Effect of aging on baroreflex function in humans

2007 ◽  
Vol 293 (1) ◽  
pp. R3-R12 ◽  
Author(s):  
Kevin D. Monahan
Keyword(s):  
Nervous System ◽  
Parasympathetic Nervous System ◽  
Pressor Response ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Impaired Ability ◽  
Baroreflex Function ◽  
Increased Risk ◽  
Vascular Stiffening ◽  
Effects Of Aging

Arterial blood pressure (BP) is regulated via the interaction of various local, humoral, and neural factors. In humans, the major neural pathway for acute BP regulation involves the baroreflexes. In response to baroreceptor activation/deactivation, as occurs during transient changes in BP, key determinants of BP, such as cardiac period/heart rate (via the sympathetic and parasympathetic nervous system) and vascular resistance (via the sympathetic nervous system), are modified to maintain BP homeostasis. In this review, the effects of aging on both the parasympathetic and sympathetic arms of the baroreflex are discussed. Aging is associated with decreased cardiovagal baroreflex sensitivity (i.e., blunted reflex changes in R-R interval in response to a change in BP). Mechanisms underlying this decrease may involve factors such as increased levels of oxidative stress, vascular stiffening, and decreased cardiac cholinergic responsiveness with age. Consequences of cardiovagal baroreflex impairment may include increased levels of BP variability, an impaired ability to respond to acute challenges to the maintenance of BP, and increased risk of sudden cardiac death. In contrast, baroreflex control of sympathetic outflow is not impaired with age. Collectively, changes in baroreflex function with age are associated with an impaired ability of the organism to buffer changes in BP. This is evidenced by the reduced potentiation of the pressor response to bolus infusion of a pressor drug after compared to before systemic ganglionic blockade in older compared with young adults.

scholarly journals The study of the odour impact on physiological, emotional, and cognitive aspects of human health under experimental conditions (literature review)

2021 ◽  
Vol 99 (12) ◽  
pp. 1370-1375
Author(s):  
Svetlana V. Ivanova ◽  
Svetlana A. Skovronskaya ◽  
Mihail E. Goshin ◽  
Olga V. Budarina ◽  
Aliya Z. Kulikova
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Literature Review ◽  
Respiratory Rate ◽  
Human Health ◽  
Experimental Research ◽  
Cognitive Functions ◽  
Blood Circulation ◽  
Parasympathetic Nervous System ◽  
Arterial Blood

The article contains a literature review devoted to research on the influence of odours on physiological, emotional, and cognitive aspects of human health. The following databases were used at literature search execution: Pubmed, Scopus, Web of Science, MedLine, Global Health, Russian Research Citation Index. A total amount of 60 sources was analyzed for 1983-2019. The experimental research results aimed at studying the influence of odours on such physiological indices a: heart rate, heart rate variability, arterial blood pressure, respiratory rate, skin conductibility reaction, sleep, are described, and emotional and cognitive characteristics of the test subjects. The response to odours exposure was shown to depend on their intensity, hedonistic tone, the chemical structure of the odorant, as well as individual peculiarities of the test subjects, including their past experiences with smelling. In most cases, exposure to unpleasant odours activates the sympathetic nervous system, therefore heart rate, respiratory rate, skin blood circulation and its conductivity increase. Attention concentration increases at the deterioration of cognitive functions. Anger and repulsion reactions are noted at the emotional level; a feeling of discomfort with a motivation to escape appears. The exposure of pleasant odours leads to parasympathetic nervous system activation, heart rate, respiratory rate, skin conductibility, and blood circulation decrease. Cognitive functions improve, the quality of problem-solving increases, attention concentration decreases. A person’s mood gets better; the sensation of happiness appears. At that literature analysis has revealed most of the studies on the human to have significant restrictions: standard exposure methods absence, the difficulty of execution blind experiments that were deemed to be ignorant by test subjects as well as the influence of individual preferences and previous personal experience on the effects generated by the odour. The authors proposed recommendations on the current restrictions prevention and optimization of conducting the experimental research on the influence of odours on humans.

