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PubMed1985

Demeclocycline-induced natriuresis and renal insufficiency: in vivo and in vitro studies.

We examined renal function and Na+ balance in a patient with congestive heart failure who was treated with demeclocycline (DMC) on three separate occasions under strict metabolic balance conditions. Natriuresis and reversible renal insufficiency, which could not be explained solely on the basis of negative Na+ balance, developed on each occasion. In contrast to reports of an association between elevated serum DMC levels and renal insufficiency in patients with cirrhotic edema, the renal insufficiency in this patient with cardiac edema occurred in the absence of high DMC levels. Consequently, markedly elevated serum DMC levels do not appear to be a prerequisite for the development of natriuresis or renal insufficiency in edematous patients receiving this drug. In an attempt to clarify the mechanism of the natriuresis, we also examined the effects of DMC on Na+ transport in an in-vitro model system, the toad urinary bladder. DMC inhibited aldosterone-stimulated Na+ transport, but had no effect on Na+ transport when the latter was jointly stimulated by ADH and theophylline. Despite this selective inhibition of the natriferic effect of aldosterone in vitro, it is unlikely that such a mechanism completely accounts for the natriuresis observed in-vivo since the natriuresis is generally of large magnitude and is usually accompanied by some degree of kaliuresis, and DMC had no consistent effect on urinary aldosterone excretion. Consequently, other mechanisms must be sought to explain the natriuretic effect of DMC in edematous patients. Likewise, mechanisms other than negative Na+ balance (perhaps primary alterations in renal hemodynamics) must underly the development of renal insufficiency in such individuals.

Administration, Oral↗
PubMed1985

Pressure dependence of exaggerated natriuresis in two-kidney, one clip Goldblatt hypertensive rats.

This study evaluated the responses of each kidney of two-kidney, one clip Goldblatt hypertensive rats to acute volume loading to delineate the contribution of elevated perfusion pressure to the mechanisms of the exaggerated natriuresis in this model of hypertension. Eleven Goldblatt animals (0.2 mm clip 3 weeks prior to study) were studied at spontaneous blood pressure for each kidney's response to volume loading. In 11 other Goldblatt animals an aortic clamp between the renal arteries allowed reduction of perfusion pressure for the left, nonclipped kidney to normal levels. Ten normal rats served as controls. Renal function was examined during control periods and following the infusion of 3.5% body wt of 154 mM X liter-1 NaCl at 22.5 ml X hr-1. An exaggerated natriuresis was observed for the left, nonclipped kidney of the hypertensive Goldblatt rats, while the clipped kidney exhibited an attenuated natriuresis compared to either kidney of normal control rats. Reduction of perfusion pressure to the nonclipped kidney of Goldblatt animals to normal levels resulted in reduced clearance and excretory function before volume loading and attenuated its natriuretic response to levels less than those for the Goldblatt group at spontaneous, hypertensive blood pressure. The exaggerated natriuresis observed at hypertensive blood pressure was attributable to increases of filtered load of Na+ and reduced fractional absorption. These observations indicate that an exaggerated natriuresis occurs in the two-kidney, one clip Goldblatt hypertensive rat and that this phenomenon depends on the elevated renal perfusion pressure to the nonclipped kidney.

Animals↗
PubMed2006

Selective endothelin B receptor blockade does not influence BNP-induced natriuresis in man.

