Importance of the renal medullary circulation in the control of sodium excretion and blood pressure

2003 ◽  
Vol 284 (1) ◽  
pp. R13-R27 ◽  
Author(s):  
David L. Mattson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Medulla ◽  
Water Excretion ◽  
Vascular Architecture ◽  
Excretory Function ◽  
Medullary Blood Flow ◽  
Arterial Blood ◽  
Renal Medullary Blood Flow ◽  
The Impact

The control of renal medullary perfusion and the impact of alterations in medullary blood flow on renal function have been topics of research interest for almost four decades. Many studies have examined the vascular architecture of the renal medulla, the factors that regulate renal medullary blood flow, and the influence of medullary perfusion on sodium and water excretion and arterial pressure. Despite these studies, there are still a number of important unanswered questions in regard to the control of medullary perfusion and the influence of medullary blood flow on renal excretory function and blood pressure. This review will first address the vascular architecture of the renal medulla and the potential mechanisms whereby medullary perfusion may be regulated. The known extrarenal and local systems that influence the medullary vasculature will then be summarized. Finally, this review will present an overview of the evidence supporting the concept that selective changes in medullary perfusion can have a potent influence on sodium and water excretion with a long-term influence on arterial blood pressure regulation.

Renal cortical and medullary blood flow responses to l-NAME and ANG II in wild-type, nNOS null mutant, and eNOS null mutant mice

2005 ◽  
Vol 289 (4) ◽  
pp. R991-R997 ◽  
Author(s):  
David L. Mattson ◽  
Carla J. Meister
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Cortex ◽  
Renal Medulla ◽  
Ang Ii ◽  
Null Mutant ◽  
Wild Type ◽  
Medullary Blood Flow ◽  
Arterial Blood ◽  
Null Mutant Mice

Experiments in wild-type (WT; C57BL/6J) mice, endothelial nitric oxide synthase null mutant [eNOS(-/-)] mice, and neuronal NOS null mutant [nNOS(-/-)] mice were performed to determine which NOS isoform regulates renal cortical and medullary blood flow under basal conditions and during the infusion of ANG II. Inhibition of NOS with Nω-nitro-l-arginine methyl ester (l-NAME; 50 mg/kg iv) in Inactin-anesthetized WT and nNOS(-/-) mice increased arterial blood pressure by 28–31 mmHg and significantly decreased blood flow in the renal cortex (18–24%) and the renal medulla (13–18%). In contrast, blood pressure and renal cortical and medullary blood flow were unaltered after l-NAME administration to eNOS(-/-) mice, indicating that NO derived from eNOS regulates baseline vascular resistance in mice. In subsequent experiments, intravenous ANG II (20 ng·kg−1·min−1) significantly decreased renal cortical blood flow (by 15–25%) in WT, eNOS(-/-), nNOS(-/-), and WT mice treated with l-NAME. The infusion of ANG II, however, led to a significant increase in medullary blood flow (12–15%) in WT and eNOS(-/-) mice. The increase in medullary blood flow following ANG II infusion was not observed in nNOS(-/-) mice, in WT or eNOS(-/-) mice pretreated with l-NAME, or in WT mice administered the nNOS inhibitor 5-(1-imino-3-butenyl)-l-ornithine (1 mg·kg−1·h−1). These data demonstrate that NO from eNOS regulates baseline blood flow in the mouse renal cortex and medulla, while NO produced by nNOS mediates an increase in medullary blood flow in response to ANG II.

Role of renal medullary blood flow in the development of L-NAME hypertension in rats

1995 ◽  
Vol 268 (2) ◽  
pp. R317-R323 ◽  
Author(s):  
K. Nakanishi ◽  
D. L. Mattson ◽  
A. W. Cowley
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Flow Distribution ◽  
Renal Medulla ◽  
Sodium Balance ◽  
Cortical Blood Flow ◽  
Medullary Blood Flow ◽  
Intrarenal Blood Flow ◽  
Renal Medullary Blood Flow ◽  
Renal Cortical Blood Flow

The effect of chronic intravenous infusion of the nitric oxide inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 8.6 mg.kg-1.day-1) on blood pressure, intrarenal blood flow distribution, and sodium and water balance was studied in conscious rats. On the 1st day of intravenous L-NAME infusion, renal medullary blood flow was reduced by 22%, renal cortical blood flow was unaltered, approximately 1 meq of sodium and 12 ml of water were retained, and blood pressure increased from 96 +/- 2 to 118 +/- 2 mmHg. Medullary blood flow was maintained at this decreased level, sodium continued to be retained, body weight continued to increase, and blood pressure remained elevated for the 5 days of L-NAME infusion. During the postcontrol period, blood flow in the renal medulla returned to levels not significantly different from control; the animals went into negative sodium balance and stopped gaining weight, and blood pressure returned to control. The present experiments indicate that decreased renal medullary blood flow and retention of sodium and water play an important role in the development of hypertension during chronic systemic L-NAME administration despite no measurable changes in renal cortical blood flow.

