Conclusion

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Hypertensives have a number of microvascular defects, which are independent of the arterioles, and affect the capillary and venular segment of the microcirculation, vessels that are not exposed to elevated blood pressure. These defects expose hypertensives to an enhanced risk for organ injury. We still have little evidence to suggest that the arterial blood pressure elevation per se induces vascular lesions similar to those encountered in hypertension. It appears that a co-factor exists that serves to enhance cell activation in the circulation. In the SHR the glucocorticoid pathway may be involved in production of reactive oxygen in endothelium, apoptosis and capillary rarefaction, inhibition of leukocyte adhesion to postcapillary venules, and suppression of the glucose receptor. These are indications of a microvascular inflammatory response, which compared to that in nor-motensives is blunted by the suppression of leukocyte rolling and adhesion to the postcapillary venules. The enhanced organ injury in hypertension may be associated with microvascular apoptosis.

Acknowledgements

Supported by NIH Grant HL-10881. I thank Drs. Makoto Suematsu, Hidekazu Suzuki, Fred Lacy, Allan Swei, Camille Vogt, and Dale Parks for numerous discussions and inspirations. Special thanks to Frank A. DeLano for the assistance with Figure 2.

References

Boegehold, M. A. (1991). Effect of salt-induced hypertension on microvascular pressures in skeletal muscle of Dahl rats. American Journal of Physiology 260, H1819-H1825. Cerwinka, W. H., and Granger, D. N. (2001). Influence of hypercholes-terolemia, and hypertension on ischemia-reperfusion induced P-selectin expression. Atherosclerosis 154, 337-344. Helmke, B. P., Bremner, S. N., Zweifach, B. W., Skalak, R., and Schmid-Schonbein, G. W. (1997). Mechanisms for increased blood flow resistance due to leukocytes. Am. J. Physiol. 273, H2884-H2890. Hutchins, P. M., and Darnell, A. E. (1974). Observations of a decreased number of small arterioles in spontaneously hypertensive rats. Circ. Res. 34-35, 161-165. The report contains the first quantitative assessment of microvascular rarefaction in arterial hypertension after repeated qualitative descriptions of the phenomenon in hypertensive patients.

Imai, T., Morita, T., Shindo, T., Nagai, R., Yazaki, Y., Kurihara, H., Suematsu, M., and Katayama, S. (2001). Vascular smooth muscle cell-directed overexpression of heme oxygenase-1 elevates blood pressure through attenuation of nitric oxide-induced vasodilation in mice. Circ. Res. 89, 55-62.

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The report summarizes the first detailed documentation of the inflammatory reaction after blockade of NO synthesis in the microcirculation. Prewitt, R. L., Chen, I. I. H., and Dowell, R. F. (1982). Development of microvascular rarefaction in the spontaneously hypertensive rat. Am. J. Physiol. 243, H243-H251. Suematsu, M., Suzuki, H., Tamatani, T., Iigou, Y., DeLano, F. A., Miyasaka, M., Forrest, M. J., Kannagi, R., Zweifach, B. W., Ishimura, Y., and Schmid-Schonbein, G. W. (1995). Impairment of selectin-mediated leukocyte adhesion to venular endothelium in spontaneously hypertensive rats. J Clin. Invest. 96, 2009-2016. An examination of the molecular mechanisms for attenuation of leukocyte adhesion to the endothelium in postcapillary venules of the SHR. Suzuki, H., DeLano, F. A., Parks, D. A., Jamshidi, N., Granger, D. N., Ishii, H., Suematsu, M., Zweifach, B. W., and Schmid-Schonbein, G. W. (1998). Xanthine oxidase activity associated with arterial blood pressure in spontaneously hypertensive rats. Proc. Natl. Acad. Sci. USA 95, 4754-4759.

Vogt, C. J., and Schmid-Schonbein, G. W. (2001). Microvascular endothe-lial cell death, and rarefaction in the glucocorticoid-induced hypertensive rat. Microcirculation 8, 129-139. Zweifach, B. W., Kovalcheck, S., DeLano, F. A., and Chen, P. (1981). Micropressure-flow relationship in a skeletal muscle of spontaneously hypertensive rats. Hypertension 3, 601-614. This report summarizes a comprehensive set of micro-hemodynamic measurements in young, and old SHR skeletal muscle.

Capsule Biography

Dr. Schmid-Schonbein has headed the Microcirculation Laboratory at the University of California San Diego since 1979. President of the Micro-circulatory Society in 2003, his laboratory primarily focuses on cell mechanics, cell activation, mechanisms of inflammation, and tissue injury. His work is supported by grants from the NIH and NSF.

Section J

Inflammation

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