scholarly journals The effects of angiotensin II and norepinephrine on afferent arterioles in the rat

1986 ◽  
Vol 30 (6) ◽  
pp. 895-905 ◽  
Author(s):  
Stephen K. Wilson
Keyword(s):  
Angiotensin Ii ◽  
Afferent Arterioles

Angiotensin II effects on microvascular diameters of in vitro blood-perfused juxtamedullary nephrons

1986 ◽  
Vol 251 (4) ◽  
pp. F610-F618 ◽  
Author(s):  
P. K. Carmines ◽  
T. K. Morrison ◽  
L. G. Navar
Keyword(s):  
Angiotensin Ii ◽  
Constant Pressure ◽  
Ang Ii ◽  
Experimental Conditions ◽  
Vasoactive Hormones ◽  
Juxtamedullary Nephron ◽  
Single Nephron ◽  
Afferent Arterioles ◽  
Dose Dependent

The purpose of this study was to determine the specific renal microvascular segments that are functionally responsive to angiotensin II (ANG II) and other vasoactive hormones. Experiments were performed on juxtamedullary tissue from captopril-treated rats during perfusion with blood at a constant pressure of 110 mmHg. Epifluorescence videomicroscopy was utilized to measure diameters of arcuate and interlobular arteries (ART), mid- (MA) and late- (LA) afferent arterioles, and efferent arterioles (EA). Norepinephrine (700 nM) significantly decreased, and sodium nitroprusside (380 nM) increased, inside diameters of all segments. Topical application of ANG II (0.01 to 1 nM) induced significant reductions in diameters of all vessel segments: ART, 17.5 +/- 2.0%; MA, 19.6 +/- 2.5%; LA, 13.5 +/- 1.5%; and EA, 16.9 +/- 2.7%. The preglomerular response to ANG II was blocked by saralasin (10 microM) and, in most cases, was dose dependent; however, an initial hypersensitivity to low ANG II doses (30% decrease in diameter) was exhibited by 38% of the preglomerular vessels studied. Under these experimental conditions, single-nephron glomerular filtration rate decreased significantly in response to 0.01 nM ANG II exposure. These observations demonstrate that physiological concentrations of ANG II can elicit receptor-dependent and reversible vasoconstriction of the juxtamedullary nephron microvasculature at both pre- and postglomerular sites.

Direct evaluation of the microvascular actions of ANP in juxtamedullary nephrons

1988 ◽  
Vol 254 (3) ◽  
pp. F440-F444 ◽  
Author(s):  
P. J. Veldkamp ◽  
P. K. Carmines ◽  
E. W. Inscho ◽  
L. G. Navar
Keyword(s):  
Angiotensin Ii ◽  
Topical Administration ◽  
Normal Kidney ◽  
Arterial Diameter ◽  
Direct Evaluation ◽  
Juxtamedullary Nephron ◽  
Afferent Arterioles ◽  
Renal Vascular ◽  
Arteriolar Diameter

The renal vascular actions of atrial natriuretic peptide (ANP) remain incompletely understood. The purpose of this study is to evaluate the effects of ANP on microvascular structures of the normal kidney. The in vitro blood-perfused juxtamedullary nephron technique was utilized to allow visualization of arcuate arteries and afferent and efferent arterioles. Donor rats were pretreated with captopril to eliminate possible interactions between angiotensin II and atriopeptin III (AP III). The effects of topical administration of 3 nM AP III were determined by videometric analysis of vessel inside diameters. Under control conditions, arcuate arterial diameter averaged 83 +/- 14 microns (n = 7), afferent arteriolar diameter was 20 +/- 4 microns (n = 7), and efferent arteriolar diameter was 16 +/- 2 microns (n = 7). During superfusion with AP III, arcuate arteries and afferent arterioles dilated 73 +/- 9 and 23 +/- 5%, respectively. Both returned to their control values when AP III was removed from the superfusate. Further experiments on arcuate arteries (n = 5) revealed that 0.3 nM AP III also vasodilated these vessels (26 +/- 9%); however, no significant effect was elicited by 0.03 nM AP III. In contrast to the vasodilator influence of AP III on preglomerular vessels, efferent arteriolar diameter was not altered by AP III exposure. These observations reveal that AP III can induce selective preglomerular vasodilation involving arcuate arteries as well as afferent arterioles, while efferent arteriolar diameter is not perceptibly influenced.

