Differences in glomerular binding and response to angiotensin II between normotensive and spontaneously hypertensive rats

1988 ◽  
Vol 75 (2) ◽  
pp. 191-196 ◽  
Author(s):  
E. A. Messenger ◽  
C. Stonier ◽  
G. M. Aber
Keyword(s):  
Angiotensin Ii ◽  
Sodium Intake ◽  
Affinity Constant ◽  
Maximal Response ◽  
Ang Ii ◽  
Shr Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
High Sodium Intake

1. Angiotensin II (ANG II) binding and the physiological response to exogenous ANG II have been studied in isolated glomerular preparations from normotensive (NTR) and spontaneously hypertensive (SHR) rats. 2. The binding of 125I-labelled ANG II by glomeruli from SHR was significantly greater than that by glomeruli from NTR, whereas the binding affinity constant (Ka) showed that the SHR ANG II glomerular receptor had a lower affinity for the hormone than the NTR glomerular receptor. 3. Glomeruli from SHR were significantly less responsive to exogenous ANG II than those from NTR. 4. Sodium loading resulted in a significant increase in ANG II binding by glomeruli from NTR, whereas a decrease in binding occurred in glomeruli from SHR. 5. Although a high sodium intake caused a reduction in the response of glomeruli from both NTR and SHR to exogenous ANG II, these changes were not statistically significant. In NTR this was associated with a decrease in the concentration of agonist required to cause half-maximal response (EC50), whereas an increase in EC50 was shown by glomeruli from SHR.

Influence of age on glomerular binding of angiotensin II in normotensive and spontaneously hypertensive rats

1989 ◽  
Vol 76 (6) ◽  
pp. 619-623 ◽  
Author(s):  
E. A. Messenger ◽  
C. Stonier ◽  
G. M. Aber
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Affinity Constant ◽  
Ang Ii ◽  
Shr Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Age Related ◽  
Age Related Changes

1. Glomerular angiotensin II (ANG II) binding has been studied in normotensive (NTR) and spontaneously hypertensive (SHR) rats at 5, 10, 15 and 20 weeks of age. 2. Binding of 125I-labelled ANG II by glomeruli from NTR and SHR was similar at 5 and 10 weeks of age, with 5 week values of 426.4 (range 384-469) and 400.2 ± 245 fmol/mg of protein; however, at 15 and 20 weeks ANG II binding by SHR glomeruli was significantly greater than by NTR, with 20 week values of 614.7 ± 245 and 308.3 ± 31.8 fmol/mg of protein, respectively (P < 0.01). 3. The ANG II binding affinity constant (Ka) of glomeruli from NTR and SHR was comparable at 5, 10 and 15 weeks of age, with values of 1.5 (range 1.1-1.9) and 1.08 ± 0.35 nmol/l, respectively, at 5 weeks; whereas at 20 weeks the Ka for SHR glomeruli was significantly greater than for NTR, with values of 1.85 ± 0.45 and 0.66 ± 0.22 nmol/l, respectively (P < 0.001). 4. Age-related changes in glomerular binding of ANG II in SHR were not found to be related to changes in either plasma renin activity or systolic blood pressure.

Effects of high sodium intake on cardiovascular aldosterone synthesis in stroke-prone spontaneously hypertensive rats

2001 ◽  
Vol 19 (Supplement) ◽  
pp. 635-639 ◽  
Author(s):  
Yoshiyu Takeda ◽  
Takashi Yoneda ◽  
Masashi Demura ◽  
Kenji Furukawa ◽  
Isamu Miyamori ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
High Sodium Intake

The Effect of Chronic Sodium Loading and Sodium Restriction on Plasma and Renal Concentrations of Prostaglandin a in Normal Wistar and Spontaneously Hypertensive Aoki Rats

1973 ◽  
Vol 45 (s1) ◽  
pp. 325s-329s ◽  
Author(s):  
R. M. Zusman ◽  
B. H. Forman ◽  
G. Schneider ◽  
B. V. Caldwell ◽  
L. Speroff ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Sodium Intake ◽  
Dietary Group ◽  
Sodium Restriction ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
High Sodium Intake ◽  
Low Sodium

1. In normal and hypertensive rats prostaglandin A (PGA) in plasma and kidney increased on low sodium intake and decreased on high sodium intake. 2. Plasma and renal concentrations of PGA were higher in spontaneously hypertensive rats than in normal Wistar rats in each dietary group.

scholarly journals Brain “ouabain,” ANG II, and sympathoexcitation by chronic central sodium loading in rats

1998 ◽  
Vol 274 (4) ◽  
pp. H1269-H1276 ◽  
Author(s):  
Bing S. Huang ◽  
Shereeni J. Veerasingham ◽  
Frans H. H. Leenen
Keyword(s):  
Wistar Rats ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
High Sodium Intake ◽  
Fab Fragments ◽  
Γ Globulins

