Combined prenatal and postnatal protein restriction influences adult kidney structure, function, and arterial pressure

Abstract

The effects of prenatal protein restriction on adult renal and cardiovascular function have been studied in considerable detail. However, little is known about the effects of life-long protein restriction, a common condition in the developing world. Therefore, we determined in rats the effects of combined pre- and postnatal protein restriction on adult arterial pressure and renal function and responses to increased dietary sodium. Nephron number was also determined. Male Sprague-Dawley rats were born to mothers fed a low [8% (wt/wt), LP] or normal [20% (wt/wt), NP] isocaloric protein diet throughout pregnancy and maintained on these diets after birth. At postnatal day 135, nephron number, mean arterial pressure (MAP), and renal function were determined. A high-NaCl [8.0% (wt/wt), high-salt] diet was fed to a subset of rats from weaning. MAP was less in LP than in NP rats (120 +/- 2 vs. 128 +/- 2 mmHg, P < 0.05) and was not significantly altered by increased salt intake. Nephron number was 31% less in LP than in NP rats (P < 0.001). The volume of individual glomeruli was also less in LP than in NP rats, as were calculated effective renal plasma flow and glomerular filtration rate. Glomerular filtration rate, but not effective renal plasma flow, appeared to be increased by high salt intake, particularly in LP rats. In conclusion, protein restriction induced a severe nephron deficit, but MAP was lower, rather than higher, in protein-restricted than in control rats in adulthood. These findings indicate that the postnatal environment plays a key role in determining the outcomes of developmental programming.

Effects of Perinatal Protein-Nacl Diets on Offspring's Blood Pressure and Renal Function in Lewis Rats

“…In some studies, a GFR of male Sprague-Dawley rats was increased with a maternal 8% LP diet and mean MAP was significantly lower (120 vs. 128 mm Hg), while offspring's 8% high salt diet did not much affect BP, although the protein restriction induced a severe nephron deficit and low glomerular volume [55]. Both the BP and GFR results were contradicted by our current results.…”

Impaired myocardial performance in a normotensive rat model of intrauterine growth restriction

“…Contrary to a number of other IUGR models, the impaired myocardial function in our study occurs independently from arterial hypertension and can therefore be considered as a primary IUGR-induced effect (10,12), which may favor the development of cardiac disease later in life. Concerning the relationship between arterial hypertension and IUGR induced by maternal protein restriction, differing reports can be found showing blood pressure elevation (13) or, alternatively, also unaffected blood pressures levels (14). This can partly be explained by different time points and methods of blood pressure assessment (e.g., telemetric blood pressure measurement vs. tail cuff plethysmography) as well as different protocols of maternal protein restriction (15).…”

Kidney Disease and Perinatal Programming of Arterial Hypertension: the Results of Experimental Researches

“…Аналогичные результаты были получены в эксперимен-тах на крысах, подвергавшихся во время беремен-ности ограничениям по потреблению белка [6,7]. При этом было показано, что голодание или недостаток белка в рационе вызывают инактивацию в плаценте фермента 11-бета-гидроксистероиддегидрогеназы, раз-рушающего глюкокортикостероиды матери, не позволяя им влиять на темпы созревания плода [6].…”