Brain natriuretic peptide (BNP) and endothelin-1 (ET-1) both exhibit natriuretic activity within the human kidney. Furthermore, they both act partly through activation of the endothelial nitric oxide pathway. Since ET-1 may cause vasodilation and natriuresis via stimulation of the ET-B receptor, the aim of the present study was to investigate whether renal ET-B receptors participate in the renal actions of BNP. In this placebo-controlled, crossover study, we infused BNP (4 pmol/kg/min) or placebo (i.v.) for 1 h, with or without co-infusion of the ET-B receptor antagonist BQ-788 (50 nmol/min) for 15 min on 4 separate days, in 10 healthy subjects (mean age 54+/-6 years.). During infusion, we measured effective renal plasma flow (ERPF), and glomerular filtration rate (GFR) using PAH/inulin clearance. Cardiac output was measured before and after infusion, using echocardiography. Blood pressure and heart rate (HR) were monitored as well. Urine and plasma samples were taken every hour to measure diuresis, natriuresis, cyclic 3',5' guanosine monophosphate, and ET-1 levels. BNP with or without ET-B receptor blockade increased natriuresis and diuresis. In addition, BNP alone increased GFR and filtered load, without changing ERPF. BQ-788 infusion did not affect renal hemodynamics or natriuresis. Neither BNP nor BQ-788 altered cardiac output, blood pressure, and heart rate. In conclusion, the present study shows that selective ET-B receptor blockade has no effect on the BNP-induced natriuresis and glomerular filtration rate.

Cross-Over Studies↗
PubMed1994

Pressure-diuresis-natriuresis response in hyperthyroid and hypothyroid rats.

1. Renal responses to changes in renal perfusion pressure were studied in anaesthetized hyperthyroid (thyroxine, 300 micrograms day-1 kg-1) and hypothyroid (methimazole, 0.03% via drinking water) rats to determine whether an abnormality in the pressure-diuresis-natriuresis phenomenon is involved in the resetting of kidney function in these disorders. 2. There were no significant differences between control and hypothyroid rats with respect to the relationships between renal perfusion pressure and absolute or fractional water and sodium excretion. However, in hyperthyroid rats the pressure-diuresis-natriuresis mechanism was impaired. 3. Renal blood flow and glomerular filtration rate were well autoregulated and there were no differences between control and hypothyroid rats at every level of renal perfusion pressure. A significantly lower glomerular filtration rate was observed in hyperthyroid rats when data were expressed per gram kidney weight, but glomerular filtration rate was similar to that of control rats when normalized by body weight. 4. The shift in the pressure-diuresis-natriuresis response of hyperthyroid rats is mainly due to an increase in tubular reabsorption. Blunting of the renal pressure-diuresis-natriuresis mechanism in hyperthyroid rats may represent the functional resetting of the kidney necessary for sustained hypertension. However, a normal pressure-natriuresis response was observed in hypothyroid rats, in which blood pressure was markedly reduced.

Animals↗
PubMed1999

Exaggerated volume expansion natriuresis in rats preloaded with hypertonic saline: a paradoxical enhancement by inhibition of prostaglandin synthesis.

In preliminary experiments rats preinfused with hypertonic saline showed exaggerated natriuresis after an additional small volume expansion (SVE). This was systematically studied in anaesthetized Wistar rats prepared for clearance studies of the left kidney and measurements of medullary blood flow (MBF, laser-Doppler technique) and tissue electrical admittance (Y ), an index of interstitial ion concentration. The rats were preinfused i.v. with 3 mL of 5% NaCl during 90 min. A subsequent injection of isotonic saline, 0.5% of body weight, increased sodium excretion (UNaV ) from 2.1 +/- 0.5 to 4.5 +/- 1.1 micromol min-1 and urine flow (V ) from 12.0 +/- 2.3 to 24.3 +/- 5.6 microL min-1 (P < 0.02). The same volume of whole blood increased UNaV from 5.0 +/- 1.4 to 8.7 +/- 1.7 micromol min-1 and V from 22.3 +/- 5.1 to 37.4 +/- 5.9 microL min-1 (P < 0.01). The glomerular filtration rate, MBF and Y did not change. In rats preinfused with 0.9% saline no natriuresis was observed after SVE. To examine if prostaglandins (PG) were involved in SVE natriuresis, indomethacin (Indo), 5 mg kg-1 or sodium meclophenamate (Meclo), 7.5 mg kg-1, were added to the injected 0.9% saline. Paradoxically, both PG synthesis inhibitors enhanced natriuresis to SVE. After Indo UNaV increased from 2.0 +/- 0.6 to 7.6 +/- 1.3 micromol min-1, significantly more than after SVE alone (P < 0.001). At higher baseline UNaV, the increase with Meclo from 4.5 +/- 1.2 to 13.5 +/- 1.8 micromol min-1 was significantly higher than after whole blood infusion (P < 0.001). MBF decreased and Y increased after both inhibitors. Further studies are required to explain the enhancement of natriuresis after blockade of PG synthesis.

