PHYSIOLOGICAL BASIS FOR EFFECTS OF LOW-PROTEIN DIETS ON BLOOD PRESSURE OF SUBTOTALLY NEPHRECTOMIZED RAT

1950 ◽  
Vol 162 (2) ◽  
pp. 368-374 ◽  
Author(s):  
Philip Handler ◽  
Frederick Bernheim
Keyword(s):  
Blood Pressure ◽  
Physiological Basis ◽  
Low Protein ◽  
Protein Diets

Maternal Carbenoxolone Treatment Lowers Birthweight and Induces Hypertension in the Offspring of Rats Fed a Protein-Replete Diet

1997 ◽  
Vol 93 (5) ◽  
pp. 423-429 ◽  
Author(s):  
Simon C. Langley-Evans
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Fetal Growth ◽  
Low Birthweight ◽  
Control Diet ◽  
Later Life ◽  
Hydroxysteroid Dehydrogenase ◽  
Fetal Exposure ◽  
Low Protein ◽  
Protein Diets

1. In the rat low birthweight and raised systolic blood pressure are the consequence of fetal exposure to maternal low protein diets. Nutritional down-regulation of the placental isoform of 11β-hydroxysteroid dehydrogenase, which may increase exposure of the fetus to maternal glucocorticoids, has been suggested to underlie effects of low protein diets on fetal growth and blood pressure. 2. Pregnant rats were fed control (18% casein) or low protein (9% casein) diets throughout gestation. Animals fed the control diet were injected with carbenoxolone, an inhibitor of 11β-hydroxysteroid dehydrogenase. Injections were administered either throughout pregnancy (days 0–22), or targeted to specific periods in early (days 0–7), mid- (days 8–14) or late (days 15–22) gestation. 3. Exposure to a low protein diet reduced birthweight and at 4 weeks of age systolic blood pressure was significantly elevated in the rats exposed to low protein. These hypertensive animals had small kidneys in proportion to body weight. 4. Fetal exposure to carbenoxolone at any period in gestation resulted in lower weight at birth. In rats exposed to the inhibitor over days 8–14, 15–22 or 0–22 systolic blood pressure at 4 weeks was significantly higher than in control animals. The greatest elevation of pressure was associated with carbenoxolone treatment in late (days 15–22) gestation. Animals with carbenoxolone-induced hypertension did not exhibit evidence of retarded renal growth. 5. Increased fetal exposure to maternal glucocorticoids impairs fetal growth and programmes elevated blood pressure in later life.

Weanling Rats Exposed to Maternal Low-Protein Diets during Discrete Periods of Gestation Exhibit Differing Severity of Hypertension

1996 ◽  
Vol 91 (5) ◽  
pp. 607-615 ◽  
Author(s):  
Simon C. Langley-Evans ◽  
Simon J. M. Welham ◽  
Rachel C. Sherman ◽  
Alan A. Jackson
Keyword(s):  
Blood Pressure ◽  
Control Diet ◽  
Plasma Renin ◽  
Late Gestation ◽  
Protein Diet ◽  
Male Rats ◽  
Low Protein Diet ◽  
Fetal Exposure ◽  
Low Protein ◽  
Protein Diets

1. In the rat, hypertension is induced by fetal exposure to maternal low-protein diets. The effect on blood pressure of undernutrition before conception and during discrete periods in early, mid or late pregnancy was assessed using an 18% casein (control) diet and a 9% casein diet to apply mild protein restriction. 2. The offspring of rats fed 9% casein developed raised blood pressure by weaning age. Feeding a low-protein diet before conception was not a prerequisite for programming of hypertension. 3. Hypertension was observed in rats exposed to low protein during the following gestational periods: days 0–7, days 8–14 and days 15–22. Blood pressure increases elicited by these discrete periods of undernutrition were lower than those induced by feeding a low-protein diet throughout pregnancy. The effect in early gestation was significant only in male animals. Post-natal growth of male rats exposed to low-protein diets was accelerated, but kidneys were small in relation to body weight. 4. Biochemical indices of glucocorticoid action in liver, hippocampus, hypothalamus and lung were elevated in rats exposed to low-protein diets in utero. The apparent hypersensitivity to glucocorticoids was primarily associated with undernutrition in mid to late gestation. 5. Plasma renin activity was elevated in rats exposed to 9% casein over days 15–22 of gestation. Animals undernourished over days 0–7 and 8–14 produced pups with lower plasma angiotensin II concentrations at weaning. 6. Fetal exposure to maternal low-protein diets for any period in gestation may programme hypertension in the rat. Alterations to renal structure, renal hormone action or the hypothalamic—pituitary-adrenal axis may all play a role in the programming phenomenon, either independently or in concert.

