Role of mesangial cell in glomerular response to volume and angiotensin II

1993 ◽  
Vol 264 (1) ◽  
pp. F158-F165 ◽  
Author(s):  
R. C. Blantz ◽  
F. B. Gabbai ◽  
B. J. Tucker ◽  
T. Yamamoto ◽  
C. B. Wilson
Keyword(s):  
Angiotensin Ii ◽  
Hydrostatic Pressure ◽  
Mesangial Cell ◽  
Physiological Role ◽  
In Vivo Studies ◽  
Ang Ii ◽  
Plasma Volume Expansion ◽  
Single Nephron

We have examined the physiological role of the mesangial cell in the regulation of glomerular hemodynamics utilizing mesangial cell lysis by the administration of antithymocyte antibody serum (ATS) 24 h before micropuncture evaluation. Plasma volume expansion (PVE) in normal NaCl-depleted rats increased single-nephron glomerular filtration rate (SNGFR) by 30% because of increases in single-nephron plasma flow (SNPF), whereas glomerular capillary hydrostatic pressure (PG) remained constant. SNGFR did not increase with PVE in NaCl-depleted ATS rats despite increases in SNPF, and PG increased significantly (51 +/- 2 to 67 +/- 3 mmHg) because of afferent arteriolar dilation, whereas efferent resistance remained elevated. Angiotensin II (ANG II) infusion in normal rats decreased SNGFR because of reductions in SNPF and the glomerular ultrafiltration coefficient (LpA), whereas the hydrostatic pressure gradient (delta P) increased. In ATS rats ANG II infusion did not change SNGFR, LpA, or delta P. These in vivo studies suggest that the mesangial cell plays an important role in the regulation of LpA, efferent arteriolar resistance, and the regulation of PG, whereas this cell exerts little effect on the afferent arteriole.

Role of angiotensin II in experimental membranous nephropathy

1988 ◽  
Vol 254 (4) ◽  
pp. F500-F506
Author(s):  
F. B. Gabbai ◽  
C. B. Wilson ◽  
R. C. Blantz
Keyword(s):  
Angiotensin Ii ◽  
Hydrostatic Pressure ◽  
Membranous Nephropathy ◽  
Enzyme Inhibitor ◽  
Chronic Administration ◽  
Ang Ii ◽  
Glomerular Injury ◽  
Single Nephron ◽  
Glomerular Hemodynamics

Glomerular hemodynamics measurements in rats with experimental membranous nephropathy [passive Heymann nephritis (PHN)] have demonstrated that the appearance of proteinuria 5 days after administration of anti-Fx1A antibody is temporally related to changes in the glomerular ultrafiltration coefficient (LpA). Previous studies in other models of glomerular injury have suggested a significant role for angiotensin II (ANG II) in the glomerular hemodynamic abnormalities. To evaluate the possible role of ANG II in the LpA decrease, converting enzyme inhibitor (CEI) was administered acutely or chronically (5 days before and after induction of PHN) to rats with PHN. Acute ANG II blockade produced a fall in mean arterial pressure (MAP), single-nephron glomerular filtration rate (SNGFR), absolute proximal reabsorption (APR), single-nephron plasma flow, single-nephron blood flow, and glomerular capillary hydrostatic pressure (PG); however, no changes in LpA were detected. Chronic administration of CEI (MK421, 5 mg.kg-1.day-1) in the drinking water was associated with a fall in MAP; however, both SNGFR and APR increased. PG and the transcapillary hydrostatic pressure gradient were unchanged, and LpA remained depressed. These results suggest that reduction of LpA in rats with PHN is ANG II independent and that other mechanisms are required to explain these changes in glomerular hemodynamics.

