Abstract 376: Prolonged Excess of Superoxide in Mouse Afferent Arterioles Causes Remodeling and Enhances Myogenic and Angiotensin II Contractions

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
En Yin Lai ◽  
Lingli Li ◽  
Di Feng ◽  
William J Welch ◽  
Christopher S Wilcox
Keyword(s):  
Angiotensin Ii ◽  
Vascular Remodeling ◽  
Perfusion Pressure ◽  
Area Ratio ◽  
Superoxide Dismutases ◽  
Strongly Correlated ◽  
Ang Ii ◽  
Wall Tension ◽  
Sod Isoforms ◽  
Afferent Arterioles

Background: Superoxide (O 2 .- ) is associated with cardiovascular disease (CVD) and inactivating SNIPs of the EC-SOD gene increased CVD, but the mechanisms are unclear. Superoxide dismutases (SODs) have three isoforms: cytoplasmic Cu/ZnSOD (SOD1), mitochondrial MnSOD (SOD2) and extracellular Cu/ZnSOD (SOD3). Complete SOD2-/- was lethal. We tested the hypothesis that these isoforms of SOD modulate angiotensin II (Ang II), myogenic responses (MRs) and remodeling of afferent arterioles (Affs). Methods and Results: MRs were assessed from the slope of the regression of active wall tension on perfusion pressure (PP) and Ang II contractions from incubation with 10 -6 M Ang II. O 2 .- was assessed from PEG-SOD inhibitable ethidium:dihydroethidium fluorescence and remodeling from media:lumen area ratio (M:L). Results: 1. Compared to +/+, increasing PP from 40 to 80 mmHg or applying 10 -6 M Ang II in Affs increased O 2 .- more in SOD1-/- (PP, 8 ± 1% vs 5 ± 1% , P<0.05; Ang II, 29 ± 7 vs 10 ± 2%, P<0.05), in SOD2+/- (PP, 15 ± 2% vs 7 ± 1%, P<0.01; Ang II, 32 ± 5 % vs 7 ± 1%, P<0.01), and in SOD3-/- ( PP, 20 ± 4% vs 7 ± 1%, P<0.05; Ang II, 32 ± 5% vs 12 ± 3%, P<0.05). However, O 2 .- did not increase in SOD1+/- and SOD3+/-. 2. Compared to +/+, MRs (dynes.cm -1 .mmHg -1 ) were significantly increased in SOD1-/- (3.49 ± 0.30 vs 2.30 ± 0.27, P<0.05), in SOD2+/- (3.85 ± 0.48 vs 1.80 ± 0.34, P<0.05), and in SOD3-/- (3.51 ± 0.20 vs 2.43 ± 0.15, P<0.01), with no increase in SOD1+/- and SOD3+/-. 3. Compared to +/+, Ang II contractions were stronger in SOD1-/- (-68 ± 2% vs -33 ± 3%, P<0.0001), in SOD2+/- (-66 ± 6% vs -42 ± 3%, P<0.01), and in SOD3-/- (-75 ± 3% vs -34 ± 3%, P<0.0001) 4. Compared to +/+, M:L ratio of Affs were greater in SOD1-/- (4.0 ± 0.2 vs 1.8 ± 0.2, P<0.0001), in SOD2+/- (3.7 ± 0.4 vs 1.8 ± 0.4, P<0.001), and in SOD3-/- (4.5 ± 0.2 vs 1.9 ± 0.1, P<0.0001), but were unchanged in SOD1+/- and SOD3+/-. M:L ratio was strongly correlated to MR (r 2 =0.32, P<0.005) and Ang II contractions (r 2 = 0.56, P<0.005) across genotypes. 5. There were no compensatory changes in expression of other SOD isoforms. Conclusions: Lifetime increases in cytosolic, mitochondrial or extracellular O 2 .- enhanced afferent arteriolar myogenic and Ang II contractions that were closely related to vascular remodeling.

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.

