Cyclic nucleotide metabolism in compensatory renal hypertrophy and neonatal kidney growth.

Schlöndorff, Detlef; Weber, Herbert

doi:10.1073/pnas.73.2.524

Cited by 42 publications

(22 citation statements)

References 15 publications

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“…We found that absolute urinary cGMP excretion increased from day 0 to day 7, consistent with the observation that both renal cGMP and guanylate cyclase activity were increased 2 d after unilateral nephrectomy (28) and with Wight et al (24), who found an increase in urinary cGMP excretion after unilateral nephrectomy that was blocked by L-NAME. In addition, Schlondorff and Weber (34) reported that after unilateral nephrectomy, there was an increase in the (NO-mediated) particulate form of guanylate cyclase. When we corrected the cGMP excretion by the changing kidney weight, we found that cGMP increased compared with controls by 2.5-fold at 2 d and remained similarly elevated at all subsequent time periods.…”

Section: Discussionmentioning

confidence: 99%

Role of Nitric Oxide in the Renal Hemodynamic Response to Unilateral Nephrectomy

Sigmon¹,

Gonzalez-Feldman

Cavasin

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Reduction of renal mass by unilateral nephrectomy results in an immediate increase in renal blood flow (RBF) to the remnant kidney, followed by compensatory renal hypertrophy. Whether the increase in RBF after unilateral nephrectomy is mediated by nitric oxide (NO) was tested. It was found that immediately after nephrectomy, blood flow to the remaining kidney increased by 8% (P Ͻ 0.01), and inhibition of NO synthesis with N-nitro-L-arginine methyl ester (L-NAME) blocked the increase in RBF. In addition, 2 d after nephrectomy, there was a 49% increase in RBF (corrected per gram of kidney weight), a 25% increase at 7 and 14 d, and a 16% increase after 28 d. Acute inhibition of NO synthesis with L-NAME in uninephrectomized rats caused a greater decrease in RBF on days 2 and 7 compared with controls, whereas by 14 and 28 d, the response to L-NAME was similar to controls. Urinary excretion of cyclic guanosine monophosphate, a marker for renal NO production, increased 2.5-fold by 2 d after uninephrectomy (P Ͻ 0.005) and remained at this level through 28 d. Pretreating rats chronically with a subpressor dose of L-NAME beginning 2 d before nephrectomy blocked the increase in RBF seen at 2 and 7 d and retarded the renal hypertrophy that should have developed by 7 d. It is concluded that after unilateral nephrectomy, immediate and sustained increases in RBF are mediated at least in part by NO. The hypertrophic response to unilateral nephrectomy may be partially initiated by the signal of hemodynamic changes.Nitric oxide (NO) is a vasodilator that contributes to the regulation of regional blood flow and BP by tonically lowering vascular resistance (1,2). This effect is mediated through activation of soluble guanylate cyclase, which increases cellular cyclic guanosine monophosphate (cGMP), resulting in vascular relaxation and decreased vascular resistance (3). In the kidney, continuous release of NO derived from the vascular endothelium is an important determinant of basal perfusion and resistance. Release of NO can be stimulated by changes in the hydromechanical forces associated with pulsatile blood flow (4 -6). Vascular shear stress is a primary stimulus for endogenous NO production from the endothelium (7-10). Miller et al. (7,8) demonstrated in vitro that chronic alterations in local blood flow, produced by opening an arteriovenous anastomosis, increased endothelium-dependent relaxation. Increasing coronary blood flow by chronic cardiac pacing or exercise also enhanced endothelium-dependent dilatation (9,10). Although the mechanism responsible for flow-induced dilatation is not completely understood, there is considerable evidence that it is mediated, in part, by [11][12][13][14][15]. Removing the endothelium or inhibiting NO synthesis blocks flow-induced dilation (13,15). Studies in dogs have demonstrated that chronic exercise enhances the release of nitrites from the coronary arteries and microvessels, accompanied by increased blood flow, and this is associated with increased expression of the endothelial i...

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Section: Discussionmentioning

confidence: 99%

Role of Nitric Oxide in the Renal Hemodynamic Response to Unilateral Nephrectomy

Sigmon¹,

Gonzalez-Feldman

Cavasin

et al. 2004

Journal of the American Society of Nephrology

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“…29 These growth factors might alter membrane phospholipid metabolism 30 or cyclic nucleotide concentration. 31 We have recently demonstrated genetic differences in cardiac phospholipid metabolism in DR and DS rats on a high salt diet, 32 differences that may also exist in the kidney and contribute to the variance observed in interstrain renal growth.…”

Section: Discussionmentioning

confidence: 99%

Differential effect of dietary salt on renal growth in Dahl salt-sensitive and salt-resistant rats.

