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Professional Experiences
Education
Publications Khraibi AA. Dobrian AD, Yu T, Solhaug MJ, Billiar RB. (2005) Role of RIHP and renal tubular sodium transporters in volume retention of pregnant rats. Am J Hypertens. 18(10):1375-1383 Solhaug MJ. (2003) Pathophysiological role of oxidative stress in geriatric vascular dysfunction. Am J Physiol Regul Integr Comp Physiol. 285(3):R524-525. Khraibi AA, Solhaug MJ, Dobrian AD, Berndt TJ. (2002) Renal interstitial hydrostatic pressure and natriuretic responses to volume expansion in pregnant rats. Am J Physiol Renal Physiol. 282(5):F821-825 Kullaprawithaya U, Wang D, Dong XQ, Dong KW, Solhaug MJ. Macula Densa and tubular neronal nitric oxide synthase, nNOS, during postnatal renal development. Am Physiol Renal Physiol. (submitted 2002) Solhaug MJ, Kullaprawithaya U, Dong XQ, Dong KW. (2001) Expression of endothelial nitric oxide synthase in the postnatal developing porcine kidney. Am J Physiol Regul Integr Comp Physiol. 280(5):R1269-R1275 Solhaug MJ, Dong XQ, Adelman RD, Dong KW. (2000) Ontogeny of neuronal nitric oxide synthase, NOS I, in the developing porcine kidney. Am J Physiol Regul Integr Comp Physiol. 278(6):R1453-1459 Solhaug MJ, Ballevre LD, Guignard JP, Granger JP, Adelman KD. (1996) Nitric oxide in the developing kidney. Pediatr Nephrol. 10(4):529-539 Research Interests & Funding Our lab is involved in the investigation of postnatal renal development, including the examination of the factors modulating newborn renal hemodynamics and function, and the processes of renal maturation to adult capability. Studies in our lab demonstrate that in the postnatal developing kidney, the potent vasodilator, nitric oxide, NO, plays a more important functional role than in the adult, counter-balancing the effects of highly activated vasoconstrictors, such as angiotensin II, AII. This increased participation of NO in the developing kidney is due to differences in the renal content and distribution of the NO synthesizing enzyme, nitric oxide synthase, NOS, from the adult. Two isoforms, NOS 1, neuronal or nNOS, and NOS 3, endothelial or eNOS, exhibit distinct developmental regulatory patterns of quantitative whole kidney and cortico-medullary expression and intrarenal distribution. These two NOS isoforms also exhibit contrasting developmental patterns in the postnatal kidney, suggesting that their functional actions may differ in this developmental period. We are currently examining the regulatory relationship between AII and these two NOS isoforms, utilizing a combination of in vivo and in vitro experiments. Present Funded Research TITLE: “Regulation of Developmental
Renal Hemodynamics”
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