Effects of angiotensin on renal cortical and papillary blood flows measured by laser-Doppler flowmetry

Nobes, Michael S; Harris, Peter; Yamada, Hiroshi; Mendelsohn, Frederick A.O.

doi:10.1152/ajprenal.1991.261.6.f998

Cited by 39 publications

(71 citation statements)

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“…MBF has been reported to increase, 20 decrease, 21 or remain unchanged 22 during Ang II infusion to the anesthetized rat. More recently, by using laser-Doppler flowmetry techniques enabling the direct and continuous recording of changes in MBF, Mattson et al 6,7 found that the medullary circulation of anesthetized Sprague-Dawley rats was very refractory to Ang II vasoconstrictor actions.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, Nobes et al 20 reported increases in papillary blood flow when even higher concentrations of Ang II (300 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 ) were infused. The relative insensitivity of the medullary circulation to Ang II may be explained in part by the stimulation of medullary prostaglandin 6 or kinin production, 20 although the long-term effects of these pathways on MBF remain to be explored. The present study, however, demonstrates that Ang II-induced NO production contributes importantly to the long-term ability of the organism to buffer against the hypertensive actions of circulating Ang II.…”

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Local Renal Medullary L-NAME Infusion Enhances the Effect of Long-Term Angiotensin II Treatment

1999

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Abstract-We hypothesized that the relatively high doses of angiotensin (Ang) II required to produce hypertension in rats were related to stimulation of renal medullary nitric oxide production, which in turn blunted reductions in medullary blood flow and the development of hypertension. Ang II was infused (5 days at 3 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 IV) to uninephrectomized Sprague-Dawley rats in the presence and absence of a continuous medullary interstitial N G -nitro-L-arginine methyl ester (L-NAME) infusion. Renal cortical and medullary blood flows were determined with the use of implanted optical fibers and laser-Doppler flowmetry. Ang II in the absence of medullary nitric oxide synthase inhibition did not change cortical or medullary blood flow or mean arterial pressure. A threshold dose of L-NAME was determined (75 g ⅐ kg Ϫ1 ⅐ h Ϫ1 ) that did not produce significant short-or long-term changes in medullary blood flow and mean arterial pressure. In rats with blunted medullary nitric oxide synthase activity, Ang II infused intravenously resulted in a 30% reduction in medullary blood flow (from 1.3 to 0.9Ϯ0.2V) and Ϸ20 mm Hg increase in mean arterial pressure with Ang II infusion over 5 days. During 70 minutes after the start of intravenous Ang II, there was an immediate reduction in medullary blood flow, with no changes in cortical blood flow or mean arterial pressure. We conclude that the relative insensitivity of rats to long-term elevations of circulating Ang II is due to the potent counterregulatory actions of the nitric oxide system, specifically within the renal medulla. The results provide novel insights of how the organism attempts to protect itself from the hypertensive effects of Ang II. Key Words: hypertension, renal Ⅲ kidney Ⅲ angiotensin II Ⅲ renal blood flow Ⅲ nitric oxide Ⅲ nitric oxide synthase I t is well recognized that elevations of circulating angiotensin (Ang) II cause resetting of the pressure-natriuresis relationship to elevated levels of arterial blood pressure through the renal retention of sodium and volume expansion. 1 Yet considerable species differences have been found in the concentrations of Ang II required to produce chronic hypertension. We have found that Ang II infused long term at concentrations of 3 to 5 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 produce Ϸ30 mm Hg increase in mean arterial pressure (MAP) over a period of 1 week in mongrel dogs maintained on a normal daily NaCl diet. 2 Humans exhibit even greater pressor sensitivity to prolonged infusions of Ang II. 3 In contrast, prolonged infusion of Ang II at 3 to 5 ng ⅐ kg Ϫ1 ⅐ min Ϫ1in Sprague-Dawley rats does not lead to a significant increase in MAP, 4 and investigators generally administer Ang II at rates of 30 to 60 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 to induce prolonged hypertension in rats. 5 A number of studies have demonstrated that the medullary vasculature of Sprague-Dawley rats is relatively refractive to the vasoconstrictor effects of Ang II compared with the cortical circulation. 6,7 Subpressor doses of Ang II administered intravenously that can significan...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Local Renal Medullary L-NAME Infusion Enhances the Effect of Long-Term Angiotensin II Treatment

1999

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“…Changes in renal CBF are not always replicated in the medullary or papillary regions because medullary hemodynamics can be regulated independently of renal CBF (Pallone et al 1990, Navar et al 1996, Mattson 2003. Vasoactive agents, including AngII, dopamine, arginine vasopressin, atrial natriuretic peptide, and bradykinin have been demonstrated to induce renal region-specific hemodynamic changes (Takezawa et al 1987, Pallone et al 1990, Nobes et al 1991, Mattson & Cowley 1993, Heyman et al 1995, Badzynska et al 2002, Igbe et al 2012. However, the effect of UII on regional RBF was unclear.…”