Blockade of chloride channels by DIDS stimulates renin release and inhibits contraction of afferent arterioles

1996 ◽  
Vol 270 (5) ◽  
pp. F718-F727 ◽  
Author(s):  
B. L. Jensen ◽  
O. Skott
Keyword(s):  
Angiotensin Ii ◽  
Chloride Channels ◽  
Channel Blocker ◽  
Inhibitory Effect ◽  
Renin Release ◽  
Disulfonic Acid ◽  
Basal Diameter ◽  
Chloride Channel Blocker ◽  
Afferent Arterioles ◽  
Dose Dependent

Calcium-activated chloride channels have been proposed to control renin release from juxtaglomerular cells and to be involved in the excitation-contraction coupling of the renal afferent arteriole. The hypothesis was tested on renin release from rat glomeruli and in microperfused rabbit afferent arterioles with the chloride channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). Renin secretion was equally enhanced by omission of extracellular calcium and by addition of 0.5 mM DIDS. The inhibitory effect of calcium was blocked by DIDS. The stimulatory effects of low calcium [with or without ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid] and DIDS were not additive. In the absence of chloride, basal renin release was suppressed and the stimulatory effect of DIDS was abolished. The DIDS-induced enhancement of renin release was not dependent on bicarbonate. Norepinephrine (5 x 10(-7)-1 x 10(-6) M) and angiotensin II (1 x 10(-8)-10(-6) M) evoked reversible and dose-dependent contractions of microperfused rabbit afferent arterioles. DIDS (0.5 mM) did not affect the basal diameter of the arterioles but strongly inhibited the response to angiotensin II and attenuated the duration of the contractile response to norepinephrine. The results support the hypothesis that DIDS-sensitive calcium-activated chloride channels are involved in regulation of renin release and in the afferent arteriolar contraction after angiotensin II but do not play a pivotal role in the response to norepinephrine.

scholarly journals Effects of Angiotensin II on Isolated Rabbit Afferent Arterioles

1994 ◽  
Vol 66 (4) ◽  
pp. 457-464 ◽  
Author(s):  
Hiroyuki Yoshida ◽  
Toshiaki Tamaki ◽  
Yasuharu Aki ◽  
Shoji Kimura ◽  
Ikumasa Takenaka ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Afferent Arterioles

Angiotensin II response in afferent arterioles of mice lacking either the endothelial or neuronal isoform of nitric oxide synthase

2008 ◽  
Vol 294 (2) ◽  
pp. R429-R437 ◽  
Author(s):  
Andreas Patzak ◽  
Andreas Steege ◽  
En Yin Lai ◽  
Jan Ole Brinkmann ◽  
Eckehardt Kupsch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Enos Gene ◽  
Angiotensin Ii Receptor ◽  
Afferent Arterioles ◽  
Dose Responses ◽  
Oxide Synthase ◽  
The Impact ◽  
Deficient Mice

The aim of the study is to evaluate the impact of nitric oxide (NO) produced by endothelial NO synthase (eNOS) and neuronal NOS (nNOS) on the angiotensin II response in afferent arterioles (Af). Dose responses were assessed for angiotensin II in microperfused Af of mice homozygous for disruption of the eNOS gene [eNOS(−/−)], or nNOS gene [nNOS(−/−)], and their wild-type controls, eNOS(+/+) and nNOS(+/+). Angiotensin II at 10−8 and 10−6 mol/l reduced the lumen to 69% and 68% in eNOS(+/+), and to 59% and 50% in nNOS(+/+). NG-nitro-l-arginine methyl ester (l-NAME) did not change basal arteriolar diameters, but augmented angiotensin II contraction, reducing diameters to 23% and 13% in eNOS(+/+), and 7% and 10% in nNOS(+/+) at 10−8 and 10−6 mol/l. The response to angiotensin II was enhanced in nNOS(−/−) mice (41% and 25% at 10−8 and 10−6 mol/l) and even more enhanced in eNOS(−/−) mice (12% and 9%) compared with nNOS(+/+) and eNOS(+/+). l-NAME led to complete constriction of Af in these groups. Media-to-lumen ratios of Af did not differ between controls and gene-deficient mice. mRNA expression of angiotensin II receptor types 1A and 1B and type 2 also did not differ. The results reveal that angiotensin II-induced release of NO from both eNOS and nNOS significantly contributes to the control of Af. Results also suggest that eNOS-derived NO is of greater importance than nNOS-derived NO in this isolated arteriolar preparation.

scholarly journals Angiotensin II receptors and renin release in rat glomerular afferent arterioles

1994 ◽  
Vol 46 (6) ◽  
pp. 1570-1573 ◽  
Author(s):  
Christos Chatziantoniou ◽  
Jean-Claude Dussaule ◽  
William J. Arendshorst ◽  
Raymond Ardaillou
Keyword(s):  
Angiotensin Ii ◽  
Renin Release ◽  
Angiotensin Ii Receptors ◽  
Afferent Arterioles

scholarly journals Involvement of Cytochrome P450 Metabolites in the Vascular Action of Angiotensin II on the Afferent Arterioles.

