Regulation Of Blood Pressure

The maintenance of postural normotension without an excessive heart rate increment requires an adequate blood volume and the integration of reflex and humoral systems in several key vascular beds. These include striated muscle, splanchnic-mesenteric, and cerebrovascular beds. An adequate blood volume is essential. Hypovolemia regularly causes OH, even if vascular reflexes are intact. Hypovolemia can also be relative. Adrenergic den-ervation decreases vascular tone and increases vascular capacity, so that these patients are relatively hypovolemic, although plasma volume is normal. A decreased red cell mass or normocytic normochromic anemia of chronic autonomic failure aggravates OH. Correcting anemia with erythropoietin improves orthostatic intolerance (4).

Vasomotor tone is controlled by two sets of baroreflexes, the arterial (or high-pressure) and venous (or low-pressure) baroreflexes. When BP falls, baroreceptors are unloaded in the carotid sinus and aortic arch (5). These are arterial baroreceptors. Afferents through the IX and X cranial nerves synapse in the nucleus of the tractus solitarius. From this nucleus, a polysynaptic cardiovagal pathway travels to the nucleus ambiguus and dorsal motor nucleus of the vagus and hence, through the vagus nerve to the sinoatrial node to control heart rate. Sympathetic function is regulated by the rostroventrolateral nucleus of medulla, which projects to the intermediolateral column of the thoracic spinal cord that in turn provides sympathetic innervation to the heart and periphery (arterioles and venules) (6). In addition to arterial baroreceptors, there are low-pressure baroreceptors, that respond to a decrease in central venous pressure. Cardiopulmonary receptors in the heart and lungs send mainly nonmyelinated vagal fibers to the nucleus of the tractus solitarius. The central pathways and efferents are the same as for arterial baroreceptors. Baroreflexes are often referred to as "buffer" nerves as they maintain BP constant in all positions. Baroreflex failure results in the triad of OH, supine hypertension, and loss of diurnal variation in BP. In normal subjects BP is lower at night than during the day. The converse occurs in baroreflex failure (7).

The splanchnic-mesenteric capacitance bed is a large-volume, low-resistance system of great importance in the maintenance of postural normotension in humans. It constitutes 25-30% of the total blood volume (8). Unlike muscle veins, splanchnic veins have an abundance of smooth muscle and a rich sympathetic innervation. The mesenteric capacitance bed is markedly responsive to both arterial and venous baroreflexes. Venoconstriction is mediated by a-adrenergic receptors (9). The nerve supply to the mesenteric bed is mostly from preganglionic axon in the greater splanchnic nerve, with cell bodies in the intermedi-olateral column (mainly T4-T9) that synapse in the celiac ganglion from where postganglionic adrenergic fibers supply effector cells. Abnormalities in the splanchnic autonomic outflow have been found in human diabetic neuropathy, indicating that preganglionic fibers can be affected (10).

Cerebral vasoregulation is important for ensuring adequate and stable flow to the brain in spite of changing systemic BP. The maintenance of constant blood flow in spite of variations in BP is termed autoregulation (11). Within a mean BP range of approximately 50-150 mmHg, a change in BP produces insignificant change in cerebral perfusion. Previous studies of patients with OH demonstrated an expansion of the autoregulated range at both the upper and lower limits, so that cerebral perfusion remained relatively constant with the patient supine (when supine hypertension might be present) and in response to standing (when OH occurs) (11-14).

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