Expression of Cell Cycle Proteins P21 waf1/Cip1 , P27 kip1 , Cyclin D1 and CDK4 in Blood Vessels of Angiotensin II-Infused Rats. Role of AT 1 Receptors.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 707-707
Author(s):  
Quy N Diep ◽  
Mohammed El Mabrouk ◽  
Rhian M Touyz ◽  
Ernesto L Schiffrin
Keyword(s):  
Cell Cycle ◽  
Angiotensin Ii ◽  
Dna Synthesis ◽  
Cyclin D1 ◽  
Blood Vessels ◽  
Thymidine Incorporation ◽  
Mesenteric Arteries ◽  
Ang Ii

P79 Angiotensin II (Ang II) is an important modulator of cell growth via AT 1 receptors, as demonstrated both in vivo and in vitro . Here, we investigated the role of different proteins involved in the cell cycle, including cyclin D1, cyclin-dependent kinase 4 (cdk4) and cdk inhibitors p21 and p27 in blood vessels of Ang II-infused rats and the effect therein of the AT 1 receptor antagonist losartan. Male Sprague Dawley rats were infused for 7 days with Ang II (120 ng/kg/min s.c.) and/or treated with losartan (10 mg/kg/day orally). DNA synthesis in mesenteric arteries was evaluated by radiolabeled 3 H-thymidine incorporation. The expression of p21, p27, cyclin D1, cdk4 and E2F, which play critical roles during G1-phase of the cell cycle process, was examined by Western blot analysis. Tail cuff systolic blood pressure (mmHg) was elevated (p<0.05, n=9) in Ang II-infused rats (161.3±8.2) vs. controls (110.1±5.3) and normalized by losartan (104.4±3.2). Radiolabeled 3 H-thymidine incorporation (cpm/100 μg DNA) showed that Ang II-infusion significantly increased DNA synthesis (152±5 vs. 102±6, p<0.05). Expression of p21 and p27 was significantly decreased in the Ang II group to 23.2±10.4% and 10.3±5.3% of controls, respectively, whereas expression of cyclin D1 and cdk4 was significantly increased in the Ang II group to 213.7±8% and 263.6±37% of controls, respectively. These effects induced by Ang II infusion was normalized in the presence of losartan. Ang II had no effect on the expression of E2F. Thus, when AT 1 receptors are stimulated in vivo , DNA synthesis is enhanced in blood vessels by activation of cyclin D1 and cdk4. Reduction in cell cycle kinase inhibitors p21 and p27 may contribute to activation of growth induced by in vivo AT 1 receptor stimulation.

scholarly journals Vitamin D and prostate cancer

2013 ◽  
Vol 66 (5-6) ◽  
pp. 259-262
Author(s):  
Goran Marusic ◽  
Dimitrije Jeremic ◽  
Sasa Vojinov ◽  
Natasa Filipovic ◽  
Milan Popov
Keyword(s):  
Prostate Cancer ◽  
Vitamin D ◽  
Physiological Role ◽  
In Vivo Studies ◽  
Vitamin D Metabolism ◽  
Genetic Changes ◽  
Metabolic Role

In addition to the metabolic role of vitamin D, which is well known and clearly defined, there have been many hypotheses regarding its anti-proliferative and pro-apoptotic role. Epidemiology and Significance of Prostate Cancer. Prostate cancer is the second most common malignancy in men. Long period of cancerogenesis, available tumor markers and high incidence make this cancer ideal for preventive measures. Physiological Role of Vitamin D and its Effect on Prostate Cancer Cells. In vitro and in vivo studies have shown the anti-proliferative and pro-apoptopic role of vitamin D. Disorders of vitamin D metabolism are noted in vitamin D gene level, vitamin D receptor, vitamin D responsive elements and androgen receptors. We present the most important effect of those changes on vitamin D metabolism. Conclusion. Available studies on vitamin D level in serum, prostate tissue, observed activity of vitamin D enzymes and genetic changes give us only a slight insight into the basic mechanisms of vitamin D action in the development of prostate cancer; therefore, further investigations are needed.

scholarly journals COX-2 mediates angiotensin II-induced (pro)renin receptor expression in the rat renal medulla

2014 ◽  
Vol 307 (1) ◽  
pp. F25-F32 ◽  
Author(s):  
Fei Wang ◽  
Xiaohan Lu ◽  
Kexin Peng ◽  
Li Zhou ◽  
Chunling Li ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Protein Expression ◽  
Renal Medulla ◽  
Receptor Expression ◽  
Ang Ii ◽  
Cox 2 ◽  
Renin Content