Animals↗
PubMed1991

Contribution of prostaglandins to pressure natriuresis in Dahl salt-sensitive rats.

To examine the role of prostaglandins on pressure natriuresis in Dahl salt-sensitive (DS) rat, the pressure-natriuresis relationships in DS and Dahl salt-resistant (DR) rats were characterized with or without indomethacin (2 mg/kg/h) by utilizing an in vivo renal perfusion study. When untreated, in the DS rat the pressure-natriuresis curve was blunted (P less than .05) and excretion of prostaglandin E2 (38 +/- 11 to 109 +/- 43 pg/min) was decreased in comparison to the DR rat. With indomethacin, the pressure-natriuresis curve in the DR rat was blunted, while no significant changes were observed in the DS rat. Plasma renin activity and concentration of atrial natriuretic peptide were not changed by the treatment of indomethacin in both strains. These results suggest that the decrease in renal prostaglandins, at least in prostaglandin E2, plays some role in blunting pressure natriuresis in DS rat.

Animals↗
PubMed1993

On the role of digoxin-like substances, ANP, and AVP in natriuresis induced by hypertonic saline infusion in dogs.

The increase of sodium concentration in cerebrospinal fluid or in plasma triggers the osmoregulatory mechanism, namely, the enhancement of renal free-water reabsorption and natriuresis. The increase of free-water reabsorption has been recognized for many years as a consequence of the osmotically released vasopressin (AVP). However, the control of renal sodium excretion in the mechanism of osmoregulation has not been clarified It has been suggested to be, at least in part, of hormonal nature, implying the decreased release of aldosterone and the increased release of atrial natriuretic peptide (ANP), digoxin-like substances (DLIS), and AVP. Neither of these factors, however, has been unequivocally linked to the mechanism of immediate natriuresis caused by an acute increase in cerebrospinal fluid or plasma sodium concentration. It was reconfirmed in our present experiments in anesthetized dogs that aldosterone, ANP, and DLIS could hardly play a role in the immediate natriuresis after the i.v. infusion of hypertonic saline (20% NaCl solution infused in 20 min in an amount that was 0.13% of body weight). However, the role of AVP in this type of natriuresis seems more promising as a V1/V2 receptor antagonist applied i.v. before the hypertonic saline loading completely prevented the increase of renal sodium excretion. Natriuresis after the isotonic saline load was not impaired by the same antagonist of vasopressin receptors.

Animals↗
PubMed1981

Pressure natriuresis in hypertension.

Pressure natriuresis, defined as the relationship between sodium excretion and mean arterial pressure (MAP), was assessed during graded reduction of arterial pressure with nitroprusside in 16 essential hypertensives (EH). In all patients, sodium excretion fell linearly with reductions in arterial pressure (r greater than 0.68; p less than 0.05). The per cent change of sodium excretion from control per mmHg change in MAP (delta UNaV/delta MAP) was less in patients with resting MAP above 120 mmHg than in those with lower blood pressure (1.4 +/- 0.1 versus 3.0 +/- 0.3; p less than 0.001), but the pressure at which urine flow extrapolated to zero (75 +/- 3 mmHg) was not significantly different in the two groups. The slope of the relationship between sodium excretion and arterial pressure was significantly correlated with resting MAP (r = -0.67; p less than 0.05) and with plasma volume (r = 0.61; p less than 0.05). Furthermore, the ratio delta UNaV/delta MAP also rose in concert with body fluid volumes when a salt load of 8 g of sodium chloride was added to the regular diet. Thus, the sensitivity of pressure natriuresis was determined by level of resting arterial pressure and body fluid volumes. These experiments suggest tht two mechanisms might be activated in EH to avoid dangerous sodium and volume depletion: 1) attenuation of pressure natriuresis at higher levels of arterial pressure, and 2) blunting of pressure natriuresis by volume contraction. By this hypothesis, the lower slope of pressure natriuresis is secondary to hypertension rather than its cause.