2001 ◽  
Vol 24 (5) ◽  
pp. 551-557 ◽  
Author(s):  
Kentaro KOHAGURA ◽  
Shuji ARIMA ◽  
Yoshimi ENDO ◽  
Yoshiroh CHIBA ◽  
Osamu ITO ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Angiotensin Ii ◽  
Afferent Arterioles

scholarly journals Purinergic P2X1 receptor, purinergic P2X7 receptor, and angiotensin II type 1 receptor interactions in the regulation of renal afferent arterioles in angiotensin II-dependent hypertension

2020 ◽  
Vol 318 (6) ◽  
pp. F1400-F1408 ◽  
Author(s):  
Supaporn Kulthinee ◽  
Weijian Shao ◽  
Martha Franco ◽  
L. Gabriel Navar
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Ang Ii ◽  
Renal Perfusion Pressure ◽  
Arteriolar Resistance ◽  
Purinergic P2x7 Receptor ◽  
Afferent Arterioles ◽  
Purinergic P2x Receptors

In ANG II-dependent hypertension, ANG II activates ANG II type 1 receptors (AT1Rs), elevating blood pressure and increasing renal afferent arteriolar resistance (AAR). The increased arterial pressure augments interstitial ATP concentrations activating purinergic P2X receptors (P2XRs) also increasing AAR. Interestingly, P2X1R and P2X7R inhibition reduces AAR to the normal range, raising the conundrum regarding the apparent disappearance of AT1R influence. To evaluate the interactions between P2XRs and AT1Rs in mediating the increased AAR elicited by chronic ANG II infusions, experiments using the isolated blood perfused juxtamedullary nephron preparation allowed visualization of afferent arteriolar diameters (AAD). Normotensive and ANG II-infused hypertensive rats showed AAD responses to increases in renal perfusion pressure from 100 to 140 mmHg by decreasing AAD by 26 ± 10% and 19 ± 4%. Superfusion with the inhibitor P2X1Ri (NF4490; 1 μM) increased AAD. In normotensive kidneys, superfusion with ANG II (1 nM) decreased AAD by 16 ± 4% and decreased further by 19 ± 5% with an increase in renal perfusion pressure. Treatment with P2X1Ri increased AAD by 30 ± 6% to values higher than those at 100 mmHg plus ANG II. In hypertensive kidneys, the inhibitor AT1Ri (SML1394; 1 μM) increased AAD by 10 ± 7%. In contrast, treatment with P2X1Ri increased AAD by 21 ± 14%; combination with P2X1Ri plus P2X7Ri (A438079; 1 μM) increased AAD further by 25 ± 8%. The results indicate that P2X1R, P2X7R, and AT1R actions converge at receptor or postreceptor signaling pathways, but P2XR exerts a dominant influence abrogating the actions of AT1Rs on AAR in ANG II-dependent hypertension.

scholarly journals Hypoxia-reoxygenation enhances murine afferent arteriolar vasoconstriction by angiotensin II

2018 ◽  
Vol 314 (3) ◽  
pp. F430-F438 ◽  
Author(s):  
Tamara Pahlitzsch ◽  
Zhi Zhao Liu ◽  
Amira Al-Masri ◽  
Diana Braun ◽  
Stefanie Dietze ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mrna Expression ◽  
Vascular Function ◽  
Calcium Transients ◽  
Surrounding Tissue ◽  
Ang Ii ◽  
Sod Activity ◽  
Afferent Arterioles ◽  
The Impact ◽  
Hypoxia Reoxygenation

We tested the hypothesis that hypoxia-reoxygenation (H/R) augments vasoreactivity to angiotensin II (ANG II). In particular, we compared an in situ live kidney slice model with isolated afferent arterioles (C57Bl6 mice) to assess the impact of tubules on microvessel response. Hematoxylin and eosin staining was used to estimate slice viability. Arterioles in the slices were located by differential interference contrast microscopy, and responses to vasoactive substances were assessed. Cytosolic calcium transients and NADPH oxidase (NOX) mRNA expression were studied in isolated afferent arterioles. SOD activity was measured in live slices. Both experimental models were subjected to control and H/R treatment (60 min). Slices were further analyzed after 30-, 60-, and 90-min hypoxia followed by 10- or 20-min reoxygenation (H/R). H/R resulted in enhanced necrotic tissue damage compared with control conditions. To characterize the slice model, we applied ANG II (10−7 M), norepinephrine (NE; 10−5 M), endothelin-1 (ET-1; 10−7 M), and ATP (10−4 M), reducing the initial diameter to 44.5 ± 2.8, 50.0 ± 2.2, 45.3 ± 2.6, and 74.1 ± 1.8%, respectively. H/R significantly increased the ANG II response compared with control in live slices and in isolated afferent arterioles, although calcium transients remained similar. TEMPOL incubation prevented the H/R effect on ANG II responses. H/R significantly increased NOX2 mRNA expression in isolated arterioles. SOD activity was significantly decreased after H/R. Enhanced arteriolar responses after H/R occurred independently from the surrounding tissue, indicating no influence of tubules on vascular function in this model. The mechanism of increased ANG II response after H/R might be increased oxidative stress and increased calcium sensitivity of the contractile apparatus.

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