Autoradiographic Identification of Kidney Angiotensin IV Binding Sites and Angiotensin IV-Induced Renal Cortical Blood Flow Changes in Rats

Coleman, John K.M.; Krebs, Luke T.; Hamilton, T. A.; Ong, B. Y.; Lawrence, Kendra Ak; Sardinia, Michael F.; Harding, Joseph W.; Wright, John W.

doi:10.1016/s0196-9781(97)00291-x

Cited by 92 publications

(74 citation statements)

References 31 publications

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“…The vasodilator effect of Ang II could be modulated by Ang IV, a vasodilator component of the renin-angiotensin system (Haberl et al, 1991;Coleman et al, 1998;Patel et al, 1998). Alternatively, Ang II could be metabolized to Ang IV by aminopeptidase A and aminopeptidase M. However, our results demonstrate that Ang IV most likely does not participate in the vasodilator effects of Ang II, since its vasodilator effect is much smaller than the vasodilator effect of Ang II.…”

Section: Rs De Moura Et Al Angiotensin Ii-dependent Vasodilation 863mentioning

confidence: 60%

The role of bradykinin, AT₂ and angiotensin 1–7 receptors in the EDRF‐dependent vasodilator effect of angiotensin II on the isolated mesenteric vascular bed of the rat

Moura

Resende

Emiliano

et al. 2004

British J Pharmacology

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1 The mechanisms involved in the vasodilator actions of angiotensin II (Ang II) have not yet been completely elucidated. We investigated the potential mechanisms that seem to be involved in the Ang II vasodilator effect using rat isolated mesenteric vascular bed (MVB). 2 Under basal conditions, Ang II does not affect the perfusion pressure of MVB. However, in vessels precontracted with norepinephrine, Ang II induces vasodilation followed by vasoconstriction. Vasoconstrictor, but not the vasodilation of Ang II, is inhibited by AT 1 antagonist (losartan). The vasodilator effect of Ang II was not inhibited by AT 2 , angiotensin IV and angiotensin 1-7 receptor antagonists alone (PD 123319, divalinal, A 779, respectively). 3 The vasodilator effect of Ang II is significantly reduced by endothelial removal (deoxycholic acid), but not by indomethacin. Inhibition of NO-synthase by N G -nitro-L-arginine methyl ester (L-NAME) and guanylyl cyclase by 1H-[1,2,3] oxadiazolo [4,4-a] quinoxalin-1-one (ODQ) reduces the vasodilator effect of Ang II. This effect is also reduced by tetraethylammonium (TEA) or L-NAME, and a combination of L-NAME plus TEA increases the inhibitory effect of the antagonists alone. However, indomethacin does not change the residual vasodilator effect observed in vessels pretreated with L-NAME plus TEA. 4 In vessels precontracted with norepinephrine and depolarized with KCl 25 mM or treated with Ca 2 þ -dependent K þ channel blockers (charybdotoxin plus apamin), the effect of Ang II was significantly reduced. However, this effect is not affected by ATP and voltage-dependent K þ channel blockers (glybenclamide and 4-aminopyridine). 5 Inhibition of kininase II with captopril significantly potentiates the vasodilator effect of bradykinin (BK) and Ang II in the rat MVB. The inhibitory effect of the B 2 receptor antagonist HOE 140 on the vasodilator effect of Ang II is further enhanced by PD 123319 and/or A 779.

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Section: Rs De Moura Et Al Angiotensin Ii-dependent Vasodilation 863mentioning

confidence: 60%

The role of bradykinin, AT₂ and angiotensin 1–7 receptors in the EDRF‐dependent vasodilator effect of angiotensin II on the isolated mesenteric vascular bed of the rat

Moura

Resende

Emiliano

et al. 2004

British J Pharmacology

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“…The affinity of Ang IV for the AT 1 and AT 2 receptors was small using SMC and HU (0.26 and 0.06 mol, respectively) [8]. Using brain membranes, Ang IV was also reported to have weak affinity for the Ang II receptor [2], Ang IV has been suggested to play a role in regulating local blood flows [5] and Ang 2-10 seems to have some opposite actions to Ang II [18]. The present hypothesis considers a coordinated action of the different peptides of the system.…”