Blood Pressure Determination↗
PubMed1992

Dopamine receptor blockade and synthesis inhibition during exaggerated natriuresis in spontaneously hypertensive rats.

The influence of dopamine receptor blockade and synthesis inhibition on natriuresis induced by isotonic saline volume expansion was investigated in anaesthetized spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. The aim of the study was to elucidate the mechanisms underlying the phenomenon of exaggerated natriuresis during volume expansion that has been observed in spontaneously hypertensive rats. Volume expansion, at 5% of body weight, resulted in a larger and faster natriuretic response in spontaneously hypertensive rats than in Wistar-Kyoto rats. Sixty minutes after commencement of volume expansion the natriuretic response (accumulated sodium excretion) in Wistar-Kyoto rats (n = 8) was only 24% of that in spontaneously hypertensive rats (n = 17). When spontaneously hypertensive rats were pretreated with the dopamine receptor blockers haloperidol (n = 14, 1 mg kg-1), SCH23390 (n = 8, 30 micrograms h-1 kg-1) or the dopamine synthesis inhibitor benserazide (n = 8, 50 mg kg-1; n = 5, 100 mg kg-1), the natriuretic response to volume expansion was only 16, 35, 59 and 42%, respectively, of that in untreated SHR. The corresponding proportion in the haloperidol-treated (n = 8) compared with untreated Wistar-Kyoto rats was 22%. In conclusion, isotonic volume loading results in more pronounced natriuresis in spontaneously hypertensive than in Wistar-Kyoto rats. Dopamine receptor blockade and synthesis inhibition attenuate the expansion of exaggerated natriuresis in spontaneously hypertensive rats and reduces the volume expansion natriuresis in Wistar-Kyoto rats, indicating that the dopamine system plays an important role.

Animals↗
PubMed1986

Drinking and natriuresis during volume expansion and intracranial angiotensin or carbachol.

Two methods of sodium loading were used to counteract the body fluid dilution resulting from natriuresis and water drinking during sustained lateral ventricular infusions of carbachol (CBC) or angiotensin II (ANG II) in rats. It was expected that preventing dilution would also prevent the precipitous decline of both drinking and natriuresis during the later hours of CBC infusion. In the first study, rats having isotonic saline as the sole drinking fluid during CBC infusions drank less fluid and had only slightly higher plasma osmolality and sodium concentration than rats drinking water, which showed extreme dilution. In the second study, rats with only water to drink were given intravenous infusions of 0.15, 0.45, or 1.00 M NaCl solutions at 1.8 ml/h concurrently with the intraventricular infusions. Significant dilution of plasma was found at the two lower rates but not at 1.00 M NaCl in CBC-infused rats. Only the latter group showed both persistent drinking and natriuresis throughout the 4-h infusion period, and this was not because of elevated plasma osmolality. Infusions of ANG II generated less severe body fluid dilution and more persistent drinking in both experiments. The study demonstrates that body fluid dilution may control the offset of both drinking and natriuresis during sustained infusions of CBC and that the more persistent drinking to ANG II vs. CBC probably occurs because of a lesser natriuresis and consequent fluid dilution.

Administration, Oral↗
PubMed1996

Pressure natriuresis following acute and chronic inhibition of nitric oxide synthase in rats.

