scholarly journals Expression of troponin subunits in the rat renal afferent arteriole

IUBMB Life ◽  
2019 ◽  
Vol 71 (10) ◽  
pp. 1475-1481 ◽  
Author(s):  
Kosuke Takeya ◽  
Iris Kathol ◽  
Cindy Sutherland ◽  
Xuemei Wang ◽  
Rodger Loutzenhiser ◽  
...  
Keyword(s):  
Afferent Arteriole

Afferent arteriolar diameter in DOCA-salt and two-kidney one-clip hypertensive rats

1983 ◽  
Vol 245 (6) ◽  
pp. F755-F762 ◽  
Author(s):  
B. M. Iversen ◽  
L. Morkrid ◽  
J. Ofstad
Keyword(s):  
Blood Pressure ◽  
Plasma Renin ◽  
Afferent Arteriole ◽  
Cortical Layers ◽  
Hypertensive Rats ◽  
Salt Hypertension ◽  
Nephron Loss ◽  
Microsphere Method ◽  
Arteriolar Diameter ◽  
Equal Thickness

The afferent arteriolar diameter (dAA) was investigated during development of hypertensive renal disease in normal and uninephrectomized control rats, in chronic DOCA-salt (DOCA), post-DOCA (p-DOCA), and chronic two-kidney one-clip (2K-1C) hypertensive rats, and in post-two-kidney one-clip (p-2K-1C) normotensive rats. dAA was measured by the microsphere method. Nephron loss was present in the kidneys exposed to elevate blood pressure. The dAA was reduced from 19.9 to 17.2 micron in the DOCA group (P less than 0.001) and from 19.1 to 16.3 micron in the nonclipped kidneys in the 2K-1C group (P less than 0.001). The dAA increased from 19.9 to 20.7 micron in the p-DOCA group. Afferent arteriolar dilatation from 19.1 to 21.0 micron (P less than 0.001) was present about 50 days after clipping in the 2K-1C group; in the clipped kidneys the dAA returned to normal (18.9 micron) after declipping. No relation between the dAA and plasma renin concentration was observed. In all models dAA was the same in three cortical layers of equal thickness. Accordingly, chronic renal DOCA-salt hypertension constricts the afferent arteriole with angiotensin-independent mechanisms. Autoregulatory dilatation of the afferent arteriole seems to be maintained for at least 50 days. When the hypertension is moderate, dAA in damaged kidneys may be dilated.

Abstract 36: Deficiency in the Production of 20-HETE Contributes to Impaired Myogenic and TGF Responses in the Afferent Arteriole of Dahl S Rats

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Ying Ge ◽  
Fan Fan ◽  
Sydney R Murphy ◽  
Jan Michael Williams ◽  
Ruisheng Liu ◽  
...  
Keyword(s):  
Renal Injury ◽  
Tubuloglomerular Feedback ◽  
Brown Norway ◽  
Sodium Reabsorption ◽  
Thick Ascending Limb ◽  
Afferent Arteriole ◽  
Synthesis Inhibitor ◽  
Renal Vasculature ◽  
Luminal Diameter ◽  
Consomic Strain

Previous studies have indicated that a deficiency in the formation of 20-HETE in the proximal tubule and thick ascending limb of Henle in Dahl S rats increases sodium reabsorption and contributes to the development of hypertension. The present study examined whether the lack of 20-HETE production in the renal vasculature contributes to the progression of renal injury by altering the myogenic or tubuloglomerular feedback (TGF) response of the afferent arteriole (Af-Art). The production of 20-HETE was significantly lower by 54% in renal microvessels isolated from the kidneys of Dahl S rats versus that seen than in SS.5BN consomic strain in which chromosome 5 from the Brown Norway (BN) rat containing the CYP4A genes responsible for the formation of 20-HETE was transferred into the Dahl S genetic background. The luminal diameter of the Af-Art decreased by 14.7± 1.5% (from 20.5 ± 0.7 to 17.5 ± 0.8 μm, n=6) in SS.5BN rats whereas the diameter of the Af-Art remained unaltered in Dahl S rats (from 20.1 ± 0.6 to 21.7 ± 0.6 μm, n=7) when the perfusion pressure was increased from 60 mmHg to 120 mmHg. In other experiments, adenosine (1 μM) reduced the diameter of the Af-Art in the SS.5BN rats by 15±0.7% (from 20.1 ±0.4 to 17.1 ± 0.9 μm, n=3) whereas the Af-Art of Dahl S rats was unaltered. However, administration of a 20-HETE synthesis inhibitor, HET0016 (1 μM, n=6), or a selective 20-HETE antagonist, 6, 15-20-HEDE (10 μM, n=6) completely blocked the myogenic and adenosine responses in the Af-Art of SS.5BN rats but it had no effect in Dahl S rats. Administration of a 20-HETE agonist, 5, 14-20-HEDE (1 μM) restored the myogenic response (from 20.7 ± 0.7 to 17.6 ± 0.6 μm, n=7) and vasoconstrictor response to adenosine in the Af-Art of Dahl S rats. These studies confirm the key role of 20-HETE in modulating the responsiveness of the Af-Art and indicate that a deficiency in the formation of 20-HETE in renal microvessels contributes to the marked susceptibility of Dahl S rats to develop hypertension induced renal injury.

