Mind the Vein

Abstract

V eins lack luster when it comes to hypertension research. Compared with the scientist working on arterial branches, heart, or kidney, the vein researcher commonly feels like being at the bottom of the cardiovascular food chain. Convincing peers that project proposals or articles dealing with venous regulation are any good can be challenging. The study by Okamoto et al 1 is a strong reminder that veins are more than blood sampling outlets, sources of blood clots, or commodities for cardiovascular surgeons. Indeed, in patients with severe autonomic failure, venous capacitance vessels, particularly those in the splanchnic area, take over command of blood pressure control. Moreover, veins can serve as a treatment target to improve blood pressure control in such patients.Veins contain ≈75% of total body blood volume such that small changes in venous capacitance or compliance substantially affect cardiac loading conditions. Venous function is governed by various feedback mechanisms and reflexes, including arterial baroreflexes. Furthermore, increased intravenous volume and associated venous distension elicit local arteriolar constriction. This so-called venoarteriolar reflex suggests that veins can truly be in charge of local hemodynamic control. With standing, ≈500 to 1000 mL of blood are rapidly redistributed from the upper body to venous capacitance vessels below the diaphragm. Human venous compliance is particularly high in splanchnic and cutaneous areas. Yet, a larger proportion of the venous pooling with standing takes place in splanchnic compared with cutaneous veins. In healthy individuals, baroreflex mechanisms adjust efferent sympathetic and parasympathetic activity, so that blood pressure is maintained with standing. Venous responses may be important in this regard as splanchnic veins are more sensitive to adrenergic stimulation and express more α 1 -and α 2 -adrenoreceptors than mesenteric arteries.In patients with autonomic failure, sympathetic and parasympathetic efferent nerves are either destroyed or disconnected from brain stem input. Thus, changes in cardiac preload with standing cannot be buffered by adjusting efferent autonomic activity and blood pressure decreases profoundly.The orthostatic hypotension can be so severe that patients are unable to stand for more than a few seconds, which dramatically restricts their quality of life.In patients with severe orthostatic hypotension, causative treatments are rare. Nonpharmacological treatments, including optimized salt and water ingestion, compression garments, and sleeping in the head-up tilt position, may not provide sufficient symptom relief in severely affected patients. Symptomatic pharmacological management with pressor agents has a slow onset of action and tends to worsen hypertension in the supine position. Therefore, Okamoto et al 1 developed and tested a servocontrolled automated inflatable abdominal binder for the treatment of orthostatic hypotension. External pressure on the abdomen likely compresses splanchnic capacitance vessels, thereby...