Abstract P435: Differential Responses of Cerebral Cortical and Renal Cortical Microvessels to Perfusion Pressure and Angiotensin II: Effect of Angiotensin II or DOCA/salt Hypertension

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Lingli Li ◽  
En Yin Lai ◽  
William J Welch ◽  
Christopher S Wilcox
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
High Salt ◽  
Ang Ii ◽  
Cerebral Microvessels ◽  
Salt Hypertension ◽  
Afferent Arterioles ◽  
Myogenic Responses ◽  
The Brain

Background: The brain and kidney autoregulate their blood flow well yet both suffer from hypertensive damage. We found that a pressor infusion of angiotensin II (Ang II) reduced renal blood flow yet did not change cerebral blood flow. Therefore, we tested the hypothesis that their myogenic and Ang II responses differed. Methods: Cerebral cortical microvessels (cerebral) and renal afferent arterioles (afferent) were isolated and perfused from mice after 4 weeks of hypertension from Ang II infusion /high salt/uninephrectomy (Ang II hypertension) or DOCA/high salt/uninephrectomy (DOCA/salt hypertension) or normotensive controls without Ang II or DOCA (n=4-6 per group). Results: Normal cerebral and afferents had similar myogenic responses (Δ diameter: cerebral -21±3 versus afferent-19±2%, NS), but bath addition of Ang II or norepinephrine contracted afferents strongly (Ang II: -48±5%, P<0.001, NE: -95±2%, P<0.001), yet cerebrals were entirely unresponsive. Myogenic responses in Ang II hypertension were reduced selectively by 40% in cerebral microvessels compared to controls (-13±3 versus -21±3%, P<0.001) yet maintained in afferents (-17±3 versus -19±2%, NS). However, myogenic responses in DOCA/salt hypertension were maintained in both groups. Contractions to Ang II in cerebral microvessels were increased in Ang II hypertension (-5±2 versus 0±1%, P<0.01) and increased in DOCA/salt hypertension (-18±8 versus -2±2%, P<0.01). In contrast, contractions to Ang II in afferent arterioles were reduced 50% in Ang II hypertension (-23±5 versus -48±5%, P<0.001) and reduced 25% in DOCA/salt hypertension (-38±6 versus -50±10%, P=0.05). Conclusions: The kidney is well protected from hypertension and excessive Ang II vasoconstriction. However, the breakdown of myogenic responses in the cerebral microvessels during Ang II hypertension and the enhanced Ang II responses in the cerebral microvessels during Ang II and DOCA/salt hypertension make the brain especially vulnerable to hypertensive ischemia or damage.

scholarly journals Intracrine angiotensin II functions originate from noncanonical pathways in the human heart

2016 ◽  
Vol 311 (2) ◽  
pp. H404-H414 ◽  
Author(s):  
Carlos M. Ferrario ◽  
Sarfaraz Ahmad ◽  
Jasmina Varagic ◽  
Che Ping Cheng ◽  
Leanne Groban ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Functional Significance ◽  
Vascular Remodeling ◽  
Human Heart ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Extended Form ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Ras Genes

Although it is well-known that excess renin angiotensin system (RAS) activity contributes to the pathophysiology of cardiac and vascular disease, tissue-based expression of RAS genes has given rise to the possibility that intracellularly produced angiotensin II (Ang II) may be a critical contributor to disease processes. An extended form of angiotensin I (Ang I), the dodecapeptide angiotensin-(1–12) [Ang-(1–12)], that generates Ang II directly from chymase, particularly in the human heart, reinforces the possibility that an alternative noncanonical renin independent pathway for Ang II formation may be important in explaining the mechanisms by which the hormone contributes to adverse cardiac and vascular remodeling. This review summarizes the work that has been done in evaluating the functional significance of Ang-(1–12) and how this substrate generated from angiotensinogen by a yet to be identified enzyme enhances knowledge about Ang II pathological actions.

Membrane potential measurements in renal afferent and efferent arterioles: actions of angiotensin II

1997 ◽  
Vol 273 (2) ◽  
pp. F307-F314 ◽  
Author(s):  
R. Loutzenhiser ◽  
L. Chilton ◽  
G. Trottier
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Membrane Potentials ◽  
Ang Ii ◽  
Ca Channels ◽  
Renal Perfusion Pressure

