Orthostatic Disorders of the Circulation

Renin-Aldosterone Paradox and Perturbed Blood Volume Regulation Underlying Postural Tachycardia Syndrome

“…Accurate plasma volume assessments can be affected by several environmental, dietary, and patient-related factors. 25 These variables may in part explain the mixed results obtained by other investigators who have tried to assess plasma volume in patients with POTS. 8,9,11,12 Several measures were undertaken in the present study to ensure that the plasma volume was measured accurately.…”

Pathogenesis of hyperadrenergic orthostatic hypotension. Evidence of disordered venous innervation exclusively in the lower limbs.

“…Eight patients with orthostatic hypotension were studied, who complained of lightheadedness, palpitations, and (frequently) syncope in the upright posture. In all patients, the blood pressure fell reproducibly by at least 20 mmHg systolic and/or 10 mmHg diastolic, and heart rate rose by 28 or to above 108 bpm in the standing posture (2). Preliminary measurements showed that there were normal increases in plasma renin activity and plasma aldosterone concentration after furosemide (40 mg i.v.)…”

“…Thus, although orthostatic venoconstriction may not be persistent in normal subjects, an abnormal orthostatic venodilatation appeared to occur in this patient and this might well have contributed to his fall in blood pressure in the upright posture. Moreover, an abundance of more recent evidence in patients with excessive gravitational pooling in the leg veins indicates that orthostatic venous contractility is important in maintaining normal venous return, cardiac filling, and cardiac output (1,2). It is difficult to explain the dramatic and repro- (17), acetylcholine (18), or histamine (19), or to a subnormal venous contractile response to the erect posture.…”

“…In these patients orthostatic hypotension is presumably due, to a large extent, to failure of the arterioles to contract in the upright posture. However, venous pooling due to failure ofthe normal venous contractile response to orthostasis is probably an important contributing factor, perhaps the most important factor, even in these patients, since an inflated MAST suit will greatly reduce the orthostatic hypotension in about 50% of patients with autonomic insufficiency (2).…”

Neurocardiogenic Syncope and Related Disorders of Orthostatic Intolerance

“…Here, the mechanoreceptors are located in the adventitia of the arterial wall. 8 The afferent impulses generated by stretch on the arterial wall are then transmitted via the sensory fibers of the carotid sinus nerve that travels with the glossopharyngeal nerve. These afferent pathways terminate in the nucleus tractus solitarii in the medulla, near the dorsal and ambiguous nuclei.…”