Increased renal sympathetic nerve activity leads to hypertension and renal dysfunction in offspring from diabetic mothers
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2013-01-01
Autores
Almeida Chaves Rodrigues, Aline Fernanda de 
Brites de Lima, Ingrid Lauren
Bergamaschi, Cassia Toledo
Campos, Ruy Ribeiro
Hirata, Aparecida Emiko
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Rodrigues AF, de Lima IL, Bergamaschi CT, Campos RR, Hirata AE, Schoorlemmer GH, Gomes GN. Increased renal sympathetic nerve activity leads to hypertension and renal dysfunction in offspring from diabetic mothers. Am J Physiol Renal Physiol 304: F189-F197, 2013. First published November 7, 2012; doi:10.1152/ajprenal.00241.2012.-The exposure of the fetus to a hyperglycemic environment promotes the development of hypertension and renal dysfunction in the offspring at adult age. We evaluated the role of renal nerves in the hypertension and renal changes seen in offspring of diabetic rats. Diabetes was induced in female Wistar rats (streptozotocin, 60 mg/kg ip) before mating. Male offspring from control and diabetic dams were studied at an age of 3 mo. Systolic blood pressure measured by tail cuff was increased in offspring of diabetic dams (146 +/- 1.6 mmHg, n = 19, compared with 117 +/- 1.4 mmHg, n = 18, in controls). Renal function, baseline renal sympathetic nerve activity (rSNA), and arterial baroreceptor control of rSNA were analyzed in anesthetized animals. Glomerular filtration rate, fractional sodium excretion, and urine flow were significantly reduced in offspring of diabetic dams. Two weeks after renal denervation, blood pressure and renal function in offspring from diabetic dams were similar to control, suggesting that renal nerves contribute to sodium retention in offspring from diabetic dams. Moreover, basal rSNA was increased in offspring from diabetic dams, and baroreceptor control of rSNA was impaired, with blunted responses to infusion of nitroprusside and phenylephrine. Thus, data from this study indicate that in offspring from diabetic mothers, renal nerves have a clear role in the etiology of hypertension; however, other factors may also contribute to this condition.
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American Journal of Physiology-renal Physiology. Bethesda: Amer Physiological Soc, v. 304, n. 2, p. F189-F197, 2013.