An adaptation of the in vitro perfused hydronephrotic rat kidney model allowing in situ measurement of arteriolar membrane potentials is described. At a renal perfusion pressure of 80 mmHg, resting membrane potentials of interlobular arteries (22 +/- 2 microns) and afferent (14 +/- 1 microns) and efferent arterioles (12 +/- 1 microns) were -40 +/- 2 (n = 8), -40 +/- 1 (n = 45), and -38 +/- 2 mV (n = 22), respectively (P = 0.75). Using a dual-pipette system to stabilize the impalement site, we measured afferent and efferent arteriolar membrane potentials during angiotensin II (ANG II)-induced vasoconstriction. ANG II (0.1 nM) reduced afferent arteriolar diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.005) and membrane potentials from -40 +/- 2 to -29 +/- mV (P = 0.012). ANG II elicited a similar vasoconstriction in efferent arterioles, decreasing diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.004), but failed to elicit a significant depolarization (-39 +/- 2 for control; -36 +/- 3 mV for ANG II; P = 0.27). Our findings thus indicate that resting membrane potentials of pre- and postglomerular arterioles are similar and lie near the threshold activation potential for L-type Ca channels. ANG II-induced vasoconstriction appears to be closely coupled to membrane depolarization in the afferent arteriole, whereas mechanical and electrical responses appear to be dissociated in the efferent arteriole.

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.

Modulation of natriuresis by sympathetic nerves and angiotensin II in conscious dogs

1989 ◽  
Vol 256 (3) ◽  
pp. F485-F489
Author(s):  
P. B. Persson ◽  
H. Ehmke ◽  
U. Kogler ◽  
H. Kirchheim
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Recovery Period ◽  
Sympathetic Nerves ◽  
Renal Perfusion ◽  
Ang Ii ◽  
Sympathetic Nerve Stimulation ◽  
Converting Enzyme Inhibition ◽  
Pressure Independent

The effects of renal perfusion pressure and reflex sympathetic nerve stimulation on sodium excretion were studied in six conscious foxhounds on a normal sodium diet. This was done before, during common carotid occlusion (CCO), and during a recovery period following CCO. Three protocols were used 1) control (n = 6), 2) converting-enzyme inhibition (CEI, n = 6), and 3) CEI combined with a constant renal artery pressure (RAP, n = 5). In protocol 1, CCO increased RAP markedly (140.5 +/- 5.1 vs. 103.0 +/- 4.4 mmHg; P less than 0.001) along with a considerable natriuresis (128.4 +/- 20.1 vs. 86.3 +/- 15.1 mumol Na+/min; P less than 0.05). In protocol 2, CEI increased control sodium excretion but did not impair the natriuresis by CCO. Maintaining RAP at control levels in protocol 3 lead to an antinatriuresis (53.1 +/- 16.8 vs. 128.3 +/- 32.2 mumol Na+/min; P less than 0.05). Creatinine clearance was unaffected by all procedures. In conclusion, a change in ANG II formation shifts but does not impair the natriuretic response to CCO. A moderate sympathetic activation has a pronounced pressure-independent antinatriuretic effect, which is not mediated by angiotensin II.

scholarly journals Androgen-Androgen Receptor System Protects against Angiotensin II-Induced Vascular Remodeling

Endocrinology ◽  
2009 ◽  
Vol 150 (6) ◽  
pp. 2857-2864 ◽  
Author(s):  
Yasumasa Ikeda ◽  
Ken-ichi Aihara ◽  
Sumiko Yoshida ◽  
Takashi Sato ◽  
Shusuke Yagi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Androgen Receptor ◽  
Angiotensin Ii ◽  
Vascular Remodeling ◽  
Collagen Type ◽  
No Synthase ◽  
Type I ◽  
Ang Ii ◽  
Endothelial No Synthase ◽  
No Bioavailability

Age-related andropause promotes cardiovascular disease in males. Although we had previously reported that the androgen-androgen receptor (AR) system plays important roles in cardiac growth and remodeling, the system’s involvement in vascular remodeling remains unclear. To clarify this role, 25-wk-old male AR knockout (ARKO) mice and littermate male wild-type (WT) mice were divided into two groups with and without angiotensin II (Ang II) administration (2.0 mg/kg · d) for 14 d, respectively. No morphological differences in the coronary artery and thoracic aorta were observed between the groups without Ang II. Ang II stimulation markedly increased medial thickness and perivascular fibrosis in ARKO mice, with enhanced TGF-β1, collagen type I, and collagen type III gene expression in the aorta. Ang II stimulation also prominently increased superoxide production, lipid peroxidation, and gene expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase components in ARKO mice compared with WT mice. In addition, phosphorylation of c-Jun N-terminal kinase (JNK) and phosphorylated (Smad2/3) was remarkably enhanced in Ang II-treated ARKO mice compared with Ang II-treated WT mice. Notably, daily urinary nitric oxide (NO) metabolites excretion as a marker of NO bioavailability, aortic endothelial NO synthase expression and phosphorylation, and Akt phosphorylation were significantly reduced in ARKO mice compared with WT mice, regardless of Ang II stimulation. In conclusion, the androgen-AR system is required for the preservation of NO bioavailability through Akt-endothelial NO synthase system activation and exerts protective effects against Ang II-induced vascular remodeling by regulating oxidative stress, c-Jun N-terminal kinase (JNK) signaling, and the TGF-β-phosphorylated Smad pathway.