Nitric oxide has been suggested to be an essential mediator of pressure natriuresis. To investigate this hypothesis, the effect of acute or chronic inhibition of nitric oxide synthase on pressure natriuresis and renal interstitial hydrostatic pressure was studied in anesthetized Sprague-Dawley rats with fixed neural and hormonal influences on the kidney. Both acute infusion (10 micrograms.kg-1.min-1 iv) and chronic administration (50 mg.kg-1.day-1 for 7 days in drinking water) of NG-nitro-L-arginine methyl ester (L-NAME) resulted in significantly increased mean arterial pressure, a 30% decrease in renal blood flow, and no change in glomerular filtration rate when compared with values in control rats. Pressure-diuresis, pressure-natriuresis, and pressure-fractional sodium excretion curves in L-NAME-treated rats were shifted to a higher pressure (by approximately 25 mmHg) when compared with those in control rats. The relationship between renal artery pressure and renal interstitial hydrostatic pressure was shifted similarly in L-NAME-treated rats. Acute administration of L-arginine completely reversed the renal effects of chronic L-NAME. These data indicate that, at the doses used in this study, both acute and chronic inhibition of nitric oxide synthase decreased the ability of the kidney to excrete sodium at least in part by a hemodynamic mechanism leading to an increased filtration fraction and a decreased renal interstitial pressure. The parallel shift of the pressure-natriuresis curve to a higher pressure suggests that nitric oxide is an important modulator but not an essential mediator of the pressure natriuresis.

Animals↗
PubMed1983

Factors causing natriuresis after hypothalamic injection of a cholinergic drug in rats.

We investigated possible mechanisms for the natriuresis seen after injection of the cholinergic drug carbamylcholine chloride (carbachol) into the lateral hypothalamus of conscious rats. In unrestrained rats injection of 1 microgram of carbachol in 1 microliter of 0.15 M NaCl solution through a permanently implanted cannula produced a significant natriuresis and kaliuresis. Injection of vehicle produced no changes. The same animals were then subjected to bilateral renal denervation (n = 13) or sham denervation (n = 13) and injected with the same solutions 1 wk later. Carbachol injection produced a natriuresis (P less than 0.0001) and a kaliuresis (P less than 0.01) in all animals studied. Both responses were of a magnitude similar to the responses seen before denervation. We studied other rats while awake but restrained, which permitted the performance of clearance studies and blood pressure measurements. Injection of carbachol produced diuresis, natriuresis, and kaliuresis in all rats, with no change in p-aminohippurate clearance and only transient change in inulin clearance. An increase in blood pressure occurred in some but not all rats. The response in rats with bilaterally denervated kidneys (n = 7) was similar to that of rats with innervated kidneys (n = 5). The natriuresis seen after cholinergic stimulation of the hypothalamus in conscious rats is not primarily mediated by inhibition of renal nerve activity and can be dissociated from changes in blood pressure, glomerular filtration rate, and renal plasma flow.

Animals↗
PubMed1987

Effect of reduction in renal artery pressure on atrial natriuretic peptide-induced natriuresis.

Studies were undertaken in anesthetized male Sprague-Dawley rats to investigate the effects of lowering renal arterial pressure within the autoregulatory range (to 85-95 mmHg) on the renal response to atriopeptin II (AP II) and atrial extract (AE). The natriuresis and diuresis produced by bolus injections of AP II at three dose levels (250-1,000 ng) was abolished or substantially reduced at lowered arterial pressure (85 mmHg). When renal artery pressure was lowered at the same time as an AE infusion was begun it completely blocked the natriuresis and diuresis. When pressure was reduced after 45 min of AE infusion the natriuresis was blunted, but not fully abolished. The effect of prior reduction in renal arterial pressure on the response to AP II (100 ng/min) and furosemide was compared; the AP II natriuresis was prevented when arterial pressure was lowered to 90 mmHg, but the natriuretic effect of furosemide was only slightly diminished. There was no significant rise in glomerular filtration rate (GFR) with AP II and no correlation between GFR changes and the Na excretory response. Reducing renal arterial pressure prior to, at the same time as, or 45 min after beginning an infusion of atrial natriuretic peptide substantially blunts or completely abolishes the natriuresis. Reductions in renal arterial pressure may block the natriuretic and diuretic effects of these compounds by interfering with their hemodynamic actions or by causing sufficient enhancement of salt reabsorption to limit delivery to terminal nephron segments.