Renal medullary blood flow: its measurement and physiology

1986 ◽  
Vol 64 (7) ◽  
pp. 873-880 ◽  
Author(s):  
W. A. Cupples
Keyword(s):  
Blood Flow ◽  
Renal Medulla ◽  
Vascular Bundles ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Countercurrent Exchange ◽  
Renal Medullary Blood Flow ◽  
Urinary Concentrating Ability ◽  
Velocity Tracking ◽  
Uptake Method

The vasculature of the mammalian renal medulla is complex, having neither discrete input nor output. There is also efficient countercurrent exchange between ascending and descending vasa recta in the vascular bundles. These considerations have hampered measurement of medullary blood flow since they impose pronounced constraints on methods used to assess flow. Three main strategies have been used: (i) indicator extraction; (ii) erythrocyte velocity tracking; and (iii) indicator dilution. These are discussed with respect to their assumptions, requirements, and limitations. There is a consensus that medullary blood flow is autoregulated, albeit over a narrower pressure range than is total renal blood flow. When normalized to gram tissue weight, medullary blood flow in the dog is similar to that in the rat, on the order of 1 to 1.5 mL∙min−1∙g−1. This is considerably greater than estimated by the radioiodinated albumin uptake method which has severe conceptual and practical problems. From both theoretical and experimental evidence it ssems that urinary concentrating ability is considerably less sensitive to changes in medullary blood flow than is often assumed.

Renal medullary interstitial infusion ofl-arginine prevents hypertension in Dahl salt-sensitive rats

1998 ◽  
Vol 275 (5) ◽  
pp. R1667-R1673 ◽  
Author(s):  
Noriyuki Miyata ◽  
Ai Ping Zou ◽  
David L. Mattson ◽  
Allen W. Cowley
Keyword(s):  
Blood Flow ◽  
Control Period ◽  
Renal Medulla ◽  
High Salt ◽  
No Production ◽  
Medullary Blood Flow ◽  
Induced Hypertension ◽  
Renal Medullary Blood Flow ◽  
Wistar Kyoto ◽  
Interstitial Infusion

Studies were designed to examine the effects of renal medullary interstitial infusion of l-arginine (l-Arg) on the development of high-salt-induced hypertension in Dahl salt-sensitive/Rapp (DS) rats. The threshold dose of l-Arg (300 μg ⋅ kg−1 ⋅ min−1) that increased the renal medullary blood flow without altering the cortical blood flow was first determined in anesthetized DS rats. Studies were then carried out to determine the effects of this dose ofl-Arg on salt-induced hypertension in DS rats. In the absence of chronic medullaryl-Arg infusion, mean arterial pressure (MAP) increased in DS rats from 125 ± 2 to 167 ± 5 mmHg by day 5 of a high-salt diet (4.0%), with no change observed in Wistar-Kyoto (WKY) or Dahl salt-resistant/Rapp (DR) rats. MAP did not change significantly with medullary infusion ofl-Arg alone in DR rats (control = 104 ± 1 mmHg) or in WKY rats (control = 120 ± 3 mmHg) and was not significantly changed from these levels during the 7 days ofl-Arg infusion combined with high-NaCl diet. The same amount of l-Arg that prevented salt-induced hypertension in DS rats when infused into the renal medulla (300 μg ⋅ kg−1 ⋅ min−1) failed to blunt salt-induced hypertension when administered intravenously to DS rats. DS rats receiving l-Arg (300 μg ⋅ kg−1 ⋅ min−1iv) exhibited an increase in plasma l-Arg from control concentrations of 138 ± 11 to 218 ± 4 μmol/l, while MAP, which averaged 124 ± 3 mmHg during the 3-day control period, rose to 165 ± 5 mmHg by day 5of high salt (4%) intake. These results indicate that the prevention of salt sensitivity in DS rats was due specifically to the action of l-Arg on renal medullary function and that DS rats may have a deficit of medullary substrate availability and NO production.

Effect of chronic renal medullary nitric oxide inhibition on blood pressure

1994 ◽  
Vol 266 (5) ◽  
pp. H1918-H1926 ◽  
Author(s):  
D. L. Mattson ◽  
S. Lu ◽  
K. Nakanishi ◽  
P. E. Papanek ◽  
A. W. Cowley
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Renal Medulla ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Nitric Oxide Inhibition ◽  
Medullary Blood Flow ◽  
Nitric Oxide Inhibitor ◽  
Oxide Inhibition

The effects of chronic nitric oxide inhibition in the renal medulla on renal cortical and medullary blood flow, sodium balance, and blood pressure were evaluated in conscious uninephrectomized Sprague-Dawley rats. During a 5-day renal medullary interstitial infusion of the nitric oxide inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 120 micrograms/h) in saline (0.5 ml/min), renal medullary blood flow was selectively decreased by 30% after 2 h and was maintained at that level for the entire infusion. The decrease in medullary blood flow was associated with sodium retention and increased blood pressure. After the cessation of L-NAME infusion, medullary blood flow returned to control, and the sodium balance became negative as blood pressure returned to baseline. These data indicate that renal medullary nitric oxide plays an important role in the regulation of renal blood flow, sodium excretion, and blood pressure.

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