scholarly journals Selective quantification of the cardiac sympathetic and parasympathetic nervous systems by multisignal analysis of cardiorespiratory variability

2008 ◽  
Vol 294 (1) ◽  
pp. H362-H371 ◽  
Author(s):  
Xiaoxiao Chen ◽  
Ramakrishna Mukkamala
Keyword(s):  
Nervous System ◽  
Transfer Function ◽  
Parasympathetic Nervous System ◽  
Transfer Functions ◽  
Low Frequency ◽  
Sympathetic Blockade ◽  
Nervous Systems ◽  
Autonomic Nervous ◽  
Arterial Blood ◽  
The Time Domain

Heart rate (HR) power spectral indexes are limited as measures of the cardiac autonomic nervous systems (CANS) in that they neither offer an effective marker of the β-sympathetic nervous system (SNS) due to its overlap with the parasympathetic nervous system (PNS) in the low-frequency (LF) band nor afford specific measures of the CANS due to input contributions to HR [e.g., arterial blood pressure (ABP) and instantaneous lung volume (ILV)]. We derived new PNS and SNS indexes by multisignal analysis of cardiorespiratory variability. The basic idea was to identify the autonomically mediated transfer functions relating fluctuations in ILV to HR (ILV→HR) and fluctuations in ABP to HR (ABP→HR) so as to eliminate the input contributions to HR and then separate each estimated transfer function in the time domain into PNS and SNS indexes using physiological knowledge. We evaluated these indexes with respect to selective pharmacological autonomic nervous blockade in 14 humans. Our results showed that the PNS index derived from the ABP→HR transfer function was correctly decreased after vagal and double (vagal + β-sympathetic) blockade ( P < 0.01) and did not change after β-sympathetic blockade, whereas the SNS index derived from the same transfer function was correctly reduced after β-sympathetic blockade in the standing posture and double blockade ( P < 0.05) and remained the same after vagal blockade. However, this SNS index did not significantly decrease after β-sympathetic blockade in the supine posture. Overall, these predictions were better than those provided by the traditional high-frequency (HF) power, LF-to-HF ratio, and normalized LF power of HR variability.

scholarly journals Angiotensin II and the Cardiac Parasympathetic Nervous System in Hypertension

2021 ◽  
Vol 22 (22) ◽  
pp. 12305
Author(s):  
Julia Shanks ◽  
Rohit Ramchandra
Keyword(s):  
Nervous System ◽  
Parasympathetic Nervous System ◽  
Angiotensin Receptor Blockers ◽  
Critical Role ◽  
Brain Regions ◽  
Nerve Endings ◽  
Vagal Activity ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Parasympathetic Nerve

The renin–angiotensin–aldosterone system (RAAS) impacts cardiovascular homeostasis via direct actions on peripheral blood vessels and via modulation of the autonomic nervous system. To date, research has primarily focused on the actions of the RAAS on the sympathetic nervous system. Here, we review the critical role of the RAAS on parasympathetic nerve function during normal physiology and its role in cardiovascular disease, focusing on hypertension. Angiotensin (Ang) II receptors are present throughout the parasympathetic nerves and can modulate vagal activity via actions at the level of the nerve endings as well as via the circumventricular organs and as a neuromodulator acting within brain regions. There is tonic inhibition of cardiac vagal tone by endogenous Ang II. We review the actions of Ang II via peripheral nerve endings as well as via central actions on brain regions. We review the evidence that Ang II modulates arterial baroreflex function and examine the pathways via which Ang II can modulate baroreflex control of cardiac vagal drive. Although there is evidence that Ang II can modulate parasympathetic activity and has the potential to contribute to impaired baseline levels and impaired baroreflex control during hypertension, the exact central regions where Ang II acts need further investigation. The beneficial actions of angiotensin receptor blockers in hypertension may be mediated in part via actions on the parasympathetic nervous system. We highlight important unknown questions about the interaction between the RAAS and the parasympathetic nervous system and conclude that this remains an important area where future research is needed.

