Afferent Baroreflex Dysfunction: Decreased or Excessive Signaling Results in Distinct Phenotypes

2020 ◽  
Vol 40 (05) ◽  
pp. 540-549
Author(s):  
Lucy Norcliffe-Kaufmann ◽  
Patricio Millar Vernetti ◽  
Jose-Alberto Palma ◽  
Bhumika J. Balgobin ◽  
Horacio Kaufmann
Keyword(s):  
Blood Pressure ◽  
Carotid Sinus ◽  
Sensory Information ◽  
Organ Damage ◽  
Direct Compression ◽  
Neck Tumors ◽  
Arterial Blood ◽  
Afferent Fibers ◽  
Acute Hypotension ◽  
Baroreflex Failure

AbstractHead and neck tumors can affect afferent baroreceptor neurons and either interrupt or intermittently increase their signaling, causing blood pressure to become erratic. When the afferent fibers of the baroreflex are injured by surgery or radiotherapy or fail to develop as in familial dysautonomia, their sensory information is no longer present to regulate arterial blood pressure, resulting in afferent baroreflex failure. When the baroreflex afferents are abnormally activated, such as by paragangliomas in the neck, presumably by direct compression, they trigger acute hypotension and bradycardia and frequently syncope, by a mechanism similar to the carotid sinus syndrome. We describe our observations in a large series of 23 patients with afferent baroreflex dysfunction and the cardiovascular autonomic features that arise when the sensory baroreceptor neurons are injured or compressed. The management of afferent baroreceptor dysfunction is limited, but pharmacological strategies can mitigate blood pressure swings, improve symptoms, and may reduce hypertensive organ damage. Although rare, the prevalence of afferent baroreflex dysfunction appears to be increasing in middle-aged men due to human papillomavirus related oropharyngeal cancer.

603 CHALLENGES IN THE MANAGEMENT OF SEVERE ORTHOSTATIC HYPOTENSION ASSOCIATED WITH SUPINE HYPERTENSION IN A PATIENT WITH AUTONOMIC DYSFUNCTION ON BACKGROUND OF NASOPHARYNGEAL CARCINOMA AND TYPE II DIABETES MELLITUS

2021 ◽  
Vol 50 (Supplement_2) ◽  
pp. ii14-ii18
Author(s):  
Q M N Rachel ◽  
K Mamun ◽  
M H Nguyen
Keyword(s):  
Blood Pressure ◽  
Nasopharyngeal Carcinoma ◽  
Orthostatic Hypotension ◽  
Carotid Sinus ◽  
Blood Pressure Monitoring ◽  
Pharmacological Interventions ◽  
Supine Hypertension ◽  
Neck Irradiation ◽  
Baroreflex Failure

Abstract Introduction Combined chemotherapy and radiotherapy increases long term survival in patients with nasopharyngeal carcinoma. However, radiotherapy of the carotid sinus or brain stem can evolve labile hypertension and orthostatic intolerance from chronic baroreflex failure. Diabetes would also cause this neuropathy. Management of patients with Supine hypertension-Orthostatic hypotension can be very challenging. Methods A case report was done on a 71-year-old man with metastatic nasopharyngeal carcinoma status post radiation therapy who was admitted with severe supine hypertension-orthostatic hypotension. Patient was managed with both non-pharmacological and pharmacological methods, and monitored for postural symptoms, complications of severe supine hypertension—which has been linked to left ventricular hypertrophy and kidney dysfunction, and placed on 24 hour ambulatory blood pressure monitoring to aid in management so as to prevent hypertension induced organ damage. Results This review outlines the pathophysiology of Supine hypertension-Orthostatic hypotension, treatment complications and potential management strategies recommendations for this group of patients. It revealed the benefit of having a 24 hour ambulatory blood pressure monitoring, which provides insight on the timing and magnitude of an individual’s blood pressure fluctuations throughout the day so as to further guide management. Conclusion Chronic baroreflex failure is a late sequela of neck irradiation for naso-pharyngeal carcinoma due to accelerated atherosclerosis in the region of the carotid sinus baroreceptor. Treatment goal is achieved with adequate control of pre-syncopal symptoms and prevention of long term complications. Non-pharmacological interventions remain the first line of therapy, followed by pharmacological interventions as necessary. Nonetheless, management of blood pressure in these elderly patients with baroreflex dysfunction remains challenging and should be individualized. Moving forward, a prospective study on the incidence of late onset, iatrogenic baroreflex failure as a late complication of neck irradiation and its particular relationship to carotid arterial rigidity should be conducted to increase awareness, timely diagnosis and management of the condition among physicians.