(Pro)renin receptor (PRR) is predominantly expressed in the distal nephron where it is activated by angiotensin II (ANG II), resulting in increased renin activity in the renal medulla thereby amplifying the de novo generation and action of local ANG II. The goal of the present study was to test the role of cycloxygenase-2 (COX-2) in meditating ANG II-induced PRR expression in the renal medulla in vitro and in vivo. Exposure of primary rat inner medullary collecting duct cells to ANG II induced sequential increases in COX-2 and PRR protein expression. When the cells were pretreated with a COX-2 inhibitor NS-398, ANG II-induced upregulation of PRR protein expression was almost completely abolished, in parallel with the changes in medium active renin content. The inhibitory effect of NS-398 on the PRR expression was reversed by adding exogenous PGE2. A 14-day ANG II infusion elevated renal medullary PRR expression and active and total renin content in parallel with increased urinary renin, all of which were remarkably suppressed by the COX-2 inhibitor celecoxib. In contrast, plasma and renal cortical active and total renin content were suppressed by ANG II treatment, an effect that was unaffected by COX-2 inhibition. Systolic blood pressure was elevated with ANG II infusion, which was attenuated by the COX-2 inhibition. Overall, the results obtained from in vitro and in vivo studies established a crucial role of COX-2 in mediating upregulation of renal medullary PRR expression and renin content during ANG II hypertension.

scholarly journals Hering-Breuer Reflex and pre-Botzinger Complex: A Literature Survey

1970 ◽  
Vol 2 ◽  
pp. 89-94
Author(s):  
M Ahmed
Keyword(s):  
Human Subjects ◽  
Respiratory Rhythm ◽  
Physiological Role ◽  
Personal Communication ◽  
In Vivo Studies ◽  
Respiratory Rhythmogenesis ◽  
Neuronal Regulation ◽  
Bötzinger Complex

The existence and physiological role of Hering-Breuer reflex and pre-Botzinger complex has long been depreciated by the Bangladesh society of physiologist (personal communication). The aim of this mini review is to highlight the recent findings on the aforementioned topics. Due to the difficulties in vivo studies in human subjects, many aspects of the neuronal regulation of the respiratory rhythm are still unclear. However, the recent localization of the pre-Botzinger complex in humans and advances in technologies necessitates further exploration of the neuronal circuits in the pre-BotC complex which will subsequently unwrap the magical box and pave the way to solve the puzzle of the mechanism of respiratory rhythmogenesis and its modulation in different pathophysiological conditions. Key Words: Physiology; Hering-Breuer reflex; pre-Botzinger complex; Rhythmic respiration  DOI:10.3329/jbsp.v2i0.988 J Bangladesh Soc Physiol. 2007 Dec;(2):89-94.  

Angiotensin II formation in dog heart is mediated by different pathways in vivo and in vitro

1996 ◽  
Vol 271 (2) ◽  
pp. H417-H421 ◽  
Author(s):  
E. Balcells ◽  
Q. C. Meng ◽  
G. R. Hageman ◽  
R. W. Palmer ◽  
J. N. Durand ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Heart Tissue ◽  
Left Ventricular ◽  
In Vivo Studies ◽  
In Vitro Assays ◽  
Ang Ii ◽  
Dog Heart ◽  
Tissue Extracts