Does endoplasmic reticulum stress mediate endothelin-1-induced renal inflammation?

2013 ◽  
Vol 305 (2) ◽  
pp. R107-R109 ◽  
Author(s):  
Carmen De Miguel ◽  
Jennifer S. Pollock
Keyword(s):  
Endoplasmic Reticulum ◽  
Thick Ascending Limb ◽  
Afferent Arteriole ◽  
Renal Vasculature ◽  
Renal Inflammation ◽  
Endothelin 1 ◽  
Collecting Ducts ◽  
Potent Vasoconstrictor ◽  
Eventual Death ◽  
Vasoconstrictor Peptide

Endothelin-1 (ET-1) is the most potent vasoconstrictor peptide known. It exerts its actions through two pharmacologically different receptors: ETA and ETB receptors. In the renal vasculature, there is a majority of ETB receptors in the efferent arteriole, whereas a greater amount of ETA receptors are located in the afferent arteriole. The nephron is rich in ETB receptors, especially in the thick ascending limb and collecting ducts, while containing a smaller amount of ETA receptors. High levels of circulating or renal ET-1 have been described in cardiovascular diseases such as hypertension or diabetes, diseases also associated to renal inflammation. Despite extensive evidence associating high levels of ET-1 to increased renal inflammation, the molecular mechanism(s) by which ET-1 leads to renal immune infiltration and/or immune activation remains unknown. In this minireview, we propose that the ET-1/ETA pathway mediates an increase in renal endoplasmic reticulum (ER) stress, initially a survival mechanism that if prolonged, leads to the eventual death of the cell via apoptosis.

Afferent arteriolar adenosine A2a receptors are coupled to KATP in in vitro perfused hydronephrotic rat kidney

1999 ◽  
Vol 277 (6) ◽  
pp. F926-F933 ◽  
Author(s):  
Lilong Tang ◽  
Michael Parker ◽  
Qing Fei ◽  
Rodger Loutzenhiser
Keyword(s):  
Rat Kidney ◽  
Afferent Arteriole ◽  
Adenosine A2a Receptors ◽  
A2a Receptors ◽  
High Affinity ◽  
Vasodilatory Response ◽  
Renal Microvasculature ◽  
Adenosine A2a ◽  
Arteriolar Vasodilation

Adenosine is known to exert dual actions on the afferent arteriole, eliciting vasoconstriction, by activating A1 receptors, and vasodilation at higher concentrations, by activating lower-affinity A2 receptors. We could demonstrate both of these known adenosine responses in the in vitro perfused hydronephrotic rat kidney. Thus, 1.0 μM adenosine elicited a transient vasoconstriction blocked by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), and 10–30 μM adenosine reversed KCl-induced vasoconstriction. However, when we examined the effects of adenosine on pressure-induced afferent arteriolar vasoconstriction, we observed a third action. In this setting, a high-affinity adenosine vasodilatory response was observed at concentrations of 10–300 nM. This response was blocked by both 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-yl-amino]ethyl)phenol (ZM-241385) and glibenclamide and was mimicked by 2-phenylaminoadenosine (CV-1808) (IC50 of 100 nM), implicating adenosine A2a receptors coupled to ATP-sensitive K channels (KATP). Like adenosine, 5′- N-ethylcarboxamidoadenosine (NECA) elicited both glibenclamide-sensitive and glibenclamide-insensitive vasodilatory responses. The order of potency for the glibenclamide-sensitive component was NECA > adenosine = CV-1808. Our findings suggest that, in addition to the previously described adenosine A1 and low-affinity A2b receptors, the renal microvasculature is also capable of expressing high-affinity adenosine A2areceptors. This renal adenosine receptor elicits afferent arteriolar vasodilation at submicromolar adenosine levels by activating KATP.

