The microcirculation in experimental hypertension. State-of-the-art review.

Information concerning the microcirculation has been obtained largely by intravital microscopy of selected tissues in the rat-skeletalrat-skeletal muscle and splanchnic viscera, as well as in the cheek pouch of the hamster. The data for the most part pertain to the spontaneous form of hypertension in the SHR strain of rats and renovascular forms of the disease involving surgical manipulation of the kidney or its blood supply. Direct measurements of pressure and flow in exteriorized skeletal muscle preparations reveal a 2- to 3-fold increase in resistance to flow. An increase in resistance appears in the terminal arterioles and their precapillary branches as early as at 4 weeks of age for SHR animals and is progressively exacerbated in older more mature animals. The increase in microvascular resistance appears to develop as a consequence of neurogenic and humoral mechanisms which act initially on larger arterioles (50–100 μm) and subsequently on the peripheral arterioles (15–25 μm in diameter). The smaller arterioles not only show an increased tone under steady state conditions but what can be referred to as a functional rarefaction in which 30° to 50° of the precapillary extensions of the arterioles are shut off for varying periods from the active muscle circulation. Structural rarefaction (a reduced number of arterioles) is seen only in the late stages of the SHR syndrome and can account for a small portion of the increase in peripheral resistance. The cause and effect relationship between the microvascular changes and the associated elevation in systemic pressure cannot be unequivocally demonstrated in intravital preparations. Hypertension induced by different experimental modalities does not have a consistent microcirculatory counterpart, leading to the conclusion that depending on the precise mechanisms involved in the initiation of the syndrome, microcirculatory derrangements can arise as either initiating or secondary phenomena. Tissue pathology is uniformly associated with a reduction in arterial supply, and uneven distribution of blood and red cell hematocrit in the network proper. On the postcapillary side, there is a trend for venular tortuosity and distension.