Animals↗
PubMed1991

Role of renal nerves on pressure natriuresis in spontaneously hypertensive rats.

An abnormal rightward shift of the pressure-natriuresis curve is a well known feature of the renal function in hypertension. The participation of intrinsic neural factors in the kidney in this phenomenon was investigated in anesthetized young and adult spontaneously hypertensive rats (SHR). At 7-8 wk of age, the renal pressure-diuresis curve and pressure-natriuresis curve were shifted to the left in denervated SHR compared with innervated animals. Fractional excretion of sodium was higher, and plasma renin activity was lower in denervated SHR. Glomerular filtration rate was not affected by renal denervation. In 13- to 15-wk-old SHR, renal denervation did not affect the pressure-diuresis and -natriuresis curves, although other parameters were changed compared with the results at 7-8 wk. In Wistar-Kyoto rats, the pressure-diuresis curve was shifted to the left by renal denervation at both ages. These results suggest that the renal nerves have an important effect on the renal pressure-diuresis and -natriuresis curves. However, renal innervation cannot be thought to cause an abnormal rightward shift of the pressure-diuresis and -natriuresis curves in SHR, especially in the established stage of hypertension.

Animals↗
PubMed1998

Bradykinin may be involved in neuropeptide Y-induced diuresis, natriuresis, and calciuresis.

Neuropeptide Y (NPY) can cause diuresis, natriuresis, and calciuresis in rats independently of the pressure-natriuresis mechanism (A. Bischoff and M. C. Michel. Pflügers Arch. 435: 443-453, 1998). Because this is seen in systemic but not intrarenal NPY infusion, we have investigated the possible mediator of tubular NPY effects in anesthetized rats. In the present study, infusion of NPY (2 micrograms . kg-1 . min-1) enhanced renovascular resistance by approximately 8 mmHg . ml-1 . min and enhanced urine and sodium excretion by approximately 450 microliter/15 min and approximately 60-85 micromol/15 min, respectively. Acute renal denervation did not alter renovascular or tubular NPY effects, indicating that a neuronally released mediator is not involved. Treatment with the angiotensin II-receptor antagonist losartan prevented the decline of the renovascular response with time but did not modify tubular NPY effects. The bradykinin B2-receptor antagonist icatibant accelerated the decline of the renovascular NPY effects with time; concomitantly, it attenuated NPY-induced diuresis and natriuresis and abolished NPY-induced calciuresis. The converting-enzyme inhibitor ramiprilat prevented the decline of the renovascular response with time; concomitantly, it magnified the NPY-induced diuresis, natriuresis, and calciuresis. We conclude that bradykinin may be involved in NPY-induced diuresis, natriuresis, and, in particular, calciuresis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Brain atrial natriuretic peptide neurons play an essential role in volume expansion-induced release of atrial natriuretic peptide and natriuresis.

The brain atrial natriuretic peptide (ANP) neuronal system appears to be involved in the increase in plasma ANP which follows blood volume expansion in the rat. To determine if this neuronal system is essential to the natriuresis and increase in plasma ANP which follow volume expansion, highly specific antiserum against ANP (ANP-AB) and/or normal rabbit serum as a control was microinjected into the third cerebral ventricle (3V) of conscious rats, and the effect on the natriuresis and increase in plasma ANP induced by intravenous injection of 2 ml/100 g body weight of 0.3 M NaCl was examined. Although there was no effect of ANP-AB on initial levels of plasma ANP or natriuresis 3 h after 3V injection, the natriuresis in response to blood volume expansion was significantly inhibited. The increase in plasma ANP which followed volume expansion was also significantly reduced at 5 min but recovered at 15 min. The results indicate that the brain ANP neuronal system plays an essential role in the mediation of volume expansion-induced increase in plasma ANP and natriuresis. The failure to block these responses completely may be due to the use of an inadequate dose of antiserum or other brain mechanisms may be able to mediate these responses.