Angiotensin-converting enzyme (ACE) inhibitors (I) have beneficial effects that are presumably mediated by decreased angiotensin II (ANG II) production. However, in vitro assays in human heart extracts have demonstrated that > 75% of ANG II-forming enzyme activity was not inhibited by captopril (Cap) and therefore did not appear to be related to ACE but was inhibited by chymostatin, suggesting that it was predominantly chymase-like activity. Previous work in our laboratory has demonstrated a similar relative contribution of ACE and chymase-like activity toward ANG II formation in vitro in dog heart tissue extracts. Accordingly, we compared Cap-inhibitable ANG II formation in vitro in heart tissue of five adult mongrel dogs to the in vivo Cap-inhibitable, ANG II-forming activity across the myocardial bed in four openchest, adult mongrel dogs. In vitro studies demonstrated that only 6 +/- 2% of ANG II formation was inhibited by Cap from heart tissue extracts of the left ventricular midwall. In in vivo studies, ANG I (0.5 nmol/min) followed by ANG I plus the ACE inhibitor Cap (0.1 mumol/min) was infused into the left anterior descending artery, and ANG II was assayed in the proximal aorta and coronary sinus. The arterial-venous (A-V) difference of ANG II across the myocardial circulation increased significantly during ANG I infusion (-13.4 +/- 23.5 to 142.8 +/- 71.4 pg/ml; P < 0.03). Subsequent coinfusion of Cap with ANG I significantly decreased the myocardial A-V difference of ANG II by 60 +/- 18% (P < 0.05). Thus, in contrast to the in vitro situation, ANG II formation in vivo is inhibited significantly by Cap in the normal dog heart. This comparison of in vivo and in vitro conversion of ANG I to ANG II by ACE and chymase-like activity suggests that in vitro assays may underestimate the functional contribution of ACE to intracardiac ANG II formation.

The renal nerve is required for regulation of proximal tubule transport by intraluminally produced ANG II

2001 ◽  
Vol 280 (3) ◽  
pp. F524-F529 ◽  
Author(s):  
Albert Quan ◽  
Michel Baum
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Renal Nerves ◽  
Ang Ii ◽  
Sham Control ◽  
Renal Nerve ◽  
Tubular Lumen ◽  
Chronic Denervation

The proximal tubule synthesizes and luminally secretes high levels of angiotensin II, which modulate proximal tubule transport independently of systemic angiotensin II. The purpose of this in vivo microperfusion study is to examine whether the renal nerves modulate the effect of intraluminal angiotensin II on proximal tubule transport. The decrement in volume reabsorption after addition of 10−4 M luminal enalaprilat is a measure of the role of luminal angiotensin II on transport. Acute denervation decreased volume reabsorption (2.97 ± 0.14 vs. 1.30 ± 0.21 nl · mm−1 · min−1, P < 0.001). Although luminal 10−4 M enalaprilat decreased volume reabsorption in controls (2.97 ± 0.14 vs. 1.61 ± 0.26 nl · mm−1 · min−1, P < 0.001), it did not after acute denervation (1.30 ± 0.21 vs. 1.55 ± 0.19 nl · mm−1 · min−1). After chronic denervation, volume reabsorption was unchanged from sham controls (2.26 ± 0.28 vs. 2.70 ± 0.19 nl · mm−1 · min−1). Addition of luminal 10−4 M enalaprilat decreased volume reabsorption in sham control (2.70 ± 0.19 vs. 1.60 ± 0.10 nl · mm−1 · min−1, P < 0.05) but not with chronic denervation (2.26 ± 0.28 vs. 2.07 ± 0.20 nl · mm−1 · min−1). Addition of 10−8 M angiotensin II to the lumen does not affect transport due to the presence of luminal angiotensin II. However, addition of 10−8 M angiotensin II to the tubular lumen increased the volume reabsorption after both acute (1.30 ± 0.21 vs. 2.67 ± 0.18 nl · mm−1 · min−1, P < 0.05) and chronic denervation (2.26 ± 0.28 vs. 3.57 ± 0.44 nl · mm−1 · min−1, P < 0.01). These data indicate that renal denervation abolished the luminal enalaprilat-sensitive component of proximal tubule transport, which is consistent with the renal nerves playing a role in the modulation of the intraluminal angiotensin II mediated component of proximal tubule transport.

