Disease relevance of Baroreflex

• Additional studies indicate that the hypertension associated with Ang II involves a resetting of the arterial baroreflex to a higher pressure [1].
• With hypoxia during baroreflex activation with PE, SNA did not increase (50 +/- 23 U/min) [2].
• CONCLUSIONS: These data indicate that increased brain ouabain plays a major role in the impairment of baroreflexes in rats with CHF after myocardial infarction [3].
• To investigate this hypothesis, parasympathetic function was assessed by arterial baroreflex sensitivity (BRS) testing (using the phenylephrine method) and by heart rate variability (HRV) analysis from 24-hour Holter recording in 68 patients at day 7-10 after infarction [4].
• Low dose of nitroglycerin failed to improve splanchnic hemodynamics in patients with cirrhosis: evidence for an impaired cardiopulmonary baroreflex function [5].

Psychiatry related information on Baroreflex

• Blood pressure (recorded continuously using the Finapres), heart rate, cardiac baroreflex sensitivity, salivary cortisol, skin conductance and breathing pattern were monitored at rest, during task performance and at recovery following tasks [6].
• Thus, individual differences in baroreflex sensitivity may explain the hemodynamic variability observed in response to cocaine [7].

High impact information on Baroreflex

• Clonidine attenuates the pressor and tachycardic surges in baroreflex failure [8].
• In several functional entities of the brain, such as the preoptic region, the hypothalamus, the olivocerebellary system, and the brainstem baroreflex arc, the colocalization of receptor mRNA, binding sites, and angiotensin immunoreactive nerve terminals suggests local synthesis and expression of angiotensin II receptors [9].
• In SHR-S, brain ANP acts at the levels of the NTS and the AHA to perturb this baroreflex regulatory pathway [10].
• Baroreflex responses were evaluated from changes in HR, BP, and MSNA that were obtained after infusions of phenylephrine and sodium nitroprusside [11].
• SYN patients also had attenuation of norepinephrine increases and lower baroreflex slope sensitivity, both during tilt and after pharmacologic testing [11].

Chemical compound and disease context of Baroreflex

• Patients with chronic renal failure develop an autonomic dysfunction with impaired baroreflex control and attenuated cardiovascular beta-adrenoceptor response to noradrenaline [12].
• These results are consistent with an abnormality in baroreflex suppression of arginine vasopressin secretion in chronic congestive heart failure and suggest that such a defect may contribute to long-term high levels of arginine vasopressin in this condition [13].
• Twenty-five patients after uncomplicated myocardial infarction underwent baroreflex sensitivity evaluation 72 to 96 h after symptom onset and after 4 days of captopril therapy [14].
• Improvement in baroreflex function by an oral angiotensin receptor antagonist in rats with myocardial infarction [15].
• These data indicate that blockade of brain "oubain" prevents sodium-induced hypertension as well as the desensitization of the arterial baroreflex in Dahl S rats [16].

Biological context of Baroreflex

• Ang II did not alter the upper plateau of the baroreflex, but decreased the lower plateau from 119.4 +/- 10.3 to 73.6 +/- 11.5 beats per minute (bpm) (P < 0.05), extending the heart rate range by 52.5 bpm [17].
• After baroreflex blockade with atropine, PE increased blood pressure but did not change heart rate [18].
• Previous studies in our laboratory demonstrate that nifedipine potentiates baroreflex control of heart rate and vascular resistance in normal human subjects [19].
• Thus, nifedipine increased the cardiopulmonary baroreflex sympathetic sensitivity (change in total MSNA per mm Hg decrease in central venous pressure during LBNP-10) from 26.5 +/- 10.7 units/mm Hg to 74.9 +/- 19.0 units/mm Hg (p less than 0.01) [19].
• Nonspecific baroreflex loading maneuvers such as head-down tilt readily suppress stimulated arginine vasopressin levels in normal humans [13].

Anatomical context of Baroreflex

• Our study was designed to determine whether the calcium channel antagonists verapamil, diltiazem, and nifedipine and the nitrate vasodilator sodium nitroprusside modulate carotid sinus (CS) baroreflex control of mean arterial pressure (MAP) and heart rate (HR) [20].
• Interactions of vasopressin with the area postrema in arterial baroreflex function in conscious rabbits [21].
• Therefore, experiments were performed to determine the effects of left circumflex coronary artery infusion of PGI2 on the baroreflex control of heart rate in conscious instrumented dogs [22].
• It seems that by day 14 to 15, the central effect of ouabain on baroreflex control prevails over its peripheral sensitizing effect on baroreceptors, leading to a tendency of desensitization [23].
• Modulatory effects of carbon monoxide on baroreflex activation in nucleus tractus solitarii of rats [24].

Associations of Baroreflex with chemical compounds

• Baroreflex control of plasma norepinephrine and heart period in healthy subjects and diabetic patients [25].
• Vasopressin reduces cardiac function and augments cardiopulmonary baroreflex resistance increases in man [26].
• Pretreatment with losartan completely abolished the pressor and cardiac baroreflex responses to Ang II [17].
• Baroreflex gain was comparable before and after cocaine [27].
• During PE alone, the baroreflex slope was 20.2 +/- 2.9 ms/mmHg (n = 10) [28].

Gene context of Baroreflex

• These observations suggest an important role for ERalpha subtype in the central modulation of baroreflex responses [29].
• Baseline cardiovascular parameters, systolic and diastolic function at different preloads, and baroreflex sensitivity were similar in FAAH-/- and FAAH+/+ mice [30].
• We conclude from these experiments that AVP and oxytocin both augment baroreflex sensitivity, although the receptor type(s) responsible are not clear [31].
• Baroreflex sensitivity and variants of the renin angiotensin system genes [32].
• We tested the hypothesis that variants in the gene (KCNMB1) coding for the BK beta1 subunit are associated with baroreflex function [33].

Analytical, diagnostic and therapeutic context of Baroreflex

• Our purpose was to evaluate the correlation and agreement between the baroreflex sensitivity obtained with phenylephrine and that obtained by two noninvasive methods: the alpha-index and sequence analysis [34].
• To further test this concept in humans, we measured sympathetic nerve discharge with intraneural microelectrodes while we used static handgrip to activate the exercise pressor reflex and nonhypotensive lower-body negative pressure (LBNP) to selectively unload the cardiac baroreflex [35].
• The gain of arterial baroreflex control of RSNA assessed by the slope of the regression line relating changes in AP and those in RSNA caused by intravenous phenylephrine or nitroglycerin did not differ before and after microinjections of L-NMMA [36].
• Open-loop performance of the CS baroreflex was determined under control conditions and after intravenous infusion of each agent for 20 minutes at four rates (nitroprusside: 0.3-10 micrograms/kg/min; verapamil and diltiazem: 1-30 micrograms/kg/min; nifedipine: 0.1-3 micrograms/kg/min) [20].
• The objectives of this study were to examine the effect of incremental lower body negative pressure (LBNP) on cardiac chamber volume and assess the relationship between cardiac chamber volume and baroreflex activation of the neurohormonal axis [37].

References