Diet and the progression of chronic kidney disease

2015 ◽  
Author(s):  
Juan Jesús Carrero ◽  
Hong Xu ◽  
Bengt Lindholm
Keyword(s):  
Blood Pressure ◽  
Protein Intake ◽  
Salt Intake ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
High Serum ◽  
Nutritional Epidemiology ◽  
Converting Enzyme Inhibitors ◽  
Early Stages ◽  
Low Protein ◽  
Protein Diets

The dietary management of non-dialysed CKD patients has focused on limiting the intake of substances which lead to accumulation of urea, potassium, phosphorus, and sodium. Recent advances in nutritional epidemiology have given us the opportunity to examine the relationships between diet and CKD. This chapter focuses on evidence relating to retarding progression of renal impairment in the early to mid stages of CKD. Limits may need to change if GFR falls. The hypothesis that a high dietary protein intake leads to progressive CKD through a mechanism of glomerular hyperfiltration has been taught for decades, and it appears effective in animals. However, the evidence that low-protein diets (LPDs) halt CKD progression in patients is weak. Their management is of course likely to include other interventions such as blood pressure control. There is risk to low-protein diets. There is some evidence that high protein intakes are harmful. We therefore recommend moderate protein intake (not low; not high – no protein supplements; around 1g/kg/day). Salt handling is impaired in most patients with CKD, probably even early stages, and hypertension is an early feature, except in salt-losing patients, to whom different rules apply. Salt intake tends to raise blood pressure, worsen proteinuria, and reduce the effects of angiotensin converting enzyme inhibitors on blood pressure and proteinuria. Very low salt intakes are difficult to comply with and limit diet. In early stages of CKD we therefore recommend restriction to moderately low levels (below 6g/day of salt; 100 mmol of sodium). Lower levels may have additional benefits, and these limits may need to be reduced as GFR declines. Potassium is associated with healthy, desirable foods such as fruit and vegetables. It should only be restricted if high serum values make this necessary.

scholarly journals THE EFFECT OF HIGH PROTEIN DIETS ON EXPERIMENTAL RENAL HYPERTENSION

1941 ◽  
Vol 74 (6) ◽  
pp. 591-600 ◽  
Author(s):  
H. Philipsborn ◽  
L. N. Katz ◽  
S. Rodbard
Keyword(s):  
Blood Pressure ◽  
Renal Hypertension ◽  
High Protein Diet ◽  
High Protein ◽  
Protein Diet ◽  
Low Protein ◽  
Experimental Renal Hypertension ◽  
High Protein Diets ◽  
Protein Diets

The effect of high and low protein diets were studied on fourteen dogs in twenty-four different experiments. In only two of these animals, both with moderate renal excretory failure, was a reversible rise in blood pressure elicited by a high protein diet. The possible mechanisms involved in meeting an increased excretory load are discussed.

Early Administration of Angiotensin-Converting Enzyme Inhibitor Captopril, Prevents the Development of Hypertension Programmed by Intrauterine Exposure to a Maternal Low-Protein Diet in the Rat

1998 ◽  
Vol 94 (4) ◽  
pp. 373-381 ◽  
Author(s):  
Rachel C. Sherman ◽  
Simon C. Langley-Evans
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Control Diet ◽  
Female Offspring ◽  
Fetal Exposure ◽  
Early Administration ◽  
Low Protein ◽  
Blood Pressures ◽  
Protein Diets

1. Associations of intrauterine exposure to maternal undernutrition with later hypertension and coronary heart disease in the human population have been duplicated in the rat. Fetal exposure to low protein diets produces offspring that develop raised systolic blood pressure by the age of weaning. This animal model of ‘programmed’ hypertension was used to investigate the role of the renin—angiotensin system in the initiation and maintenance of high blood pressure. 2. Pregnant rats were fed diets containing 18 or 9% casein from conception until littering. The offspring from these pregnancies were administered captopril either between 2 and 4 weeks of age, or from 10 to 12 weeks of age. 3. The feeding of low protein diets in pregnancy had no effect upon the reproductive ability of female rats and the offspring generated were of normal birthweight. By 4 weeks of age the male and female offspring of low-protein-fed dams had systolic blood pressures that were 24–25 mmHg higher than those of rats exposed to a control diet in utero. 4. Treatment of 10-week-old female offspring with captopril for 2 weeks indicated that angiotensin II formation may play a role in the maintenance of high blood pressure in low-protein-exposed rats. While captopril had no significant effect upon systolic pressures of rats exposed to the control diet in intrauterine life, the systolic blood pressures of low-protein animals rapidly declined by 31 mmHg. 5. Administration of captopril to male and female offspring between 2 and 4 weeks of age exerted long-term effects upon systolic blood pressure. Eight weeks after cessation of treatment, at an age where maximal blood pressures are achieved, captopriltreated, low-protein-exposed rats had similar blood pressures to normotensive rats exposed to the protein-replete diet in utero. 6. In conclusion, we have demonstrated that the elevation of adult blood pressure associated with fetal exposure to a maternal low-protein diet, is prevented by early administration of an angiotensin-converting enzyme inhibitor. The actions of angiotensin II in the late suckling period may be a critical determinant of long-term cardiovascular functions in these animals.