Both brain ouabain-like activity (“ouabain”) and brain angiotensin II (ANG II) contribute to the sympathoexcitatory and pressor responses to high sodium intake in spontaneously hypertensive (SHR) and Dahl salt-sensitive (Dahl S) rats. To assess whether increases in cerebrospinal fluid (CSF) sodium can mimic this pattern of changes, Wistar rats were chronically infused with artificial CSF (aCSF) or sodium-rich aCSF (0.8 or 1.2 M sodium) intracerebroventricularly through osmotic minipumps for 14 days. Sodium-rich aCSF (0.8 M) was also infused intracerebroventricularly for 2 wk concomitantly with either antibody Fab fragments that bind ouabain and related steroids with high affinity, γ-globulins as control (200 μg/day for both), or the AT1blocker losartan (1 mg ⋅ kg−1 ⋅ day−1). Sodium-rich aCSF increased CSF sodium from 146 ± 2 to 152 ± 2 (0.8 M) and 160 ± 3 (1.2 M) mmol/l, and increased brain “ouabain” in the hypothalamus, pituitary, and pons. In conscious rats, sodium-rich aCSF increased baseline mean arterial pressure (MAP), enhanced MAP, heart rate (HR), and renal sympathetic nerve activity (RSNA) responses to intracerebroventricular α2-adrenoceptor agonist guanabenz and air stress, and desensitized arterial and cardiopulmonary baroreflex control of HR and RSNA. These effects were largely prevented by intracerebroventricular Fab fragments or losartan. Thus, in Wistar rats, both brain “ouabain” and the brain renin-angiotensin system contribute to sympathoexcitation, impairment of baroreflexes, and hypertension caused by chronically increased CSF sodium. The similar patterns of changes caused by CSF sodium in Wistar rats and by high sodium intake in SHR and Dahl S rats indicate that if high sodium intake increases central sodium, such changes may contribute to sympathoexcitation and hypertension.

Role of aldosterone in angiotensin II-induced hypertension in rats

1990 ◽  
Vol 259 (1) ◽  
pp. R102-R109 ◽  
Author(s):  
N. L. Kanagy ◽  
C. M. Pawloski ◽  
G. D. Fink
Keyword(s):  
Angiotensin Ii ◽  
Sodium Intake ◽  
Chronic Administration ◽  
Plasma Aldosterone ◽  
Ang Ii ◽  
Plasma Aldosterone Concentration ◽  
High Sodium ◽  
High Sodium Intake ◽  
Induced Hypertension ◽  
Commercial Radio

Initial experiments demonstrated that a 1-h infusion of 10 ng/min angiotensin II (ANG II) into rats causes an increase in plasma aldosterone concentration (PAC) and that chronic administration of aldosterone alone to rats on increased sodium intake causes hypertension. We therefore hypothesized that a portion of the hypertensive effect of chronic ANG II infusion is accompanied by and dependent on chronic release of aldosterone. To test this hypothesis, 10 ng/min ANG II or saline was infused into chronically instrumented rats housed in metabolism cages. Fifteen rats were maintained on a high sodium intake (6 meq/day); 10 received ANG II and 5 received saline. Ten other rats were maintained on a normal sodium intake (2 meq/day); five received ANG II and five received saline. PAC was measured using a commercial radio-immunoassay kit. Mean arterial pressure (MAP), heart rate, water intake, urine output, and urine electrolytes were measured daily during 3-day control, 16- or 28-day infusion, and 4-day recovery periods. Compared with saline-infused rats, ANG II-infused rats on high sodium intake had normal values for all variables except MAP, which was significantly elevated during ANG II infusion. In the normal sodium group, none of the variables were consistently different during ANG II infusion compared with control. These results suggest that ANG II-induced hypertension in the rat is sodium dependent, that plasma aldosterone does not play a major role in ANG II-induced hypertension in the rat, and that a small chronic increase in circulating ANG II does not necessarily lead to a detectable sustained increase in PAC.

scholarly journals High Na intake increases renal angiotensin II levels and reduces expression of the ACE2-AT2R-MasR axis in obese Zucker rats

2012 ◽  
Vol 303 (3) ◽  
pp. F412-F419 ◽  
Author(s):  
Preethi Samuel ◽  
Quaisar Ali ◽  
Rifat Sabuhi ◽  
Yonnie Wu ◽  
Tahir Hussain
Keyword(s):  
Sodium Intake ◽  
Zucker Rats ◽  
Kidney Cortex ◽  
Complex Nature ◽  
Ang Ii ◽  
Pronounced Increase ◽  
High Sodium ◽  
High Sodium Intake ◽  
Obese Rats ◽  
Obese Zucker Rats

High sodium intake is known to regulate the renal renin-angiotensin system (RAS) and is a risk factor for the pathogenesis of obesity-related hypertension. The complex nature of the RAS reveals that its various components may have opposing effects on natriuresis and blood pressure regulation. We hypothesized that high sodium intake differentially regulates and shifts a balance between opposing components of the renal RAS, namely, angiotensin-converting enzyme (ACE)-ANG II-type 1 ANG II receptor (AT1R) vs. AT2-ACE2-angiotensinogen (Ang) (1–7)-Mas receptor (MasR), in obesity. In the present study, we evaluated protein and/or mRNA expression of angiotensinogen, renin, AT1A/BR, ACE, AT2R, ACE2, and MasR in the kidney cortex following 2 wk of a 8% high-sodium (HS) diet in lean and obese Zucker rats. The expression data showed that the relative expression pattern of ACE and AT1BR increased, renin decreased, and ACE2, AT2R, and MasR remained unaltered in HS-fed lean rats. On the other hand, HS intake in obese rats caused an increase in the cortical expression of ACE, a decrease in ACE2, AT2R, and MasR, and no changes in renin and AT1R. The cortical levels of ANG II increased by threefold in obese rats on HS compared with obese rats on normal salt (NS), which was not different than in lean rats. The HS intake elevated mean arterial pressure in obese rats (27 mmHg) more than in lean rats (16 mmHg). This study suggests that HS intake causes a pronounced increase in ANG II levels and a reduction in the expression of the ACE2-AT2R-MasR axis in the kidney cortex of obese rats. We conclude that such changes may lead to the potentially unopposed function of AT1R, with its various cellular and physiological roles, including the contribution to the pathogenesis of obesity-related hypertension.

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