Section: Introductionmentioning

confidence: 99%

Angiotensinase activities in the kidney of renovascular hypertensive rats

et al. 2003

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In spite of the well-known contribution of angiotensin II (Ang II) in the pathogenesis of Goldblatt two-kidney one clip (G2K1C) hypertension, the importance of other Ang peptides, such as Ang III, Ang IV or Ang 2-10, is scarcely understood. The functional status of these peptides depends on the action of several aminopeptidases called angiotensinases. The metabolism of Ang III to Ang IV by aminopeptidase M (AlaAP) and of Ang I to Ang 2-10 by aspartyl aminopeptidase (AspAP) was evaluated in the renal cortex and medulla of normotensive (Sham-operated) and hypertensive (G2K1C) rats, treated or not with the AT 1 receptor antagonist valsartan. The results demonstrated a highly significant increase of membrane-bound (MEMB) AlaAP in the cortex of the non-ischemic kidney of G2K1C rats compared with the kidney of normal rats and with the clipped kidney of G2K1C rats. This suggests an increased formation of Ang IV in the non-clipped kidney of G2R1C rats. Valsartan reduced MEMB AlaAP and AspAP activities in the renal cortex of normotensive and in the clipped kidney of hypertensive rats. The reduced metabolism of Ang III may prolong its half-life in valsartan-treated animals. These results suggest a role for AlaAP in renovascular hypertension. In addition, the higher AspAP activity of the renal cortex compared to medulla reflects its relative functional difference between both locations.

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“…L-NAME, an NO synthase inhibitor, also blocked this vasodilator response. 60 In the same line, studies on the pulmonary and cerebral vasculature also suggested that Ang IV produced an endothelium-dependent vasodilatation associated with increased endothelial NO and cGMP production. [127][128][129] In addition, Ang IV was reported to promote the release of vasodilating prostaglandins.…”

Section: Angiotensin II At 1 and At 2 Receptorsmentioning

confidence: 95%

“…44,47,62,125 Studies on the effects of Ang IV in the kidney have yielded conflicting results. Infusion of Ang IV directly in renal arteries was reported to increase renal CBF in anesthetized rats as measured by laser Doppler flowmetry, 60,126 an effect blocked by the specific 'AT 4 receptor' antagonist, Divalinal-Ang IV, but not by selective AT 1 and AT 2 receptor antagonists. L-NAME, an NO synthase inhibitor, also blocked this vasodilator response.…”

Section: Angiotensin II At 1 and At 2 Receptorsmentioning

confidence: 97%

“…55,56 AT 1 receptor-mediated renal effects of Ang II Systemic administration 57 and i.r. administration [58][59][60][61] of Ang II produced dose-dependent decreases in total renal blood flow (RBF) and renal cortical blood flow (CBF), and increases in renal vascular resistance and renal cortical vascular resistance, which were blocked by AT 1 receptor antagonists. 47,62 Within the microvasculature, Ang II constricted both the afferent and efferent arterioles, 63,64 although the efferent arterioles are much more sensitive.…”

Section: Angiotensin II At 1 and At 2 Receptorsmentioning

confidence: 99%

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Blood pressure and renal hemodynamic effects of angiotensin fragments

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Dupont³

2011

Hypertens Res

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Autoradiographic Identification of Kidney Angiotensin IV Binding Sites and Angiotensin IV-Induced Renal Cortical Blood Flow Changes in Rats

Cited by 92 publications

References 31 publications

The role of bradykinin, AT₂ and angiotensin 1–7 receptors in the EDRF‐dependent vasodilator effect of angiotensin II on the isolated mesenteric vascular bed of the rat

The role of bradykinin, AT₂ and angiotensin 1–7 receptors in the EDRF‐dependent vasodilator effect of angiotensin II on the isolated mesenteric vascular bed of the rat

Angiotensinase activities in the kidney of renovascular hypertensive rats

Blood pressure and renal hemodynamic effects of angiotensin fragments

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Autoradiographic Identification of Kidney Angiotensin IV Binding Sites and Angiotensin IV-Induced Renal Cortical Blood Flow Changes in Rats

Cited by 92 publications

References 31 publications

The role of bradykinin, AT2 and angiotensin 1–7 receptors in the EDRF‐dependent vasodilator effect of angiotensin II on the isolated mesenteric vascular bed of the rat

The role of bradykinin, AT2 and angiotensin 1–7 receptors in the EDRF‐dependent vasodilator effect of angiotensin II on the isolated mesenteric vascular bed of the rat

Angiotensinase activities in the kidney of renovascular hypertensive rats

Blood pressure and renal hemodynamic effects of angiotensin fragments

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The role of bradykinin, AT₂ and angiotensin 1–7 receptors in the EDRF‐dependent vasodilator effect of angiotensin II on the isolated mesenteric vascular bed of the rat

The role of bradykinin, AT₂ and angiotensin 1–7 receptors in the EDRF‐dependent vasodilator effect of angiotensin II on the isolated mesenteric vascular bed of the rat