Animals↗
PubMed2004

Renal interstitial guanosine cyclic 3', 5'-monophosphate mediates pressure-natriuresis via protein kinase G.

Pressure-natriuresis is the physiological protective mechanism whereby elevation of blood pressure induces a rapid increase in renal sodium (Na+) excretion. Pressure-natriuresis abnormalities are common to all forms of hypertension. We tested the hypothesis that pressure-natriuresis is mediated by renal interstitial (RI) cGMP and protein kinase G (PKG). We used anesthetized, uninephrectomized Sprague-Dawley rats and a standard pressure-natriuresis model in which bilateral adrenalectomy and renal denervation was done on rats. Renal perfusion pressure (RPP) was adjusted by manipulating clamps above and below the renal artery, and RI cGMP was quantified by microdialysis. RI cGMP increased from 3.1+/-0.5 to 5.5+/-0.4 fmol/min (P<0.05) when RPP was raised from 100 to 140 mm Hg. This increase in RI cGMP was eliminated by RI infusion of soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,2-alpha]quinoxalin-1-one (ODQ). Raising RPP from 100 to 140 mm Hg increased urinary sodium excretion from 0.2+/-0.1 to 0.8+/-0.1 micromol/min, fractional sodium excretion from 0.2+/-0.1% to 0.8+/-0.1%, and fractional lithium excretion from 20.1+/-3.0% to 62.7+/-3.7% (all P<0.05). These responses were eliminated by RI infusion of nitric oxide synthase inhibitor N-nitro-l-arginine methyl ester, ODQ, and PKG inhibitors Rp-8-pCPT-cGMP and Rp-8-Br-cGMP. Increasing RPP from 100 to 140 mm Hg decreased fractional proximal sodium reabsorption without influencing fractional distal Na+ reabsorption or glomerular filtration rate. In conclusion, pressure-natriuresis is mediated by RI cGMP and a PKG signaling pathway in target renal proximal tubule cells.

Adrenalectomy↗
PubMed1997

Indirect assessment of glomerular capillary pressure from pressure-natriuresis relationship: comparison with direct measurements reported in rats.

It is examined whether glomerular hemodynamics can be indirectly estimated from the pressure-natriuresis relationship. There are only two animal studies reported, one in normal and the other in 5/6 nephrectomized Munick-Wistar rats, which permits plotting the pressure-natriuresis relationship and comparison of indirect estimations with directly measured glomerular hemodynamic data. Normal and extensive renal ablation rats were placed on relatively high and low sodium diets. Plotting mean arterial pressure (MAP) on the x-axis and 24 h urinary sodium excretion rate on the y-axis, the pressure-natriuresis relationship was drawn. As the difference between MAP (121 +/- 1 and 169 +/- 12 mmHg) on relatively high sodium diet and the extrapolated x-intercept (122 and 138 mmHg) of the pressure-natriuresis relationship, based on previous proposal, the effective filtration pressure across the glomerular capillary walls was estimated to be-1 and 31 mmHg for normal and 5/6 nephrectomized rats. Then, the glomerular capillary hydraulic pressure (PGC) was calculated to be 33 and 64 mmHg. Micropuncture studies showed that directly measured PGC of 47 +/- 1 and 65 +/- 2 mmHg was close agreement with those estimated indirectly. Therefore, an approach from the pressure-natriuresis relationship provides a noninvasive means to predict an approximation of PGC. This approach to estimating glomerular hemodynamics may have invaluable implications for clinical practice; in the early detection of loss of filtration capacity and in the assessment of an important risk factor for the development of chronic renal failure.

Animals↗