Angiotensin II binding sites in aortic endothelium of domestic fowl

1990 ◽  
Vol 258 (3) ◽  
pp. R777-R782 ◽  
Author(s):  
J. N. Stallone ◽  
H. Nishimura ◽  
A. Nasjletti
Keyword(s):  
Angiotensin Ii ◽  
Domestic Fowl ◽  
Angiotensin Receptors ◽  
Ang Ii ◽  
Aortic Endothelium ◽  
Specific Receptors ◽  
Layer Chromatography

In domestic fowl, angiotensin II (ANG II) produces a unique vasodepressor response in vivo and endothelium-dependent relaxation of aortic rings in vitro that appear to be a direct effect on vascular smooth muscle mediated through vascular angiotensin receptors. To explore the possible role of the endothelium in ANG II-induced vasodilation, ANG II binding to aortic membrane fractions and intact endothelium and prostaglandin (PG) production were examined in fowl aortas. 125I-[Ile5]ANG II binding by endothelium-intact aortic membrane fractions was consistently higher than binding by identically prepared endothelium-deleted membrane fractions at virtually all concentrations of ligand (10 pM-0.20 microM). Incubation of intact aortic rings with 125I-[Ile5]ANG II (0.50 nM) resulted in specific endothelial binding that increased linearly with time from 5.5 +/- 1.7 (SE) fmol/mg protein at 5 min to 13.7 +/- 1.8 at 30 min. Endothelial ANG II binding increased linearly with the dose of ligand, from 2.7 +/- 0.3 fmol/mg protein at 0.1 nM to 21.0 +/- 2.2 at 1.0 nM. Specific ANG II binding to aortic endothelium was competitively displaced 73 +/- 11% by unlabeled ANG II (0.1 microM) but not by bradykinin (0.1 microM). Incubation of intact aortic rings with [14C]arachidonic acid resulted in the formation of radioactive metabolites that comigrated in thin-layer chromatography with authentic PGE2 but not with 6-keto-PGF1 alpha. PGE2 production by aortic rings (44.4 +/- 4.5 ng.mg dry tissue-1.h-1) was not stimulated by addition of ANG II. These results suggest that specific receptors for ANG II exist in fowl aortic endothelium and that PGs are not involved in ANG II-induced vasodilation of the fowl aorta.

Effects of angiotensin II on electrolyte transport in the early and late distal tubule in rat kidney

1996 ◽  
Vol 271 (1) ◽  
pp. F143-F149 ◽  
Author(s):  
T. Wang ◽  
G. Giebisch
Keyword(s):  
Angiotensin Ii ◽  
Rat Kidney ◽  
Distal Tubule ◽  
Distal Convoluted Tubule ◽  
Ang Ii ◽  
Hormone Effect ◽  
Collecting Tubule ◽  
High Doses

We have demonstrated in previous studies that luminal administration of low doses of angiotensin II (ANG II) stimulate and high doses of ANG II inhibit fluid and HCO3- transport in proximal tubules of rat kidney. However, the role of ANG II on Na+ and HCO3- transport in the distal nephron has not yet been fully elucidated. The superficial early and late distal tubules (DT) of the nephron segments correspond to the distal convoluted tubule and initial collecting tubule. Accordingly, we investigated the effects of ANG II on Na+, HCO3-, and K+ transport in the early and late DT by separate perfusion of these tubule segments in vivo. [3H]inulin, Na+, K+, and total CO2 concentrations were measured in the perfusate and collected fluid, and transport of sodium (JNa), bicarbonate (JHCO3), potassium (JK), and fluid (JV) were analyzed as an index of the hormone effect. Intravenous infusion of the ANG II receptor antagonist [Sar1,Ile8]ANG II (1 microgram.kg-1.min-1) decreased JV, JNa, and JHCO3 in the early DT and decreased Jv and JNa in the late DT. Addition of ANG II (10(-11) M) to the tubular perfusate significantly increased the Jv, JNa, and JHCO3 in the early DT. Similar studies in late DT demonstrated an increase in Jv and JNa, decrease in JK, but no effect on JHCO3. The effects of ANG II on fluid and ion transport were abolished by the luminal application of amiloride (10(-3) M) and of the angiotensin-receptor blocker [Sar1,Ile8]ANG II (10(-6) M). These results suggest that ANG II stimulates Na+/H+ exchange in the early DT (distal convoluted tubule) and amiloride-sensitive Na+ transport (Na+ channels) in the late DT (initial collecting tubule) of cortical nephrons.

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