ solution was 
      shifted downwards by the addition of 10(-8) M ANP, indicating that, at any given 
      [Ca2+]i, the tension generated by high K+ solution was considerably inhibited by 
      the addition of 10(-8) M ANP. The [Ca2+]i-tension curve of the contraction 
      obtained by the cumulative application of external Ca2+ (0-3.75 mM) during 
      depolarization with 118 mM K+ solution was shifted to the left by 3 x 10(-7) M 
      NA. This NA-induced [Ca2+]i-tension relationship was shifted to the right by 
      10(-8) M ANP, indicating that the ANP-induced reduction of Ca(2+)-sensitivity 
      operates during the contraction induced by NA. 5. In alpha-toxin-permeabilized 
      preparations, ANP induced relaxation of tissues precontracted with a mixture of 3 
      x 10(-7) M Ca2+, 10(-5) M guanosine 5'-triphosphate (GTP) and 10(-6) M NA. Thus a 
      component of ANP-induced relaxation took place by way of a reduction in the Ca2+ 
      sensitivity of the myofilaments, independent of changes in [Ca2+]i. 6. These 
      results indicate that ANP induces relaxation of the porcine renal artery by: (1) 
      reducing [Ca2+]i mainly via the activation of the Ca2+ pumps located on the 
      sarcoplasmic reticulum and sarcolemma, as well as via inhibition of 
      agoinist-induced release of Ca2+ from the intracellular store; and (2) decreasing 
      the Ca(2+)-sensitivity of the contractile elements.
FAU - Seguchi, H
AU  - Seguchi H
AD  - Division of Molecular Cardiology, Faculty of Medicine, Kyushu University, 
      Fukuoka, Japan.
FAU - Nishimura, J
AU  - Nishimura J
FAU - Toyofuku, K
AU  - Toyofuku K
FAU - Kobayashi, S
AU  - Kobayashi S
FAU - Kumazawa, J
AU  - Kumazawa J
FAU - Kanaide, H
AU  - Kanaide H
LA  - eng
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 (Solutions)
RN  - 85637-73-6 (Atrial Natriuretic Factor)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - RWP5GA015D (Potassium)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Atrial Natriuretic Factor/*pharmacology
MH  - Calcium/metabolism
MH  - In Vitro Techniques
MH  - Muscle Relaxation/drug effects
MH  - Potassium/chemistry
MH  - Renal Artery/*drug effects/metabolism/physiology
MH  - Solutions
MH  - Swine
MH  - Type C Phospholipases/pharmacology
PMC - PMC1909626
EDAT- 1996/05/01 00:00
MHDA- 1996/05/01 00:01
PMCR- 1997/05/01
CRDT- 1996/05/01 00:00
PHST- 1996/05/01 00:00 [pubmed]
PHST- 1996/05/01 00:01 [medline]
PHST- 1996/05/01 00:00 [entrez]
PHST- 1997/05/01 00:00 [pmc-release]
AID - 10.1111/j.1476-5381.1996.tb15408.x [doi]
PST - ppublish
SO  - Br J Pharmacol. 1996 May;118(2):343-51. doi: 10.1111/j.1476-5381.1996.tb15408.x.