Effect of acute exposure to 3,660 m altitude on orthostatic responses and tolerance

2003 ◽  
Vol 95 (2) ◽  
pp. 591-601 ◽  
Author(s):  
A. P. Blaber ◽  
T. Hartley ◽  
P. J. Pretorius
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Parasympathetic Nervous System ◽  
Cerebral Blood Flow Velocity ◽  
Coarse Graining ◽  
Cerebral Vasoconstriction ◽  
Arterial Blood ◽  
Nervous System Activity ◽  
Head Up Tilt ◽  
Sympathetic Nervous

Orthostatic reflexes were examined at 375 m and after 60 min of exposure in a hypobaric chamber at 3,660 m using a 20-min 70° head-up tilt (HUT) test. Mean arterial blood pressure, R wave-R wave interval (RRI), and mean cerebral blood flow velocity (MFV) were examined with coarse-graining spectral analysis. Of 14 subjects, 7 at 375 m and 12 at 3,660 m were presyncopal. Immediately on arrival to high altitude, breathing frequency and MFV increased, and endtidal PCO2, RRI, RRI complexity, and the parasympathetic nervous system indicator decreased. MFV was similar in HUT at both altitudes. The sympathetic nervous system indicator increased with tilt at 3,660 m, whereas parasympathetic nervous system indicator decreased with tilt at both altitudes. Multiple regression analysis of supine variables from either 375 or 3,660 m and the time to presyncope at 3,660 m indicated that, after 1 h of exposure, increased presyncope at altitude was the result of 1) ineffective peripheral vasoconstriction, despite increased cardiac sympathetic nervous system activity with HUT, and 2) insufficient cerebral perfusion owing to cerebral vasoconstriction as the result of hypoxic hyperventilation-induced hypocapnia.

Nonadrenergic noncholinergic autonomic mediation of pressor response to feeding in lambs

1993 ◽  
Vol 265 (3) ◽  
pp. R530-R536 ◽  
Author(s):  
S. A. Jones ◽  
B. L. Langille ◽  
S. Frise ◽  
S. L. Adamson
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Adrenergic Blockade ◽  
Arterial Blood ◽  
Plasma Angiotensin ◽  
Muscarinic Cholinergic ◽  
Alpha Beta

We examined factors mediating a 70% increase in arterial blood pressure that occurs during feeding in newborn lambs. We report that the increase in blood pressure during feeding was significantly reduced (to approximately 50%) and delayed in onset by combined alpha- and beta-adrenergic blockade. Plasma angiotensin and vasopressin levels did not increase significantly during feeding, nor was the pressor response to feeding attenuated while using captopril to block the production of angiotensin II. Adrenalectomy or muscarinic cholinergic blockade with atropine was also unsuccessful in attenuating the pressor response to feeding. We demonstrated that the component of the pressor response to feeding that was insensitive to alpha, beta, and muscarinic blockade was mediated by the autonomic nervous system because it was completely eliminated by ganglionic blockade with hexamethonium. Thus nonadrenergic noncholinergic autonomic mechanisms mediate approximately half the pressor response to feeding in lambs.

Effects of fetal ovine adrenalectomy on sympathetic and baroreflex responses at birth

2002 ◽  
Vol 283 (2) ◽  
pp. R460-R467 ◽  
Author(s):  
Jeffrey L. Segar ◽  
Timothy Van Natta ◽  
Oliva J. Smith
Keyword(s):  
Plasma Cortisol ◽  
Late Gestation ◽  
Renal Nerve ◽  
Baroreflex Control ◽  
Fetal Sheep ◽  
Cesarean Section Delivery ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Baroreflex Function ◽  
Before And After

