PMID- 37511174
OWN - NLM
STAT- MEDLINE
DCOM- 20230807
LR  - 20230807
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 24
IP  - 14
DP  - 2023 Jul 13
TI  - Interaction of Angiotensin II AT1 Receptors with Purinergic P2X Receptors in 
      Regulating Renal Afferent Arterioles in Angiotensin II-Dependent Hypertension.
LID - 10.3390/ijms241411413 [doi]
LID - 11413
AB  - In angiotensin II (Ang II)-dependent hypertension, Ang II activates angiotensin 
      II type 1 receptors (AT1R) on renal vascular smooth muscle cells, leading to 
      renal vasoconstriction with eventual glomerular and tubular injury and 
      interstitial inflammation. While afferent arteriolar vasoconstriction is 
      initiated by the increased intrarenal levels of Ang II activating AT1R, the 
      progressive increases in arterial pressure stimulate the paracrine secretion of 
      adenosine triphosphate (ATP), leading to the purinergic P2X receptor 
      (P2XR)-mediated constriction of afferent arterioles. Thus, the afferent 
      arteriolar tone is maintained by two powerful systems eliciting the co-existing 
      activation of P2XR and AT1R. This raises the conundrum of how the AT1R and P2XR 
      can both be responsible for most of the increased renal afferent vascular 
      resistance existing in angiotensin-dependent hypertension. Its resolution implies 
      that AT1R and P2XR share common receptor or post receptor signaling mechanisms 
      which converge to maintain renal vasoconstriction in Ang II-dependent 
      hypertension. In this review, we briefly discuss (1) the regulation of renal 
      afferent arterioles in Ang II-dependent hypertension, (2) the interaction of AT1R 
      and P2XR activation in regulating renal afferent arterioles in a setting of 
      hypertension, (3) mechanisms regulating ATP release and effect of angiotensin II 
      on ATP release, and (4) the possible intracellular pathways involved in AT1R and 
      P2XR interactions. Emerging evidence supports the hypothesis that P2X1R, P2X7R, 
      and AT1R actions converge at receptor or post-receptor signaling pathways but 
      that P2XR exerts a dominant influence abrogating the actions of AT1R on renal 
      afferent arterioles in Ang II-dependent hypertension. This finding raises 
      clinical implications for the design of therapeutic interventions that will 
      prevent the impairment of kidney function and subsequent tissue injury.
FAU - Kulthinee, Supaporn
AU  - Kulthinee S
AD  - Department of Physiology, Hypertension and Renal Center of Excellence, Tulane 
      University School of Medicine, New Orleans, LA 70112, USA.
FAU - Tasanarong, Adis
AU  - Tasanarong A
AD  - Chulabhorn International College of Medicine, Thammasat University, Klong Luang 
      12120, Thailand.
FAU - Franco, Martha
AU  - Franco M
AUID- ORCID: 0000-0003-4073-524X
AD  - Department of Cardio-Renal Physiopathology, Instituto Nacional de Cardiologia 
      "Ignacio Chavez", Mexico City 14080, Mexico.
FAU - Navar, Luis Gabriel
AU  - Navar LG
AUID- ORCID: 0000-0002-3777-7564
AD  - Department of Physiology, Hypertension and Renal Center of Excellence, Tulane 
      University School of Medicine, New Orleans, LA 70112, USA.
LA  - eng
GR  - NIGMS; CoBRE P30GM103337/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20230713
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - 11128-99-7 (Angiotensin II)
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Receptors, Angiotensin)
RN  - 0 (Receptors, Purinergic P2X)
SB  - IM
MH  - Humans
MH  - Adenosine Triphosphate/metabolism
MH  - *Angiotensin II/metabolism
MH  - Arterioles/metabolism
MH  - *Hypertension/metabolism
MH  - *Kidney/blood supply
MH  - *Receptor, Angiotensin, Type 1/metabolism
MH  - Receptors, Angiotensin/metabolism
MH  - *Receptors, Purinergic P2X/metabolism
PMC - PMC10380633
OTO - NOTNLM
OT  - AT1 receptors
OT  - P2X receptors
OT  - afferent arteriole
OT  - angiotensin II infusions
OT  - hypertension
COIS- The authors declare no conflict of interest.
EDAT- 2023/07/29 11:45
MHDA- 2023/07/31 06:43
PMCR- 2023/07/13
CRDT- 2023/07/29 01:22
PHST- 2023/06/02 00:00 [received]
PHST- 2023/07/09 00:00 [accepted]
PHST- 2023/07/31 06:43 [medline]
PHST- 2023/07/29 11:45 [pubmed]
PHST- 2023/07/29 01:22 [entrez]
PHST- 2023/07/13 00:00 [pmc-release]
AID - ijms241411413 [pii]
AID - ijms-24-11413 [pii]
AID - 10.3390/ijms241411413 [doi]
PST - epublish
SO  - Int J Mol Sci. 2023 Jul 13;24(14):11413. doi: 10.3390/ijms241411413.