Influence of plasma osmolality on baroreflex control of sympathetic activity

Abstract

The purpose of this study was to determine if plasma osmolality alters baroreflex control of sympathetic activity when controlling for a change in intravascular volume; we hypothesized that baroreflex control of sympathetic activity would be greater during a hyperosmotic stimulus compared with an isoosmotic stimulus when intravascular volume expansion was matched. Seven healthy subjects (25 +/- 2 yr) completed two intravenous infusions: a hypertonic saline infusion (HSI; 3% NaCl) and, on a separate occasion, an isotonic saline infusion (ISO; 0.9% NaCl), both at a rate of 0.15 ml x kg(-1) x min(-1). To isolate the effect of osmolality, comparisons between HSI and ISO conditions were retrospectively matched based on hematocrit; therefore, baroreflex control of sympathetic outflow was determined at 20 min of a HSI and 40 min of an ISO. Muscle sympathetic outflow (MSNA) was directly measured using the technique of peroneal microneurography; osmolality and blood pressure (Finometer) were assessed. The baroreflex control of sympathetic outflow was estimated by calculating the slope of the relationship between MSNA and diastolic blood pressure during controlled breathing. Plasma osmolality was greater during the HSI compared with the ISO (HSI: 292 +/- 0.9 mosmol/kg and ISO: 289 +/- 0.8 mosmol/kg, P < 0.05). Hematocrits were matched (HSI: 39.1 +/- 1% and ISO: 39.1 +/- 1%, P > 0.40); thus, we were successful in isolating osmolality. The baroreflex control of sympathetic outflow was greater during the HSI compared with the ISO (HSI: -8.3 +/- 1.2 arbitrary units x beat(-1) x mmHg(-1) vs. ISO: -4.0 +/- 0.8 arbitrary units x beat(-1) x mmHg(-1), P = 0.01). In conclusion, when controlling for intravascular volume, increased plasma osmolality enhances baroreflex control of sympathetic activity in humans.

Influence of increased plasma osmolality on sympathetic outflow during apnea

“…The results of this study demonstrate that an acute elevation of plasma osmolality has an overall effect on MSNA, confirming previous findings in humans (9,12,44) and animals (4,22,27,43). Additionally, in humans, increased plasma osmolality enhances sensitivity of baroreflex control of MSNA (9,44).…”

“…Hypercapnia acts primarily on centrally located chemoreceptors, potentially located on the medullary surface (7); hypoxia exerts effects principally through the peripheral receptors located on the carotid bodies (24, 41). Hypercapnia and hypoxia increased muscle sympathetic nerve activity (MSNA) when assessed both during spontaneous breathing and during a voluntary apnea (19,23,26,33).Experimentally induced changes in plasma osmolality also influence the control of sympathetic outflow in both animals (4,22,27,30,43) and humans (9,12,44). Acute administration of hypertonic saline in anesthesized animals increased splanchnic, adrenal, and lumbar sympathetic activity and blunted renal sympathetic activity (4,22,27,43).…”

“…Experimentally induced changes in plasma osmolality also influence the control of sympathetic outflow in both animals (4,22,27,30,43) and humans (9,12,44). Acute administration of hypertonic saline in anesthesized animals increased splanchnic, adrenal, and lumbar sympathetic activity and blunted renal sympathetic activity (4,22,27,43).…”

Cerebrospinal Fluid Hypernatremia Elevates Sympathetic Nerve Activity and Blood Pressure via the Rostral Ventrolateral Medulla

“…Indeed, our current findings document, for the first time, that acute ICV infusion of hypertonic NaCl produced a differential activation of lumbar and adrenal SNA but inhibition of renal SNA and no change in splanchnic SNA. In agreement, several studies have acutely raised NaCl concentrations in different species and through different routes to produce qualitatively similar responses and include: 1) IV infusion in rodents produce a similar differential SNA response 34 , 2) intracarotid infusion of NaCl to produce physiological changes decreases renal SNA 35 , and 3) IV infusion in humans increases muscle SNA 36, 37 . This SNA pattern may promote increased sodium excretion through a pressure-natriuresis mechanism and concurrent inhibition of renal SNA through a direct Na + -sympathoinhibitory pathway or a baroreceptor-mediated inhibition of RVLM discharge.…”

Neurogenic and Sympathoexcitatory Actions of NaCl in Hypertension

“…Similar to studies in animals, acute intravenous infusion of hypertonic NaCl to raise serum sodium and osmolality has been reported to increase ABP by ~6–10 mmHg [48–52]. In a subset of these studies, the pressor response was associated with significant increases in plasma norepinephrine (~30–40 %) [49–51].…”