Studies were performed to test the hypothesis that the absence of adrenal glucocorticoids late in gestation alters sympathetic and baroreflex responses before and immediately after birth. Fetal sheep at 130–131 days gestation (term 145 days) were subjected to bilateral adrenalectomy before the normal prepartum increase in plasma cortisol levels. One group of fetuses ( n = 5) received physiological cortisol replacement with a continuous infusion of hydrocortisone (2 mg · day−1 · kg−1 for 10 days), whereas the other group received 0.9% NaCl vehicle ( n = 5). All animals underwent a second surgery 48 h before the study for placement of a renal nerve recording electrode. Heart rate (HR), mean arterial blood pressure (MABP), renal sympathetic nerve activity (RSNA), and baroreflex control of HR and RSNA were studied before and after cesarean section delivery. At the time of study (140–141 days gestation), fetal plasma cortisol concentration was undetectable in adrenalectomized (ADX) fetuses and 58 ± 9 ng/ml in animals receiving cortisol replacement (ADX + F). Fetal and newborn MABP was significantly greater in ADX + F relative to ADX animals. One hour after delivery, MABP increased 13 ± 3 mmHg and RSNA increased 91 ± 12% above fetal values in ADX + F (both P < 0.05) but remained unchanged in ADX lambs. The midpoint pressures of the fetal HR and RSNA baroreflex function curves were significantly greater in ADX + F (54 ± 3 and 56 ± 3 mmHg for HR and RSNA curves, respectively) than ADX fetuses (45 ± 2 and 46 ± 3 mmHg). After delivery, the baroreflex curves reset toward higher pressure in ADX + F but not ADX lambs. These results suggest that adrenal glucocorticoids contribute to cardiovascular regulation in the late-gestation fetus and newborn by modulating arterial baroreflex function and sympathetic activity.

Parasympathetic impairment of baroreflex control of heart rate in Dahl S rats

1990 ◽  
Vol 259 (1) ◽  
pp. R76-R83 ◽  
Author(s):  
S. A. Whitescarver ◽  
C. E. Ott ◽  
T. A. Kotchen
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Sodium Nitroprusside ◽  
Baroreflex Sensitivity ◽  
Parasympathetic Nervous System ◽  
Baroreflex Control ◽  
High Salt Diet ◽  
Salt Diet ◽  
Reflex Bradycardia ◽  
Before And After

To test the hypothesis that impaired baroreflex control of heart rate in Dahl salt-sensitive (S) rats is due to an impairment of the parasympathetic limb of the bradycardic response, baroreflex sensitivity was evaluated in conscious, chronically instrumented Dahl S and salt-resistant (R) animals. Sensitivity was impaired in Dahl S rats when bolus doses of phenylephrine were administered (0.863 +/- 0.042 vs. 1.43 +/- 0.055 ms/mmHg), but it was not different than in R rats when tested with sodium nitroprusside. When the sensitivities before and after blocking the parasympathetic nervous system with atropine were compared, it was revealed that 82% of the reflex bradycardia resulting from bolus doses of phenylephrine was due to the parasympathetic nervous system, whereas the majority (73%) of the bradycardia induced by 5-min infusions of phenylephrine was due to withdrawal of sympathetic tone. Neither baroreflex sensitivity to infusions of phenylephrine (73% sympathetic) or to infusions after atropine (100% sympathetic) were significantly different between S and R rats. Therefore, the impairment of the heart rate reflex in Dahl S rats is due to an impairment of the parasympathetic limb of the response. In addition, a high-salt diet before the development of hypertension did not alter baroreflex sensitivity in either Dahl S or R rats.

Role of endogenous ANG II and AT1 receptors in regulating arterial baroreflex responses in newborn lambs

1997 ◽  
Vol 272 (6) ◽  
pp. R1862-R1873 ◽  
Author(s):  
J. L. Segar ◽  
A. Minnick ◽  
A. M. Nuyt ◽  
J. E. Robillard
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Ang Ii ◽  
Central Administration ◽  
Arterial Baroreflex ◽  
Response Curves ◽  
Baroreflex Control ◽  
At1 Receptors ◽  
Arterial Blood ◽  
Baroreflex Function

