Distinct modulation of superficial and juxtamedullary arterioles by prostaglandin in vivo.
Renal afferent (AFF) and efferent arteriolar (EFF) responsiveness to angiotensin II (ANG II) in superficial and juxtamedullary nephrons in vivo remains undetermined, nor has it been clarified what role intrarenal autocrines/paracrines play in modulating the renal microvascular response. The present study characterized the responsiveness to ANG II (1-30 ng/kg/min) of AFF and EFF of canine superficial and juxtamedullary nephrons under pentobarbital anesthesia, using intravital CCD-videomicroscopy that allowed direct in vivo visualization of the renal microcirculation. Furthermore, the effect of prostaglandins (PG) and nitric oxide (NO) on ANG II-induced tone was examined. In superficial nephrons, ANG II induced a similar dose-dependent constriction of both AFF (46 +/- 5% constriction) and EFF (53 +/- 3%). In juxtamedullary arterioles, ANG II induced a dose-dependent constriction of EFF, whereas AFF responses were diminished (17 +/- 4% vs. 37 +/- 4% at 10 ng/kg/min). The PG inhibition by indomethacin enhanced the ANG II-induced constriction of juxtamedullary AFF, whereas no augmentation was observed in other arterioles. In contrast, NO inhibition by nitro-L-arginine methylester (L-NAME) enhanced the ANG II-induced constriction, with greater augmentation in juxtamedullary AFF and EFF. Finally, renal interstitial PG and nitrite/nitrate contents were greater in the medulla than the superficial cortex under basal and ANG II-stimulated conditions. Taken together, the results of the intravital CCD-videomicroscopy reveal that the renal microvascular action of ANG II had both zonal (juxtamedullary vs. superficial nephrons) and segmental (AFF vs. EFF) heterogeneity under the present experimental conditions. This heterogeneity was associated with a difference in the intrarenal production of prostaglandin E2 (PGE2) and NO; PGE2 contributed to segmental and zonal differences whereas NO was responsible for the zonal heterogeneity in arteriolar responsiveness.
Matsuda
Hiroto
H
Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Hayashi
Koichi
K
Arakawa
Koki
K
Kubota
Eiji
E
Honda
Masanori
M
Tokuyama
Hirobumi
H
Suzuki
Hiromichi
H
Yamamoto
Tokunori
T
Kajiya
Fumihiko
F
Saruta
Takao
T
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000502:physiology; D015232:Dinoprostone / Q000378:metabolism; D004285:Dogs; D007668:Kidney / Q000378:metabolism; D007679:Kidney Medulla / Q000098:blood supply*; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D009399:Nephrons / Q000098:blood supply*; D009566:Nitrates / Q000378:metabolism; D009569:Nitric Oxide / Q000502:physiology; D009573:Nitrites / Q000378:metabolism; D011453:Prostaglandins / Q000502:physiology*; D012079:Renal Circulation / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects
D009566:Nitrates; D009573:Nitrites; D011453:Prostaglandins; D000804:Angiotensin II; D009569:Nitric Oxide; D015232:Dinoprostone