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  • Title: Importance of the renal nerves in the pathogenesis of experimental hypertension.
    Author: Winternitz SR, Oparil S.
    Journal: Hypertension; 1982; 4(5 Pt 2):III108-14. PubMed ID: 7049925.
    Abstract:
    Anatomical studies have demonstrated sympathetic innervation of the renal arterioles, juxtaglomerular apparatus, and renal tubules. Physiologic studies of the effects of the renal efferent nerves on renin release and renal sodium handling indicate that they play an important role in body fluid homeostasis and cardiovascular regulation. In addition, evidence is accumulating that stimulation of intrarenal mechanoreceptors and chemoreceptors causes in increase in renal afferent nerve activity and that alterations in renal afferent nerve traffic are, in turn, associated with changes in blood pressure and in vasoconstrictor tone in the contralateral kidney. Further, recent studies have demonstrated functionally significant connections between renal afferent nerves and the central nervous system. Interruption of the renal sympathetic nerves has been shown to prevent or attenuate hypertension in a number of animal models, suggesting that the renal nerves have an important role in the pathogenesis of experimental hypertension. In the spontaneously hypertensive rate of the Okamoto strain (SHR) and the DOCA-NaCl rat, the delay in the development of hypertension produced by renal denervation is due in part to increased sodium excretion thought to be secondary to interruption of the renal efferent nerves. In contrast, in one-kidney, one clip and two-kidney, one clip Goldblatt hypertension in the rat and coarctation hypertension in the dog, the depressor effect of renal denervation is unrelated to changes in urinary sodium excretion or plasma renin activity. In these models the attenuation of hypertension following renal denervation appears to be secondary to a decrease in peripheral sympathetic activity. Evidence in the one-kidney model suggests that interruption of the renal afferent nerves lower blood pressure via an effect on central noradrenergic mechanisms.
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