The present study was designed to test the hypothesis that endogenous angiotensin II (ANG II) influences baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) early in life and to determine whether these actions are mediated by angiotensin AT1 or AT2 receptors. To test this hypothesis, we studied the effects of systemic and central administration of losartan, a selective AT1 receptor antagonist, and PD-123319, a selective AT2 antagonist, on baroreflex-mediated control of HR and RSNA in conscious newborn lambs. Systemic administration of losartan decreased resting mean arterial blood pressure (MABP) from 70 +/- 3 to 58 +/- 4 mmHg (P < 0.05) without producing reflex increases in HR or RSNA. The baroreflex response curves were shifted to the left as indicated by a decrease in the arterial pressure at the midpoint of the curve for HR (83 +/- 3 to 75 +/- 4 mmHg) and RSNA (74 +/- 2 to 69 +/- 3 mmHg; P < 0.05 for both). Losartan also reset HR and RSNA baroreflex curves when changes in baseline blood pressure were prevented by simultaneous infusion of phenylephrine. In contrast, a sustained decrease in arterial pressure of 10-12 mmHg with nitroprusside failed to shift the baroreflex function curves. PD-123319 had no effect on baseline HR, MABP, RSNA, or baroreflex responses. Lateral ventricle administration of losartan but not PD-123319 also produced a decrease in arterial pressure (81 +/- 4 to 73 +/- 3 mmHg, P < 0.05) and reset the baroreflex for HR and RSNA toward lower pressure. These results demonstrate that, early in life, endogenous ANG II exerts a tonic effect on baroreflex control of HR and RSNA to shift the curves toward higher pressure levels. The alterations in arterial baroreflex function appear independent of direct ANG II effects on arterial pressure and are mediated by AT1 receptors.

scholarly journals Severe haemophilia A in a preterm girl with Turner syndrome: case report – a diagnostic and therapeutic challenge for a paediatrician (Part 2)

2021 ◽  
Vol 47 (1) ◽  
Author(s):  
Berendt Agnieszka ◽  
Wójtowicz-Marzec Monika ◽  
Wysokińska Barbara ◽  
Kwaśniewska Anna
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Family History ◽  
Factor Viii ◽  
Turner Syndrome ◽  
Factor Viii Inhibitor ◽  
Haemophilia A ◽  
Severe Haemophilia ◽  
Prolonged Bleeding ◽  
Increased Risk

Abstract Background Haemophilia A is an X-linked genetic condition which manifests itself mainly in male children in the first 2 years of life, during gross motor skill development. This disorder is rare in females. The clinical manifestation of severe haemophilia in preterm infants poses a great challenge to the therapeutic team. As extreme prematurity is linked to an increased risk of central nervous system or gastrointestinal bleeding, a well-informed and balanced treatment from the first days of life is crucial to prevent long-term damage. Haemophilia is most commonly caused by inheriting defective genes, and can also be linked to skewed X inactivation and Turner syndrome. The coincidental occurrence of haemophilia A and Turner syndrome is extremely rare, with only isolated cases described to date. Hence, a multidisciplinary approach is needed. Case presentation The authors report on a preterm girl (gestational age 28 weeks) diagnosed with haemophilia and Turner syndrome. The first manifestation of haemophilia was prolonged bleeding from injection sites on the second day of life. Indeterminate aPTT and factor VIII level < 1% confirmed the diagnosis of haemophilia A. Dysmorphic features which did not match the typical clinical picture of haemophilia, the female sex, and a negative paternal family history led to the diagnosis of Turner syndrome. While in hospital, the girl received multiple doses of recombinant factor VIII in response to prolonged bleedings from the injection sites and from a nodule on the girl’s head, and before and after retinal laser photocoagulation. No central nervous system or abdominal cavity bleeding was observed. The substitutive therapy was complicated by the development of factor VIII inhibitor (anti-factor VIII (FVIII) antibodies). Treatment was continued with recombinant factor VIIa. This article aims at demonstrating the complexity of the diagnostics and treatment of a preterm child with two genetic disorders. Conclusions Haemophilia should always be considered in the differential diagnosis of prolonged bleeding, even in patients with a negative family history. In the case of coinciding atypical phenotypic features, further diagnostics for another genetic disease are recommended. Infant care should follow current care standards, while considering certain individual features.

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