Role of renal medullary inducible nitric oxide synthase in the regulation of arterial pressure

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TAN Dun-Yong()
Journal Title:
Volume 52, Issue 02, 2000
Key Word:
nitric oxide;blood pressure;renal medulla

Abstract: In the present work, we have examined the effects of selective inhibition of the inducible isoform of nitric oxide synthase (iNOS) in rat medulla by aminoguanidine (AG) on the arterial pressure of Dahl salt sensitive (DS), Dahl salt-resistant (DR) and Sprague Dawley (SD) rats by chronic in vivo hemodynamic experiment, the effect of sodium chloride (NaCl) or NaCl plus AG infusion on urinary nitrate/nitrite (urinary NO3/NO2,UNOx), the end product of nitric oxide (NO), excretion, glomerular filtration rate (GFR), effective renal plasma flow (ERPF) and plasma renin activity (PRA). Furthermore, an iNOS activity assay was also made. The results showed that AG infusion significantly augmented the pressor response of DS and SD rats to high NaCl (8%) intake, and decreased GFR, ERPF and PRA of DS rats. In addition, in DS rats, renal medullary interstitial administration of high NaCl significantly elevated the iNOS activity of renal tissue, especially inner medulla and outer medulla, and greatly increased UNOx excretion. Therefore, it is concluded that inducible NOS is an important modulator of blood pressure in case of NaCl-induced hypertension.

  • [1]Furchgott RF. Endothelial dependent relaxations in systemic arterioles in: Endothelium-derived vasoactive substance. In: PM Vanbott ed. Human Press Clifton. NJ, 1987.
  • [2]Tan DY, Cernadas MR, Aragoncillo PA et al. Role of nitric oxide-related mechanisms in renal function in aging rats. Nephrology Dialysis Transplantation. 1998, 13: 594601.
  • [3]Tan DY, Meng SM, Manning RD Jr. Role of neuronal nitric oxide synthase in dahl salt sensitive hypertension. Hypertension, 1999, 33 (Pt 1): 456~461.
  • [4]Anderson TJ, Meredith IT, Ganz P et al. Nitric oxide and nitrovasodilators: similarities, differences and potential interactions. J Am Coll Cardiol,1994, 24: 555~566.
  • [5]Deng AY, Rapp JP. Locus for the inducible, but not a constitutive, nitric oxide synthase cosegregates with blood pressure in the Dahl salt-sensitive rat. J Clin Invest, 1995, 95: 2170~2177.
  • [6]Qiu C, Muchant D, Beierwaltes WH et al. Evolution of chronic nitric oxide inhibition hypertension. Hypertension, 1998, 31 (Pt 1): 21~26.
  • [7]Hecker M, Cattaruzza M, Wagner AH et al. Regulation of inducible nitric oxide synthase gene expression in vascular smooth muscle cells. Gen Pharmacol, 1999, 32 (1): 9~16.
  • [8]Mattson DL, Bellehumeur TG. Neural nitric oxide synthase in the renal medulla and blood pressure regulation. Hypertension, 1996, 28 (2): 297~303.
  • [9]Mattson DL, Higgins DJ. Influence of diatary sodium intake on renal medullary nitric oxide synthase and L-NAME hypertension. Hypertension, 1996, 27: 688~692.
  • [10]LaPointe MC, Isenovic E. Interleukin-1 beta regulation of inducible nitric oxide synthase and cyclooxygenase-2 involves the p42/44 and p38 MAPK signaling pathways in cardiac myocytes. Hypertension, 1999, 33 (1 Pt 2): 276~282.
  • [11]Morton JJ, Beattie EC, Speirs A et al. Persistent hypertension following inhibition of nitic oxide formation in the young Wistar rat: role of renin and vascular hypertrophy. J Hypertension, 1993, 11: 1083~1088.
  • [12]Zou AP, Wu F, Cowley AW Jr et al. Protective effect of angiotensin Ⅱ-induced increase in nitric oxide in the renal medullary circulation. Hypertension, 1997, 31 (Pt 1): 271~276.
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