Abstract 062: Regulation of Nephron Afferent Arteriole Resistance in Obesity: Role of Connecting Tubule Glomerular Feedback

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Sumit R Monu ◽  
Mani Maheshwari ◽  
Hong Wang ◽  
Ed Peterson ◽  
Oscar Carretero
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Tubuloglomerular Feedback ◽  
Afferent Arteriole ◽  
Connecting Tubule ◽  
Single Nephron ◽  
Renal Micropuncture ◽  
The Difference

In obesity, renal damage is caused by increase in renal blood flow (RBF), glomerular capillary pressure (P GC ), and single nephron glomerular filtration rate but the mechanism behind this alteration in renal hemodynamics is unclear. P GC is controlled mainly by the afferent arteriole (Af-Art) resistance. Af-Art resistance is regulated by mechanism similar to that in other arterioles and in addition, it is regulated by two intrinsic feedback mechanisms: 1) tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to an increase in sodium chloride (NaCl) in the macula densa, via sodium–potassium-2-chloride cotransporter-2 (NKCC2) and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation and is mediated by connecting tubule via epithelial sodium channel (ENaC). CTGF is blocked by the ENaC inhibitor benzamil. Attenuation of TGF reduces Af-Art resistance and allows systemic pressure to get transmitted to the glomerulus that causes glomerular barotrauma/damage. In the current study, we tested the hypothesis that TGF is attenuated in obesity and that CTGF contributes to this effect. We used Zucker obese rats (ZOR) while Zucker lean rats (ZLR) served as controls. We performed in-vivo renal micropuncture of individual rat nephrons while measuring stop-flow pressure (P SF ), an index of P GC. TGF response was measured as a decrease in P SF induced by changing the rate of late proximal perfusion from 0 to 40nl/min in stepwise manner.CTGF was calculated as the difference of P SF value between vehicle and benzamil treatment, at each perfusion rate. Maximal TGF response was significantly less in ZOR (6.16 ± 0.52 mmHg) when compared to the ZLR (8.35 ± 1.00mmHg), p<0.05 , indicating TGF resetting in the ZOR. CTGF was significantly higher in ZOR (6.33±1.95 mmHg) when compared to ZLR (1.38±0.89 mmHg), p<0.05 . When CTGF was inhibited with the ENaC blocker Benzamil (1μM), maximum P SF decrease was 12.30±1.72 mmHg in ZOR and 10.60 ± 1.73 mmHg in ZLR, indicating that blockade of CTGF restored TGF response in ZOR. These observations led us to conclude that TGF is reset in ZOR and that enhanced CTGF contributes to this effect. Increase in CTGF may explain higher renal blood flow, increased P GC and higher glomerular damage in obesity.

scholarly journals Effect of denervation on the afferent arteriole in the SHR.

1984 ◽  
Vol 25 (5) ◽  
pp. 745-753 ◽  
Author(s):  
Vincent H. II GATTONE ◽  
Michael SHATTUCK ◽  
Friedrich C. LUFT ◽  
J. Marc OVERHAGE ◽  
L.R. WILLIS ◽  
...  
Keyword(s):  
Afferent Arteriole

Angiotensin II induces a tachyphylactic calcium response in the rabbit afferent arteriole

1997 ◽  
Vol 160 (2) ◽  
pp. 165-173 ◽  
Author(s):  
M. KORNFELD ◽  
A. M. GUTIÉRREZ ◽  
A. E. G. PERSSON ◽  
M. SALOMONSSON
Keyword(s):  
Angiotensin Ii ◽  
Afferent Arteriole ◽  
Calcium Response

Immunocytochemical localization of renin in the developing ovine fetus

1996 ◽  
Vol 8 (1) ◽  
pp. 97 ◽  
Author(s):  
NM Rawashdeh ◽  
JC Rose ◽  
MS Rogers ◽  
C Giammattei ◽  
SS Iskandar
Keyword(s):  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Afferent Arteriole ◽  
Vascular Tree ◽  
Developmentally Regulated ◽  
Newborn Lamb ◽  
Adult Sheep ◽  
Ovine Fetus ◽  
Ovine Fetal ◽  
Renin Content

The ontogeny of renin distribution in the outer cortical segments was studied by immunocytochemistry in two groups of ovine fetal kidneys; one set of fetal kidneys was obtained at 104-106 days (0.73 gestation, n = 6), and the other at 138-140 days (0.96 gestation, n = 6). Similar studies were performed in kidneys obtained from a lamb (2 weeks old) and from non-pregnant adult sheep, n = 4. Using rabbit anti-mouse renin antiserum that was proven to cross react with sheep renin and 0.033% 3',3'-diamino benzidine tetrachloride as a chromogen, immunoreactivity was found to be localized in the classical juxtaglomerular apparatus and the afferent arteriole in the immature fetuses, newborn lamb and adult sheep. In the mature fetuses a more extensive distribution was noted. Immunoreactivity was found in the afferent arteriole and the juxtaglomerular apparatus as well as other segments of the arterial vascular tree. These findings suggest that renal renin distribution in the lamb fetus is developmentally regulated. The results also correlate well with reports about renal cortical renin content and plasma renin activity at the stages studied. These observations further support the hypothesis that increased renal renin expression occurs in the fetus just prior to birth.

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