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.

Role of angiotensin II and alpha-adrenergic receptors during estrogen-induced vasodilation in ewes

1992 ◽  
Vol 263 (5) ◽  
pp. E837-E843 ◽  
Author(s):  
L. E. Davis ◽  
R. R. Magness ◽  
C. R. Rosenfeld
Keyword(s):  
Angiotensin Ii ◽  
Adrenergic Receptors ◽  
Perfusion Pressure ◽  
Cardiovascular Effects ◽  
Ang Ii ◽  
Uterine Blood Flow ◽  
Renin Angiotensin ◽  
Alpha Adrenergic Receptors ◽  
Adrenergic Systems

Estradiol-17 beta (E2 beta) produces uterine and systemic vasodilation in nonpregnant ewes without altering mean arterial pressure (MAP). Mechanisms responsible for maintaining MAP and thus uterine blood flow (UBF) may include activation of the renin-angiotensin and/or adrenergic systems. We therefore investigated the effects of systemic blockade of angiotensin II (ANG II) and/or alpha-adrenergic receptors in nonpregnant, castrated ewes, using saralasin (Sar) and/or phentolamine (Phen) in the presence or absence of intravenous E2 beta (1.0 microgram/kg). In nonestrogenized ewes neither antagonist alone had substantial cardiovascular effects; however, Sar + Phen decreased systemic vascular resistance (SVR) 20 +/- 7.4% (SE) and increased heart rate (HR) 50 +/- 19% (P < 0.01); MAP and UBF were unaffected. Following E2 beta treatment SVR fell 17 +/- 2.4% (P < 0.01), UBF increased more than fourfold, and MAP was unchanged. Compared with E2 beta alone, Phen + E2 beta decreased SVR 42 +/- 4.7%, and MAP fell 11 +/- 1.8% (P < 0.05) despite 40–50% increases in HR and cardiac output (P < 0.05). Responses to Sar + E2 beta were similar to E2 beta alone, except for a fall in MAP, whereas responses to Sar + Phen + E2 beta resembled those of Phen + E2 beta. E2 beta-induced uterine vasodilation was unaltered by Sar and/or Phen. During E2 beta-induced vasodilation, MAP is maintained by enhanced activation of the alpha-adrenergic and renin-angiotensin systems; however, uterine vascular responses to E2 beta are independent of both systems and perfusion pressure.

Segmental effects of norepinephrine and angiotensin II on isolated renal microvessels

1983 ◽  
Vol 244 (5) ◽  
pp. F526-F534 ◽  
Author(s):  
R. M. Edwards
Keyword(s):  
Angiotensin Ii ◽  
Contractile Response ◽  
Intraluminal Pressure ◽  
Lumen Diameter ◽  
Rabbit Kidney ◽  
Ang Ii ◽  
Efferent Arteriole ◽  
Afferent Arterioles ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Interlobular arteries and superficial afferent and efferent arterioles were isolated from rabbit kidney, and the effects of intraluminal pressure, norepinephrine (NE), and angiotensin II (ANG II) on lumen diameter were examined. A single microvessel was dissected and one end was cannulated. The other end of the vessel was occluded and lumen diameter was measured at fixed intraluminal pressures. With step increases in intraluminal pressure over the range of 70-180 mmHg, lumen diameters of the interlobular arteries and afferent arterioles remained constant or decreased by up to 11%. In contrast, lumen diameters of efferent arterioles continued to increase as intraluminal pressure was elevated. In all three vessels NE (10(-9) to 10(-5) M) caused a dose-dependent decrease in lumen diameter. However, only the efferent arteriole responded to ANG II (10(-12) to 10(-8) M). The contractile response of the efferent arteriole to NE or ANG II was localized to the first 50-75 micrometers of the vessel as it emerged from the glomerulus. This finding suggests that smooth muscle cells are located only in this portion of the efferent arteriole. It is concluded that at least part of the autoregulation of renal blood flow can be explained by a myogenic mechanism in preglomerular vessels and that ANG II acts primarily on postglomerular segments of the rabbit renal microcirculation.

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