[The contribution of endogenous vasodilators to the control of glomerular hemodynamics].
Preglomerular afferent (Af-) and postglomerular efferent arterioles (Ef-Arts) are crucial vascular segments in the control of glomerular hemodynamics. However, their vascular reactivity is not fully understood. We examined: 1) their responses to angiotensin II (AII) or norepinephrine (NE), and 2) the possible modulatory roles of nitric oxide (NO) and prostaglandins (PGs) in these responses. Rabbit Af- or Ef-Arts were microperfused in vitro. Ef-Arts were perfused in either the orthograde direction from the distal end of Af-Arts through the glomerulus (OP) or the retrograde direction from its distal end to eliminate the influence of the glomerulus (RP). Although AII and NE constricted both arterioles in a dose-dependent manner, sensitivity to AII was higher in Ef-Arts. AII began to cause significant (P < 0.01) constriction from 10(-9) M (11 +/- 3%, n = 11) in Af-Arts, and from 10(-11) M in Ef-Arts (OP; 11 +/- 4%, n = 9. RP; 10 +/- 2%, n = 5). In addition, both AII and NE produced stronger constriction of Ef-Arts in RP than OP; AII at 10(-8) M or NE at 10(-6) M decreased the diameter by 35 +/- 4% or 25 +/- 4% in OP and 74 +/- 4% or 62 +/- 7% in RP. NO synthesis inhibitor nitro-L-arginine (L-NAME; 10(-4) M) increased the sensitivity of Af-Art to AII without affecting the reactivity of Ef-Art; in L-NAME-pretreated Af-Arts, AII began to cause significant constriction from 10(-10) M (14 +/- 4%, n = 9, P < 0.01). Thus, L-NAME-pretreatment significantly decreased the differences in sensitivity to AII between Af- and Ef-Arts without affecting different vascular responses between OP and RP. Indomethacin (5 x 10(-5) M) significantly augmented the AII- or NE-induced Ef-Art constriction only in OP; AII at 10(-8) M or NE at 10(-6) M decreased the diameter by 72 +/- 5% (n = 8) or 48 +/- 3% (n = 7). Thus, indomethacin-pretreatment markedly diminished the differences in responses between OP and RP. These results suggest that 1) NO modulates AII action only in the Af-Art, contributing to the difference in sensitivity to AII between Af- and Ef-Art, and 2) the glomerulus controls vascular reactivity of the downstream Ef-Art by releasing PGs.
Arima
S
S
Department of Clinical Biology and Hormonal Regulation, Tohoku University School of Medicine, Sendai, Japan.
Ito
S
S
Abe
K
K
D000804:Angiotensin II / Q000494:pharmacology / Q000502:physiology*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D006439:Hemodynamics / Q000187:drug effects; D066298:In Vitro Techniques; D007678:Kidney Glomerulus / Q000098:blood supply*; D008297:Male; D009569:Nitric Oxide / Q000494:pharmacology / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology / Q000502:physiology*; D010477:Perfusion; D011453:Prostaglandins / Q000494:pharmacology / Q000502:physiology*; D011817:Rabbits; D014664:Vasodilation / Q000502:physiology*
D011453:Prostaglandins; D000804:Angiotensin II; D009569:Nitric Oxide; D009638:Norepinephrine