Role of renal interstitial hydrostatic pressure in the pressure diuresis response

1989 ◽  
Vol 256 (1) ◽  
pp. F63-F70 ◽  
Author(s):  
J. Garcia-Estan ◽  
R. J. Roman
Keyword(s):  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Capsule ◽  
Interstitial Pressure ◽  
Renal Perfusion Pressure ◽  
Residual Response

The present study examines the role of renal interstitial hydrostatic pressure (RIHP) in the pressure-diuretic and -natriuretic response. The relationships between RIHP, sodium excretion, and renal perfusion pressure (RPP) were determined in antidiuretic and volume-expanded (VE) rats with an intact or decapsulated kidney. RIHP was measured by use of the implanted capsule technique. RIHP increased significantly from 7.5 +/- 0.8 to 12.0 +/- 1.4 mmHg in VE animals and from 3.3 +/- 0.4 to 5.2 +/- 0.7 mmHg in antidiuretic rats after RPP was varied from 100 to 150 mmHg. The pressure-natriuretic response of the antidiuretic rats was blunted compared with that observed in the VE rats. Decapsulation of the kidney in VE rats lowered RIHP and reduced, but did not eliminate, the pressure-natriuretic response. To determine whether this residual response was related to changes in interstitial pressure in the medulla, cortical (CIHP) and medullary interstitial hydrostatic pressures (MIHP) were simultaneously measured in VE rats with an intact or decapsulated kidney. In control rats CIHP and MIHP were similar at all levels of RPP studied. In rats with the renal capsule removed MIHP was higher than CIHP and rose significantly from 6.7 +/- 0.8 to 9.2 +/- 0.8 mmHg when RPP was varied from 100 to 150 mmHg. These results indicate that pressure diuresis and natriuresis is accompanied by changes in RIHP and the response is modulated by the basal level of RIHP. These findings suggest that changes in MIHP may serve as an intrarenal signal for this response.

L-arginine improves transmission of perfusion pressure to the renal interstitium in Dahl salt-sensitive rats

1994 ◽  
Vol 266 (6) ◽  
pp. R1730-R1735 ◽  
Author(s):  
A. R. Patel ◽  
J. P. Granger ◽  
K. A. Kirchner
Keyword(s):  
Hydrostatic Pressure ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Capsule ◽  
Renal Perfusion Pressure ◽  
Renal Interstitium ◽  
Pressure Natriuresis ◽  
Acute Changes ◽  
The Relationship

L-Arginine normalizes pressure natriuresis in Dahl salt-sensitive (DS) rats. To determine the role of renal interstitial hydrostatic pressure (RIHP) in this phenomenon, we measured RIHP determined by servo-null during acute changes in renal perfusion pressure in anesthetized DS rats receiving L-arginine (300 mg.kg-1.day-1 ip) or vehicle for 3 wk. Dahl salt-resistant (DR) rats were controls. As observed previously, the slope of the pressure-natriuresis relationship was greater (P < 0.05) in L-arginine-treated DS rats than vehicle DS rats and not different from DR rats. The slope of the relationship between renal perfusion pressure and RIHP was greater (P < 0.05) in DR rats than vehicle DS rats. In L-arginine-treated DS rats the slope of this relationship was greater (P < 0.05) than that in vehicle DS rats and not different from DR rats. Removal of the renal capsule blunted the pressure-natriuresis relationship in L-arginine-treated DS rats but had no effect in vehicle DS rats. Thus L-arginine improves transmission of perfusion pressure into the renal interstitium in DS rats and may contribute to the improved pressure-natriuresis response.

Effect of Renal Perfusion Pressure on Renal Interstitial Hydrostatic Pressure and Sodium Excretion

Hypertension ◽  
1995 ◽  
Vol 25 (4) ◽  
pp. 866-871 ◽  
Author(s):  
Tetsuya Nakamura ◽  
Tetsuo Sakamaki ◽  
Toshiaki Kurashina ◽  
Kunio Sato ◽  
Zenpei Ono ◽  
...  
Keyword(s):  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure

Effect of renal perfusion pressure on renal interstitial hydrostatic pressure in rats

1989 ◽  
Vol 256 (1) ◽  
pp. F165-F170 ◽  
Author(s):  
A. A. Khraibi ◽  
J. A. Haas ◽  
F. G. Knox
Keyword(s):  
Hydrostatic Pressure ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Fractional Excretion ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Polyethylene Matrix ◽  
Renal Perfusion Pressure ◽  
Fractional Excretion Of Sodium

The purpose of this study was to investigate the hypothesis that changes in renal perfusion pressure may be transmitted to the renal interstitium and cause alterations in renal interstitial hydrostatic pressure and sodium excretion. A method that utilizes a chronically implanted polyethylene matrix that allows for direct continuous measurement of renal interstitial hydrostatic pressure, and agrees well with subcapsular measurement in rats, was developed. Renal interstitial hydrostatic pressure, fractional excretion of sodium, and urine flow rate were 3.0 +/- 0.3 mmHg, 0.35 +/- 0.13%, and 19.44 +/- 3.00 microliter/min, respectively, when renal perfusion pressure was 101 +/- 0.8 mmHg. When renal perfusion pressure was increased to 123 +/- 0.9 mmHg renal interstitial hydrostatic pressure, fractional excretion of sodium, and urine flow rate increased significantly to 5.8 +/- 0.6 mmHg, 1.29 +/- 0.29%, and 50.76 +/- 8.83 microliter/min, respectively, in anesthetized male Sprague-Dawley rats. These changes occur despite a well-autoregulated glomerular filtration rate and renal blood flow. In conclusion, increasing renal perfusion pressure caused a significant increase in renal interstitial hydrostatic pressure as measured directly by the implanted polyethylene matrix method and was associated with a significant increase in sodium excretion.