1989

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A high salt diet has been shown to increase renal mass of intact rats, although the mechanism by which this occurs has not been investigated. We used Dahl rats that are sensitive (DS) or resistant (DR) to the hypertensinogenic effect of salt to examine changes in renal size and composition caused by a high salt diet. Renal index, deoxyribonudeic add (DNA), protein, water content, protein/DNA ratio, and cell number and size were measured in age-matched DR and DS on a high salt diet for 7,14, or 28 days. The results were compared with those obtained from respective rats on a low salt diet. High salt diet elevated renal index and protein hi DR and DS rats at each time point. After 7 days of a high salt diet, DNA increased in DS only. Protein/DNA ratio was progressively decreased by a high salt diet in DS and remained unchanged in DR rats. Cell number was increased 35% in DS versus only 13% in DR rats at 4 weeks. Cell size decreased 24% in DS and only 11% in DR rats. These results indicate that renal growth due to hyperplasia accompanies ingestion of a high salt diet in both DR and DS rats, but the rate of growth and the mechanism through which it occurs differ between strains. This difference may be important in delineating salt sensitivity and future development of hypertension. {Hypertension 1989;13:122-127) N umerous studies of renal enlargement have been conducted after reduction of renal mass. The mechanism by which compensatory renal growth occurs has been ascribed mainly to hypertrophy, 1 although a component of hyperplasia has been found in at least one study.2 Compensatory renal growth occurs independent of changes in blood pressure and many factors are known to modify its extent, including age, 3 hormones, 4 and diet. 5 We found only one published report of the effect of salt intake on renal growth in the absence of renal ablation.6 That study demonstrated increased renal mass after ingestion of a high salt diet by normal rats, but the mechanism of growth was not investigated. In order to gain further insight into this question, we have studied the effect of salt consumption on renal size and composition in Dahl rats Received August 29, 1988; accepted October 19, 1988. sensitive (DS) or resistant (DR) to the hypertensinogenic effect of salt. The data permit analysis of the degree to which renal growth on a high salt diet is due to hyperplasia or hypertrophy and the detection of differences between the two strains. Materials and MethodsMale DR and DS rats were obtained as 26-to 32-day-old weanlings from Brookhaven National Laboratories (Upton, New York), housed individually, and maintained on low salt chow containing 0.4% NaCl until introduction of high salt chow containing 8.0% NaCl. All animals in this study consumed standard rodent laboratory chow (5001, Purina Laboratories, Richmond, Indiana) with a protein content of 23% and a potassium content of 1.1%. The NaCl content of this chow was adjusted to yield either a low or high salt diet. Three experimental groups and one control group were designated...

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“…(a) Before then, hyperplasia is the dominant mechanism for renal compensatory growth. After then, both hyperplasia and hypertrophy are the major mechanisms (20,26,27). (b) At 14 days of age, the levels of RNA in the renal cortex decrease transiently with respect to DNA (20).…”

Section: Introductionmentioning

confidence: 99%

Choline pathways during normal and stimulated renal growth in rats.

Bean¹,

Lowenstein²

1978

J. Clin. Invest.

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A B S T R A C T Celluilar membrane synthesis ocecurs during normal and stimutlated renal growNth. Choline in the kidney is utilized as a precuirsor for membrane synthesis via the choline kinase reaction. We investigated choline phosphorylation dturing normal and stimulated renal growth. Rapidly growing neonatal rat kidneys contained relatively high levels of choline kinase activity (61 pmol phosphoryleholine/min per mg protein). Choline kinase activity and phosphorvlcholine production then fell gradually over the 1st mo of life; by 1 mo phosphorylcholine produiction was 34 pmol phosphorylcholine/min per mg protein. Choline kinase activity increased by 27% (P < 0.001) in 28-dayold rats when renal growth was stimtulated by contralateral nephrectomy; the increase occuirred wvithin 2 h after suirgery. Thus, changes in the activity of this important enzyme in the initiation of membrane svnthesis is associated both with normal renal development and with adaptation to nephron loss. The findings further stuggest that the cell membrane may be involved in the initiation of compensatory renal growth.

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Cyclic nucleotide metabolism in compensatory renal hypertrophy and neonatal kidney growth.

Cited by 42 publications

References 15 publications

Role of Nitric Oxide in the Renal Hemodynamic Response to Unilateral Nephrectomy

Role of Nitric Oxide in the Renal Hemodynamic Response to Unilateral Nephrectomy

Differential effect of dietary salt on renal growth in Dahl salt-sensitive and salt-resistant rats.

Choline pathways during normal and stimulated renal growth in rats.

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