Since arterial hypertension is diagnosed by elevated blood pressure in central arteries, it is frequently regarded as a condition that is almost exclusively affected by hemody-namic resistance in the small arteries and arterioles. This point of view has lead for several decades to a focus on arteries and arterioles as mediators of the syndrome and as focus for therapeutic targets. But microvascular studies indicate that several forms of arterial hypertension may be affected by more general mechanisms, which not only involve the arteries and arterioles, but a range of pathophy-siological mechanisms.
This chapter will be focused on the manifestations of hypertension in capillaries and venules, microvessels that are not exposed to blood pressure elevation. Capillaries and venules are involved in blood flow regulation and exchange functions. They are also an integral part of the inflammatory cascade, a potentially important aspect of hypertension as a vascular disease with cell and organ damage. We will summarize an array of pathophysiological phenomena in hypertension for which there is still no conclusive evidence for a pressure-mediated mechanism and which instead point towards a more general metabolic and regulatory defect.
The majority of the evidence cited here has been obtained in the spontaneously hypertensive rat (SHR) and its nor-motensive control, the Wistar Kyoto (WKY) rat, as well as in the salt dependent Dahl-S hypertensive rat with its nor-motensive control, the salt resistant Dahl-R strain. Both of these models have a strong genetic linkage. Unless indicated otherwise, these models serve as the main basis for current knowledge at the microvascular level.
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