Effects of Renal Perfusion Pressure on Renal Interstitial Hydrostatic Pressure and Na+ Excretion: Role of Endothelium-Derived Nitric Oxide

Nephron ◽  
1997 ◽  
Vol 78 (1) ◽  
pp. 104-111 ◽  
Author(s):  
Tetsuya Nakamura ◽  
Antonio M. Alberola ◽  
F. Javier Salazar ◽  
Yuichiro Saito ◽  
Toshiaki Kurashina ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrostatic Pressure ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure

Effects of meclofenamate on the renin response to aortic constriction in the rat

1984 ◽  
Vol 247 (3) ◽  
pp. R546-R551 ◽  
Author(s):  
D. Villarreal ◽  
J. O. Davis ◽  
R. H. Freeman ◽  
W. D. Sweet ◽  
J. R. Dietz
Keyword(s):  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Release ◽  
Aortic Constriction ◽  
Renal Perfusion Pressure ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Intact Kidney ◽  
Stimulus Secretion Coupling

This study examines the role of the renal prostaglandin system in stimulus-secretion coupling for renal baroreceptor-dependent renin release in the anesthetized rat. Changes in plasma renin activity (PRA) secondary to suprarenal aortic constriction were evaluated in groups of rats with a single denervated nonfiltering kidney (DNFK) with and without pretreatment with meclofenamate. Suprarenal aortic constriction was adjusted to reduce renal perfusion pressure to either 100 or 50 mmHg. In addition, similar experiments were performed in rats with a single intact filtering kidney. Inhibition of prostaglandin synthesis with meclofenamate failed to block or attenuate the increase in PRA in response to the decrement in renal perfusion pressure after both severe and mild aortic constriction for both the DNFK and the intact-kidney groups. The adequacy of prostaglandin inhibition was demonstrated by complete blockade with meclofenamate of the marked hypotensive and hyperreninemic responses to sodium arachidonate. The results in the DNFK indicate that in the rat, renal prostaglandins do not function as obligatory mediators of the isolated renal baroreceptor mechanism for the control of renin release. Also the findings in the intact filtering kidney suggest that prostaglandins are not essential in the renin response of other intrarenal receptor mechanisms that also are stimulated by a reduction in renal perfusion pressure.

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.

Interaction of renal beta 1-adrenoceptors and prostaglandins in reflex renin release

1983 ◽  
Vol 244 (4) ◽  
pp. F418-F424 ◽  
Author(s):  
U. Kopp ◽  
G. F. DiBona
Keyword(s):  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Prostaglandin Synthesis ◽  
Urinary Sodium ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Renal Perfusion Pressure

Anesthetized dogs with isolated carotid sinus preparation were used to examine the mechanisms involved in the increase in renin secretion rate produced by carotid baroreceptor reflex renal nerve stimulation (RNS) at constant renal perfusion pressure. Lowering carotid sinus pressure by 41 +/- 5 mmHg for 10 min increased mean arterial pressure and heart rate, caused no or minimal renal hemodynamic changes, decreased urinary sodium excretion, and increased renin secretion rate. Metoprolol, a beta 1-adrenoceptor antagonist, given in the renal artery, did not affect the decrease in urinary sodium excretion but attenuated the increase in renin secretion rate, from 1,764 +/- 525 to 412 +/- 126 ng/min (70 +/- 8%). Indomethacin or meclofenamate, prostaglandin synthesis inhibitors, did not affect the decrease in urinary sodium excretion but attenuated the increase in renin secretion rate, from 1,523 +/- 416 to 866 +/- 413 ng/min (51 +/- 18%). Addition of metoprolol to indomethacin-pretreated dogs attenuated the increase in renin secretion rate from 833 +/- 327 to 94 +/- 60 ng/min (86 +/- 10%). These results indicate that reflex RNS at constant renal perfusion pressure results in an increase in renin secretion rate that is largely mediated by renal beta 1-adrenoceptors and is partly dependent on intact renal prostaglandin synthesis. The beta 1-adrenoceptor-mediated increase in renin secretion rate is independent of and not in series with renal prostaglandins.

Role of the Renal Nerves in Renin Release during Suprarenal Aortic Stenosis in Cats

1976 ◽  
Vol 51 (s3) ◽  
pp. 85s-87s
Author(s):  
A. Stella ◽  
F. Calaresu ◽  
A. Zanchetti
Keyword(s):  
Aortic Stenosis ◽  
Time Course ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renin Release ◽  
Renal Nerves ◽  
Renal Perfusion Pressure ◽  
The Difference

1. Renin release from an intact, innervated kidney and from the contralateral denervated kidney was measured before and during a period of suprarenal aortic stenosis. 2. Aortic stenosis of 10 min duration reduced renal perfusion pressure to 50 mmHg and increased renin release from both kidneys, but the response from the innervated kidney was greater. 3. A study of the time-course of the response during 30 min of aortic stenosis showed that the difference in rate of renin release between the innervated and the denervated kidney is greatest during the first few minutes of aortic stenosis.

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