PMID- 34929695
OWN - NLM
STAT- MEDLINE
DCOM- 20220308
LR  - 20220308
IS  - 1423-0313 (Electronic)
IS  - 0031-7012 (Linking)
VI  - 107
IP  - 3-4
DP  - 2022
TI  - Soluble Guanylate Cyclase-Mediated Relaxation in Aortas from Rats with 
      Renovascular Hypertension.
PG  - 235-240
LID - 10.1159/000520655 [doi]
AB  - Soluble guanylate cyclase (sGC) plays an important role in nitric oxide 
      (NO)-mediated regulation of vascular tone; however, NO bioavailability is often 
      reduced in diseased blood vessels. Accumulating evidence suggests that a shift of 
      sGC from the NO-sensitive form to the NO-insensitive form could be an underlying 
      cause contributing to this reduction. Herein, we investigated the impact of 
      renovascular hypertension on NO-sensitive and NO-insensitive sGC-mediated 
      relaxation in rat aortas. Renovascular hypertension was induced by partially 
      clipping the left renal artery (2-kidneys, 1-clip; 2K1C) for 10 weeks. Systolic, 
      diastolic, and mean arterial pressures were significantly increased in the 2K1C 
      group when compared with the sham group. In addition, plasma thiobarbituric acid 
      reactive substances and aortic superoxide generation were significantly enhanced 
      in the 2K1C group when compared with those in the sham group. The vasorelaxant 
      response of isolated aortas to the sGC stimulator BAY 41-2272 (NO-sensitive sGC 
      agonist) was comparable between the sham and 2K1C groups. Likewise, the sGC 
      activator BAY 60-2770 (NO-insensitive sGC agonist)-induced relaxation did not 
      differ between the sham and 2K1C groups. In addition, the cGMP mimetic 8-Br-cGMP 
      (protein kinase G agonist) induced similar relaxation in both groups. 
      Furthermore, there were no differences in BAY 41-2272-stimulated and BAY 
      60-2770-stimulated cGMP generation between the groups. These findings suggest 
      that the balance between NO-sensitive and NO-insensitive forms of sGC is 
      maintained during renovascular hypertension. Therefore, sGC might not be 
      responsible for the reduced NO bioavailability observed during renovascular 
      hypertension.
CI  - (c) 2021 S. Karger AG, Basel.
FAU - Tawa, Masashi
AU  - Tawa M
AD  - Department of Pathological and Molecular Pharmacology, Faculty of Pharmacy, Osaka 
      Medical and Pharmaceutical University, Takatsuki, Japan.
FAU - Shimosato, Takashi
AU  - Shimosato T
AD  - Shiga University of Medical Science, Otsu, Japan.
FAU - Nakagawa, Keisuke
AU  - Nakagawa K
AD  - Department of Pathological and Molecular Pharmacology, Faculty of Pharmacy, Osaka 
      Medical and Pharmaceutical University, Takatsuki, Japan.
FAU - Okamura, Tomio
AU  - Okamura T
AD  - Shiga University of Medical Science, Otsu, Japan.
FAU - Ohkita, Mamoru
AU  - Ohkita M
AD  - Department of Pathological and Molecular Pharmacology, Faculty of Pharmacy, Osaka 
      Medical and Pharmaceutical University, Takatsuki, Japan.
LA  - eng
PT  - News
DEP - 20211220
PL  - Switzerland
TA  - Pharmacology
JT  - Pharmacology
JID - 0152016
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 4.6.1.2 (Guanylate Cyclase)
RN  - EC 4.6.1.2 (Soluble Guanylyl Cyclase)
RN  - H2D2X058MU (Cyclic GMP)
SB  - IM
MH  - Animals
MH  - Aorta
MH  - Cyclic GMP
MH  - *Guanylate Cyclase
MH  - *Hypertension, Renovascular
MH  - Nitric Oxide
MH  - Rats
MH  - Soluble Guanylyl Cyclase
OTO - NOTNLM
OT  - Renovascular hypertension
OT  - Soluble guanylate cyclase stimulator
OT  - Soluble guanylate cyclase; Soluble guanylate cyclase activator
OT  - Vasorelaxation
EDAT- 2021/12/21 06:00
MHDA- 2022/03/09 06:00
CRDT- 2021/12/20 20:32
PHST- 2021/09/02 00:00 [received]
PHST- 2021/10/31 00:00 [accepted]
PHST- 2021/12/21 06:00 [pubmed]
PHST- 2022/03/09 06:00 [medline]
PHST- 2021/12/20 20:32 [entrez]
AID - 000520655 [pii]
AID - 10.1159/000520655 [doi]
PST - ppublish
SO  - Pharmacology. 2022;107(3-4):235-240. doi: 10.1159/000520655. Epub 2021 Dec 20.