Increased Systolic Blood Pressure in Adult Rats Induced by Fetal Exposure to Maternal Low Protein Diets

1994 ◽  
Vol 86 (2) ◽  
pp. 217-222 ◽  
Author(s):  
Simon C. Langley ◽  
Alan A. Jackson
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Maternal Nutrition ◽  
Control Group ◽  
Chow Diet ◽  
Adult Rats ◽  
Pregnant Rats ◽  
Low Protein ◽  
Protein Diets ◽  
In Pregnancy

1. Possible associations between maternal nutrition in pregnancy and non-communicable diseases of adulthood were assessed using a rat model. Rats were habituated to diets containing a range of protein levels (18, 12, 9 and 6% by weight), over a 14 day period, before mating. The low protein diets were maintained throughout pregnancy. Lactating mothers and their offspring were transferred to a standard chow diet (20% protein). 2. Pregnant rats demonstrated a graded response to the diets, with those fed 9 and 6% protein tending to consume less energy and gain less weight than 18% protein fed controls. Litter size and newborn death rates were not significantly altered by the low protein diets. 3. Offspring of 12 and 9% protein fed dams were grossly normal, gaining weight at a similar rate to those born to 18% protein fed control rats. Offspring of the 6% protein fed dams were smaller than pups from all other groups, over a 21 week period. 4. At 9 weeks of age, systolic blood pressure was determined in the offspring. All offspring from the three low protein groups were found to have significantly elevated blood pressure (15–22 mmHg) relative to the control group. An inverse relationship between maternal protein intake and the systolic blood pressure of the offspring was observed. Blood pressure remained elevated in the offspring of the 9 and 6% protein fed dams until 21 weeks of age. The observed hypertension was associated with increased pulmonary angiotensin-converting enzyme activity in the low protein groups. 5. The data are consistent with the hypothesis that poor maternal nutrition in pregnancy may irreversibly impair aspects of physiological and biochemical function in the fetus. This has potential adverse consequences for the later health of the offspring.

scholarly journals Prenatal programming of angiotensin II type 2 receptor expression in the rat

2004 ◽  
Vol 91 (1) ◽  
pp. 133-140 ◽  
Author(s):  
Sarah McMullen ◽  
David S. Gardner ◽  
Simon C. Langley-Evans
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
In Utero ◽  
Protein Restriction ◽  
Receptor Expression ◽  
Female Rats ◽  
Low Protein ◽  
Protein Diets ◽  
Renal Expression

Exposure to undernutrition during fetal life has been proposed as an underlying cause of adult hypertension. Epidemiological studies demonstrating relationships between low birth weight and later CVD are supported by animal experiments indicating that manipulations of the maternal diet in pregnancy exert programming effects upon blood pressure control. Pregnant female Wistar rats were fed a control diet (n 13) or a low-protein diet (n 12) throughout pregnancy. At delivery all animals were fed the same standard laboratory chow diet. Analysis of nephron number in kidneys obtained from 4-week-old offspring showed that this was significantly (P<0·05) reduced in animals exposed to maternal protein restriction. At this age rats exposed to low-protein diets in utero had systolic blood pressures that were significantly greater than those of control animals (+23 mmHg, P<0·05). Administration of ascending doses of angiotensin II (1–40 ng/kg body weight intravenously) to 10-week-old anaesthetised female rats showed that the pressor response to the peptide was greater and more prolonged in animals exposed to low-protein diets in utero. Renal expression of mRNA for the angiotensin II type 1A receptor was similar in the two groups of rats, but low-protein-exposed animals had significantly lower renal expression of the type 2 receptor (P=0·023). These results suggest that maternal nutritional status programmes expression of the renal angiotensin II type 2 receptor. This may play a key role in the impairment of renal development and the elevation of blood pressure noted in rats exposed to intra-uterine protein restriction.

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