The Role of Sodium Intake, the Na+-K+ Pump and a Ouabain-Like Humoral Agent in the Genesis of Reduced Renal Mass Hypertension

1983 ◽  
Vol 3 (2-3) ◽  
pp. 92-99 ◽  
Author(s):  
Stephen J. Huot ◽  
Motilal B. Pamnani ◽  
David L. Clough ◽  
Francis J. Haddy
Keyword(s):  
Renal Mass ◽  
Sodium Intake ◽  
Humoral Agent

Role of serotonergic 5-HT1A and oxytocinergic receptors of the lateral septal area in sodium intake regulation

2010 ◽  
Vol 209 (2) ◽  
pp. 260-266 ◽  
Author(s):  
Gabriela Maria Pavan de Arruda Camargo ◽  
Luiz Antônio de Arruda Camargo ◽  
Wilson Abrão Saad
Keyword(s):  
Sodium Intake ◽  
Septal Area ◽  
Lateral Septal Area ◽  
Intake Regulation

scholarly journals The Role of Renal Natriuretic Depressor Systems on Hypertensive Mechanisms in Reduced Renal Mass Hypertensive Rats

1995 ◽  
Vol 18 (SupplementI) ◽  
pp. S53-S57 ◽  
Author(s):  
Kazuaki Shimamoto ◽  
Nobuyuki Ura ◽  
Toshiya Ishiguro ◽  
Motoya Nakagawa ◽  
Osamu Iimura
Keyword(s):  
Renal Mass ◽  
Hypertensive Rats

scholarly journals Role of the endothelium-dependent relaxing factor nitric oxide on renal function.

1992 ◽  
Vol 2 (9) ◽  
pp. 1371-1387 ◽  
Author(s):  
J C Romero ◽  
V Lahera ◽  
M G Salom ◽  
M L Biondi
Keyword(s):  
Nitric Oxide ◽  
Renal Function ◽  
Perfusion Pressure ◽  
Sodium Intake ◽  
Systemic Circulation ◽  
Renal Perfusion ◽  
Renin Release ◽  
High Sodium ◽  
Renal Perfusion Pressure

The role of nitric oxide in renal function has been assessed with pharmacologic and physiologic interventions. Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. However, prostaglandins and nitric oxide do not participate in the renal effects produced by endothelium-independent vasodilators such as atrial natriuretic peptide, prostaglandin I2, and nitroprusside. Physiologically, nitric oxide and prostaglandins exert a strong regulation on the effects produced by changes in renal perfusion pressure. Increments in renal perfusion pressure within the range of RBF autoregulation appear to inhibit prostaglandin synthesis while simultaneously enhancing the formation of nitric oxide. Nitric oxide modulates autoregulatory vasoconstriction and at the same time inhibits renin release. Conversely, a decrease of renal perfusion pressure to the limit of or below RBF autoregulation may inhibit the synthesis of nitric oxide but may trigger the release of prostaglandins, whose vasodilator action ameliorates the fall in RBF and stimulates renin release. Nitric oxide and prostaglandins are also largely responsible for mediating pressure-induced natriuresis. However, unlike prostaglandins, mild impairment of the synthesis of nitric oxide in systemic circulation produces a sustained decrease in sodium excretion, which renders blood pressure susceptible to be increased during high-sodium intake. This effect suggests that a deficiency in the synthesis of nitric oxide could constitute the most effective single disturbance to foster the development of a syndrome similar to that seen in salt-sensitive hypertension.

scholarly journals MP61-07 HIGH RISK DISEASE AND POOR FOLLOWUP: THE ROLE OF RENAL MASS BIOPSY IN A VA COHORT

2021 ◽  
Vol 206 (Supplement 3) ◽  
Author(s):  
Kseniya Anishchenko ◽  
Samuel Antoine ◽  
Rachel Lenzmeier ◽  
Simon Kim ◽  
Granville Lloyd
Keyword(s):  
High Risk ◽  
Renal Mass ◽  
High Risk Disease ◽  
Renal Mass Biopsy

Abstract P244: Role of the Na-H Exchanger Regulatory Factor 1 (NHERF1) in Hypertension of Aging Animals