Section: Discussionmentioning

confidence: 99%

Pressor and renal regional hemodynamic effects of urotensin II in neonatal pigs

Soni¹,

Adebiyi²

2013

Journal of Endocrinology

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Renal expression of the peptide hormone urotensin II (UII) and its receptor (UTR) are dependent on kidney maturation and anatomical regions. However, renal regional hemodynamic effects of UII in neonates are unclear. Here, we investigated regional hemodynamic responses to acute intrarenal arterial administration of UII in newborn pigs. Western immunoblotting and immunofluorescence confirmed UTR expression and membrane localization in newborn pig renal afferent arterioles and afferent arteriolar smooth muscle cells respectively. Intrarenal arterial bolus injections of human UII (hUII; 1-100 ng/kg) resulted in a dose-dependent decrease in total renal blood flow (RBF) and an increase in mean arterial pressure (MAP) and renal vascular resistance (RVR) in newborn pigs. Moreover, hUII dose dependently reduced cortical blood flow (CBF) but increased medullary blood flow (MBF) in the piglets. hUII-induced MAP elevation and hemodynamic changes were inhibited by urantide, a UTR antagonist, but not losartan, a type 1 angiotensin II receptor antagonist. U-73122, a phospholipase C (PLC) inhibitor, and 2-aminoethoxydiphenyl borate, an inositol 1,4,5 trisphosphate (IP 3 ) receptor antagonist, attenuated hUII-induced MAP and RVR elevations, RBF and CBF reductions, but not MBF increase. These findings indicate that intrarenal arterial administration of hUII elevates blood pressure and induces region-selective renal hemodynamic changes in newborn pigs. Our data also suggest that the PLC/IP 3 signaling pathway contributes to hUII-induced alterations in MAP, RBF, RVR, and CBF but not MBF in newborn pigs.

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“…Recently, Manotham et al (2004) demonstrated a reduced PTC blood flow and interstitial hypoxia before the development of structural damage to renal tissues in an early phase of remnant kidney model rats. Although the precise mechanisms responsible for the pathogenesis of peritubular ischemia are currently unclear, a potential contribution of the renin-angiotensin system has been suggested (Nobes et al, 1991;Lombardi et al, 1999;Omoro et al, 2000;Franco et al, 2001;Norman et al, 2003;Welch et al, 2003aWelch et al, ,b, 2005Manotham et al, 2004). Acute infusion of angiotensin II (AngII) resulted in renal cortical vasoconstriction (Nobes et al, 1991) or hypoxia (Norman et al, 2003).…”

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confidence: 99%

“…Although the precise mechanisms responsible for the pathogenesis of peritubular ischemia are currently unclear, a potential contribution of the renin-angiotensin system has been suggested (Nobes et al, 1991;Lombardi et al, 1999;Omoro et al, 2000;Franco et al, 2001;Norman et al, 2003;Welch et al, 2003aWelch et al, ,b, 2005Manotham et al, 2004). Acute infusion of angiotensin II (AngII) resulted in renal cortical vasoconstriction (Nobes et al, 1991) or hypoxia (Norman et al, 2003). Likewise, cortical hypoxia was observed in the kidneys of chronically AngII-infused hypertensive rats (Welch et al, 2005) and in the clipped kidney at an early phase of twokidney, one-clip Goldblatt hypertensive rats (Welch et al, 2003b).…”

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confidence: 99%

Effects of Calcium Channel Blockade on Angiotensin II-Induced Peritubular Ischemia in Rats

Kondo

Kiyomoto

Yamamoto

et al. 2005

J Pharmacol Exp Ther

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Recent studies have indicated that derangement of peritubular capillary (PTC) circulation with consequent tubulointerstitial hypoxia plays a pivotal role in the pathogenesis of renal injury. The present study was performed to determine whether azelnidipine, a new dihydropyridine calcium channel blocker, attenuates angiotensin II (AngII)-induced peritubular ischemia in anesthetized rats. The superficial PTCs were visualized directly using an intravital fluorescence videomicroscope system, and the PTC blood flow was evaluated by analyzing the velocity of fluorescein isothiocyanate-labeled erythrocytes. Intravenous infusion of AngII (50 ng/kg/min, 10 min) significantly increased mean arterial pressure (MAP) and renal vascular resistance (RVR) (by 35 Ϯ 3% and 110 Ϯ 32%, respectively), and decreased total renal blood flow (RBF) and PTC erythrocyte velocity (by Ϫ34 Ϯ 4 and Ϫ37 Ϯ 1%, respectively). Treatment with azelnidipine (5 g/kg/min i.v., 10 min) had no effect on basal MAP, RBF, RVR, or PTC erythrocyte velocity. However, azelnidipine markedly attenuated the AngII-induced increases in MAP (7 Ϯ 3%) and RVR (40 Ϯ 4%) and decreases in RBF (Ϫ24 Ϯ 1%) and PTC erythrocyte velocity (Ϫ22 Ϯ 1%). Similar attenuation in the AngII-induced responses of MAP, RBF, RVR, and PTC erythrocyte velocity were observed in rats treated with a higher dose of azelnidipine (20 g/kg/min i.v., 10 min), which significantly decreased basal MAP and RVR and increased RBF and PTC erythrocyte velocity. These data suggest that calcium channel blockade attenuates AngII-induced peritubular ischemia, which may be involved in its beneficial effects on renal injury.

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Effects of angiotensin on renal cortical and papillary blood flows measured by laser-Doppler flowmetry

Cited by 39 publications

References 0 publications

Local Renal Medullary L-NAME Infusion Enhances the Effect of Long-Term Angiotensin II Treatment

Local Renal Medullary L-NAME Infusion Enhances the Effect of Long-Term Angiotensin II Treatment

Pressor and renal regional hemodynamic effects of urotensin II in neonatal pigs

Effects of Calcium Channel Blockade on Angiotensin II-Induced Peritubular Ischemia in Rats

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