Precapillary sphincter

In humans, injection or infusion of histamine causes a decrease in systolic and diastolic blood pressure and an increase in heart rate. The blood pressure changes are caused by the direct vasodilator action of histamine on arterioles and precapillary sphincters the increase in heart rate involves both stimulatory actions of histamine on the heart and a reflex tachycardia. Flushing, a sense of warmth, and headache may also occur during histamine administration, consistent with the vasodilation. Vasodilation elicited by small doses of histamine is caused by H -receptor activation and is mediated primarily by release of nitric oxide from the endothelium (see Chapter 19). The decrease in blood pressure is usually accompanied by a reflex tachycardia. Higher doses of histamine activate the H2-mediated cAMP process of vasodilation and direct cardiac stimulation. In humans, the cardiovascular effects of small doses of histamine can usually be antagonized by Hi-receptor antagonists alone. 

In most patients with hypertension, the disease, cardiac output is about normal while resistance to the flow of blood in the tissues is raised. Blood viscosity and blood volume are also normal. The question is Where is the resistance increased which results in elevated blood pressure Most of the older evidence pointed to the arterioles or small arteries, and this is still believed. But it should be extended farther down the line to the precapillary sphincter area, a region that has much to do with the control of the exit of fluid from the blood. 

The classical view of blood flow control involved the action of vasomotor influences on a set of vessels called the resistance vessels, generally arterioles and small arteries smaller than about 100 to 150 )u.m in diameter, which controlled flow to and within an organ [56]. The notion of precapillary sphincters that control flow in individual capillaries has been abandoned in favor of the current notion that the terminal arterioles control the flow in small capfllary networks that branch off of these arterioles. In recent years, it has become clear that the resistance to blood flow is distributed over a wider range of vessel branching orders with diameters up to 500 /um. There are mechanisms to be discussed in Section 59.4.2 that are available for coordinating the actions of local control processes over wider regions. 

The autoregulation response should ultimately arise from the action of multiple precapillary sphincters and resistance arterioles in the microcirculation. The control of flow in a microvascular model was analyzed by Mayrovitz et al. (1978). This model included muscular arterial and venous vasomotion, capillary filtration and reabsorption, and lymph flow. Tissue pressure was assumed to be regulated and was used to provide the control pathway for activation of the precapillary sphincter. Local flow was found to vary considerably with periodic sphincter activity. This model demonstrated that autoregulation of flow is likely to find its genesis at the microcirculatory level. 

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