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Sathnur Pushpakumar ◽  
Corey J Ketchem ◽  
Michelle T Barati ◽  
Utpal Sen ◽  
Pedro J Jose ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Brown Norway ◽  
Proximal Tubule Cells ◽  
Left Femoral Artery ◽  
Old Rats ◽  
Dopamine Signaling ◽  
Old Mice

Aging animals develop hypertension when challenged with high salt diet due, in part, to desensitization of dopamine receptors (DR) in renal proximal tubules (RPT). We have demonstrated that NHERF1 associates with DR1 and Na-K ATPase (NKA) and is important for regulation of NKA in RPT. Preliminary data showed loss of NHERF1 expression in 22m old F344 rats. We hypothesized that loss of NHERF1 results in increased blood pressure (BP) and lack of natriuretic response to dopamine (DA) in aging animals. To address this hypothesis, Fischer Brown Norway (FBN) rats (1m, 4m, 12m, and 24m old) were fed diet containing 1% or 8% NaCl for one week and, BP was measured in anesthetized animals using an indwelling left femoral artery catheter. 8% NaCl did not increase BP in 1m or 4 month old rats. By contrast, 8% NaCl diet increased BP in 12m (84.3±3.5 vs 90.8±2.36) and 24m (73.5±7.58 vs 104±1.6) old animals. To determine if lack of NHERF1 is responsible for the increase in BP, we measured BP in 12 m old WT and NHERF1 KO mice. By contrast to WT mice, 8% NaCl diet did not increase BP in NHERF1 KO mice (84±4.9 vs 96.5±3.56 (WT) and 78.2±3.89 vs 81.8±9.2 (NHERF1 KO mice)). To confirm that NHERF1 is required for DA-mediated inhibition of NKA, NKA activity in primary proximal tubule cells (PTC) from young and old mice in culture was measured in the presence or absence of DA. DA decreased NKA activity in PTC from young animals (67.2±3.8 vs 32.7±5.3) but not in PTC from old animals. Transfection of NHERF1 restored NKA regulation by DA in PTC from old rats (58.4±4.2 vs 64.4±4.3 (in untransfected cells) 54.2±3.8 vs 31.1±3.4 (in NHERF1 transfected cells)). We conclude that NHERF1 regulates DA-mediated proximal tubule sodium handling; however, other factors modulate BP response to dietary sodium intake in young and old animals. The contribution of NHERF1 and dopamine signaling to sodium homeostasis requires further study.

The expanding role of renal mass biopsy

2019 ◽  
Vol 25 (10) ◽  
pp. 379-389
Author(s):  
Sean R. Williamson
Keyword(s):  
Renal Mass ◽  
Renal Mass Biopsy

Role of renal nerves in sodium depletion-induced salt appetite

1996 ◽  
Vol 271 (3) ◽  
pp. R806-R812 ◽  
Author(s):  
R. L. Thunhorst ◽  
R. F. Kirby ◽  
A. K. Johnson
Keyword(s):  
Enzyme Inhibitor ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Salt Appetite ◽  
Subcutaneous Injections ◽  
Intact Control ◽  
Water And Sodium Excretion

The ingestion of water and 0.3 M NaCl solution and the secretion of key hormones were studied in groups of intact and bilaterally renal-denervated rats after extracellular fluid depletion. Hypovolemia with mild hypotension was produced by subcutaneous injections of the diuretic furosemide (10 mg/kg) followed by injections of the angiotensin-converting enzyme inhibitor captopril (5 mg/kg s.c.). Denervated rats drank significantly less of a concentrated saline solution in response to depletion than intact control rats did, but drank similar amounts of water. Denervated rats finished testing in significantly greater negative water and sodium balance compared with controls. Renal denervation did not impair the secretion of renin and aldosterone or the formation of angiotensin I. The diminished sodium intake of denervated rats is not attributable to reduced water and sodium excretion in response to the hypovolemic protocol. These results indicate that the integrity of the renal nerves is important for the normal elaboration of salt appetite in response to hypovolemia/hypotension.

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