Cardiovascular and neuroendocrine responses to baroreceptor denervation in baboons

1990 ◽  
Vol 258 (4) ◽  
pp. R930-R938 ◽  
Author(s):  
R. E. Shade ◽  
V. S. Bishop ◽  
J. R. Haywood ◽  
C. K. Hamm
Keyword(s):  
Blood Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Vasopressin Secretion ◽  
Blood Pressure Responses

The purpose of this study was to describe the hormonal and blood pressure responses to partial (carotid sinus) and complete (carotid sinus + aortic arch) baroreceptor denervation in baboons. Experiments were performed in eight adult male baboons maintained on a tether system for the continuous measurement of mean arterial blood pressure (MAP) and heart rate (HR). Bilateral carotid sinus denervation (CSD) immediately increased MAP from 83 +/- 2.2 to 124 +/- 7.3 mmHg. MAP gradually decreased over the next 14 days to intact levels. There were also transient decreases in HR variability and increases in blood pressure variability after CSD. Subsequent denervation of the aortic arch to produce sinoaortic denervation (SAD) resulted in another abrupt large increase in MAP followed by a small but significant increase in MAP of 11 mmHg that was maintained for up to 4 wk after SAD. The short-term variability of HR and blood pressure was chronically decreased and increased, respectively, after SAD. Plasma renin activity, vasopressin, and epinephrine were not changed from intact levels either after CSD or SAD. Plasma norepinephrine was only transiently increased by CSD and chronically elevated by 72% over intact levels after SAD. Thus CSD in the baboon does not produce a sustained increase in MAP. SAD chronically increases MAP and is associated with evidence for an increased sympathetic tone. There is no indication that either increased renin secretion or vasopressin secretion contributes to the chronic cardiovascular effects of SAD in baboons.

Role of sinoaortic reflexes in hemodynamic patterns of natural defense behaviors in the cat

1981 ◽  
Vol 240 (3) ◽  
pp. H421-H429 ◽  
Author(s):  
G. Baccelli ◽  
R. Albertini ◽  
A. Del Bo ◽  
G. Mancia ◽  
A. Zanchetti
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Carotid Sinus ◽  
Emotional Behavior ◽  
Natural Defense ◽  
Arterial Blood ◽  
Hemodynamic Pattern ◽  
Before And After

To evaluate whether sinoaortic afferents contribute to the hemodynamic pattern of fighting, cardiovascular changes associated with fighting were studied in cats before and after sinoaortic denervation. Sinoaortic denervation exaggerates the decrease in heart rate, cardiac output, and arterial pressure during immobile confrontation (hissing, staring but no movement). During nonsupportive fighting (fighting with forelimbs while lying on one side) and supportive fighting ( fighting while standing on four feet) sinoaortic denervation reduces the increase in heart rate and cardiac output, minimizes the mesenteric vasoconstriction, induces a fall in arterial blood pressure, but does not affect iliac vasoconstriction or vasodilatation. The hemodynamic pattern of fighting is similarly changed by temporary inactivation of carotid sinus baroreflexes by common carotid occlusion as by chronic section of sinoaortic nerves. It is concluded that sinoaortic reflexes play an important role in the cardiovascular patterns accompanying natural fighting. They favor cardiac action and allow a marked visceral vasoconstriction to occur, thus minimizing or preventing a fall in blood pressure during emotional behavior.

Acute hypotension induced by aortic clamp vs. PTH provokes distinct proximal tubule Na+ transporter redistribution patterns

2004 ◽  
Vol 287 (4) ◽  
pp. R878-R885 ◽  
Author(s):  
Patrick K. K. Leong ◽  
Li E. Yang ◽  
Harrison W. Lin ◽  
Niels H. Holstein-Rathlou ◽  
Alicia A. McDonough
Keyword(s):  
Blood Pressure ◽  
Proximal Tubule ◽  
Subcellular Distribution ◽  
Urine Output ◽  
Volume Flow ◽  
High Dose ◽  
Arterial Blood ◽  
Acute Hypotension ◽  
High Doses ◽  
Cortical Membranes

Renal parathyroid hormone (PTH) action is often studied at high doses (100 μg PTH/kg) that lower mean arterial pressure significantly, albeit transiently, complicating interpretation of studies. Little is known about the effect of acute hypotension on proximal tubule Na+ transporters. This study aimed to determine the effects of acute hypotension, induced by aortic clamp or by high-dose PTH (100 μg PTH/kg), on renal hemodynamics and proximal tubule Na/H exchanger isoform 3 (NHE3) and type IIa Na-Pi cotransporter protein (NaPi2) distribution. Subcellular distribution was analyzed in renal cortical membranes fractionated on sorbitol density gradients. Aortic clamp-induced acute hypotension (from 100 ± 3 to 78 ± 2 mmHg) provoked a 62% decrease in urine output and a significant decrease in volume flow from the proximal tubule detected as a 66% decrease in endogenous lithium clearance. There was, however, no significant change in glomerular filtration rate (GFR) or subcellular distribution of NHE3 and NaPi2. In contrast, high-dose PTH rapidly (<2 min) decreased arterial blood pressure to 51 ± 3 mmHg, decreased urine output, and shifted NHE3 and NaPi2 out of the low-density membranes enriched in apical markers. PTH at much lower doses (<1.4 μg·kg−1·h−1) did not change blood pressure and was diuretic. In conclusion, acute hypotension per se increases proximal tubule Na+ reabsorption without changing NHE3 or NaPi2 subcellular distribution, indicating that trafficking of transporters to the surface is not the likely mechanism; in comparison, hypotension secondary to high-dose PTH blocks the primary diuretic effect of PTH but does not inhibit the PTH-stimulated redistribution of NHE3 and NaPi2 to the base of the microvilli.

Interplay among carotid sinus, cardiopulmonary, and carotid body reflexes in dogs

1976 ◽  
Vol 230 (1) ◽  
pp. 19-24 ◽  
Author(s):  
G Mancia ◽  
JT Shepherd ◽  
DE Donald
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Dominant Role ◽  
Arterial Blood ◽  
Carotid Bodies ◽  
Sinus Pressure

Interactions among vascular reflexes evoked from carotid sinuses, carotid bodies, and cardiopulmonary region were examined in anesthetized, atropinized, and respired dogs with aortic nerves cut. The carotid sinuses were perfused at 220, 150, and 40-50 mmHg; the chemoreceptors were stimulated by perfusion with hypoxic hypercapnic blood. Cardiopulmonary vasomotor inhibition was interrupted by vagal cold block. Measurements were made of arterial blood pressure and of kidney and hindlimb vascular resistance. At sinus pressures less than 170-160 mmHg, cardiopulmonary vasomotor inhibition increased with increase in blood volume. At high sinus pressure, interruption of this augmented cardiopulmonary inhibition was as ineffective in changing vascular resistance as interruption of the lesser inhibition present during normovolemia. Chemoreceptor stimulation increased the response to vagal block at intermediate but not at high or low sinus pressure. The studies demonstrate the dominant role of the carotid sinus reflex when the three systems interact and the ineffectiveness of chemoreceptor stimulation when carotid or cardiopulmonary inhibition is maximal.

Dynamic cerebral autoregulation during and after handgrip exercise in humans

2010 ◽  
Vol 108 (6) ◽  
pp. 1701-1705 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Kohei Sato ◽  
Toshinari Akimoto ◽  
Anna Oue ◽  
Ai Hirasawa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cerebral Autoregulation ◽  
Valsalva Maneuver ◽  
Maximum Voluntary Contraction ◽  
Static Exercise ◽  
Handgrip Exercise ◽  
Arterial Blood ◽  
Significant Difference ◽  
Acute Hypotension ◽  
Dynamic Cerebral Autoregulation

The purpose of the present study was to examine the effect of static exercise on dynamic cerebral autoregulation (CA). In nine healthy subjects at rest before, during, and after static handgrip exercise at 30% maximum voluntary contraction, the response to an acute drop in mean arterial blood pressure and middle cerebral artery mean blood velocity was examined. Acute hypotension was induced nonpharmacologically via rapid release of bilateral thigh occlusion cuffs. Subjects were instructed to avoid executing a Valsalva maneuver during handgrip. To quantify dynamic CA, the rate of regulation (RoR) was calculated from the change in cerebral vascular conductance index during the transient fall in blood pressure. There was no significant difference in RoR between rest (mean ± SE; 0.278 ± 0.052/s), exercise (0.333 ± 0.053/s), and recovery (0.305 ± 0.059/s) conditions ( P = 0.747). In addition, there was no significant difference in the rate of absolute cerebral vasodilatory response to acute hypotension between three conditions ( P = 0.737). This finding indicates that static exercise and related elevations in blood pressure do not alter dynamic CA.

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