Disease relevance of Carotid Sinus

• Alpha-methyldopa and carotid-sinus hypersensitivity [1].
• After interruption of the reflex are with the alpha-adrenergic receptor antagonist, dibozane, carotid sinus hypotension and the same increase in aortic pressure (15 mm Hg) resulted in only a 5% increase in diastolic coronary resistance [2].
• A reduced baroreflex responsiveness was demonstrated in hypertensive patients as compared with normal subjects by evaluating both the reflex bradycardia evoked by intravenous administration of phenylephrine and the reflex increase in blood pressure during carotid sinus hypotension [3].
• Baroreflex sensitivity measured by the phenylephrine pressor test in patients with carotid sinus and sick sinus syndromes [4].
• The respiratory depression seen in moderate hypoxia (partial pressure of inspired O2, PI,O2, 80-100 mmHg) 3 days after bilateral carotid sinus nerve section disappeared by day 10 [5].

High impact information on Carotid Sinus

• Alpha-methyldopa and carotid-sinus hypersensitivity [6].
• Neither indomethacin nor prostacyclin (n = 5) influenced the pressure-diameter relation of the carotid sinus [7].
• Baroreceptor activity was recorded from the vascularly isolated carotid sinus during slow ramp increases in pressure in rabbits anesthetized with pentothal and chloralose [7].
• Timolol, carotid sinus hypersensitivity, and elderly patients [8].
• METHODS AND RESULTS: Renal function studies were performed in seated healthy volunteers (n = 12; age range, 20 to 34 years) during sustained neck suction at -60 mm Hg, aiming to selectively activate the carotid sinus arterial baroreceptors [9].

Chemical compound and disease context of Carotid Sinus

• Digoxin and ASI-222 were infused i.v. at rates which produced cardiac arrhythmias in about 100 min in dogs either: 1) with intact nerves, 2) pretreated with atropine, 3) without reflex receptors (without vagus and carotid sinus nerves, 4) without cardiac sympathetic nerves and adrenals or 5) pretreated with metoprolol [10].
• The present experiments were designed to measure and characterize direct hemodynamic effects of propranolol on vascularly isolated carotid sinuses. dl-Propranolol, when restricted to the isolated carotid sinuses, inhibited in a dose-dependent manner the reflex increases in heart rate and mean arterial pressure during carotid sinus hypotension [11].
• Substance P immunoreactivity in type I cells was dramatically attenuated by hypoxia in both intact and chronic carotid sinus nerve-denervated preparations, but this effect was reduced following chronic sympathectomy [12].
• Denervation and retrograde tracing experiments have revealed that these fibers arise from NOS-immunoreactive and nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase-positive neuronal cell bodies located in the petrosal ganglion and the carotid body, and dispersed along the glossopharyngeal and carotid sinus nerves (CSN) [13].
• Studies on the site of action revealed that nimodipine (0.3 and 1.0 micrograms/kg/min i.v. at 20 min) attenuated the reflex vagal bradycardia evoked by pressure elevations in the isolated carotid sinus, but did not change the reflex responses elicited by electrical stimulation of afferent fibers in the carotid sinus nerve [14].

Biological context of Carotid Sinus

• Arterial baroreceptors in the carotid sinus (CBR) and aortic arch (ABR) regions exert important control over heart rate and peripheral vascular responses to changes in arterial pressure [15].
• This study examined the role of arginine vasopressin in the pressor response to vagal cold block and evaluated a possible interaction between vasopressin and the sympathetic nervous system during vagal block in conscious dogs with (carotid sinus intact) and without (sinoaortic denervated) functional arterial baroreflexes [16].
• Interaction of carotid sinus and aortic arch reflex control of total peripheral resistance was studied in eight dogs anesthetized with sodium pentobarbital and placed on constant flow cardiac bypass [17].
• To quantify the importance of the carotid sinus baroreceptor reflex and the interaction with epinephrine infusion on total pulmonary vascular capacity and resistance, I have simultaneously measured total pulmonary vascular compliance, changes in pulmonary blood volumes, and changes in resistances in seven sodium pentobarbital-anesthetized dogs [18].
• This pacemaker was slowed by maneuvers that enhanced vagal tone, including carotid sinus massage, the postrelease phase of the Valsalva maneuver and phenylephrine [19].

Anatomical context of Carotid Sinus

• Activity was recorded from physiologically identified baroreceptor or chemoreceptor fibers in carotid sinus nerves of urethane-anesthetized spontaneously breathing rabbits [20].
• Combined lesions of the contralateral NTS and C1 area ipsilateral to the stimulated vagus nerve maintained AP and HR at normal levels, and totally blocked the VDR to vagal stimulation and carotid sinus stretch [21].
• Carotid baroreceptor function, the compliance of the carotid sinus wall, and the structure of the carotid artery were examined in dogs with elevated plasma norepinephrine (2,000-4,000 pg/ml) for 28 days [22].
• Bilateral lesions of the C1 area decreased arterial pressure (AP) and heart rate (HR) to spinal cord transection levels and blocked the VDR induced by vagal stimulation and carotid sinus stretch [21].
• Baroreceptor activity was recorded from single fibers innervating the isolated carotid sinus of dogs anesthetized with chloralose after removal of the endothelium (balloon denudation) and after replacing into the denuded sinus bovine aortic endothelial cells cultured on microcarrier beads [23].

Associations of Carotid Sinus with chemical compounds

• Junctional diastolic slopes were recorded in 11 of 15 patients (73.3%) with junctional rhythm that occurred spontaneously, after intravenous administration of atropine (1 mg), or during carotid sinus massage [24].
• This dose of ouabain had no effect on pressure-discharge relations or carotid sinus diameters in normal dogs.(ABSTRACT TRUNCATED AT 250 WORDS)[25]
• NP was applied during sustained PE infusion to eliminate the increase in transmural carotid sinus pressure and thus remove CBR activation, thereby causing ABR stimulation alone [15].
• Static and pulsatile pressure were applied to the isolated carotid sinus of dogs anesthetized with chloralose [26].
• Baroreceptor activity was recorded from the vascularly isolated carotid sinus of rabbits anesthetized with sodium pentobarbital [27].

Gene context of Carotid Sinus

• Moreover, initial data obtained using antisense oligonucleotides to AT1 receptors suggest that, in the NTS, the effect of endogenous AngII on the baroreceptor reflex is mainly due to presynaptic actions on vagal or carotid sinus afferent fibres [28].
• The carotid sinus nerve and carotid body contained numerous calbindin D-28k-ir nerve fibers but few parvalbumin-ir nerve fibers [29].
• 2. A series of studies suggests a significant role for substance P in the acute cardiovascular and carotid sinus chemoreceptor facilitatory actions of AngII in the NTS [28].
• A selective 5-HT3 agonist, 2-methyl-5-HT, also produced a dose-dependent increase in the carotid sinus nerve activity [30].
• Neither methysergide (3 x 10(-7) mol/kg), which possesses both 5-HT1-like partial agonistic and 5-HT2 antagonistic actions, nor ketanserin (3 x 10(-7) mol/kg), a selective 5-HT2 antagonist, affected the 5-HT-induced increase in carotid sinus nerve activity [30].

Analytical, diagnostic and therapeutic context of Carotid Sinus

• In the heart-failure group, perfusion of the carotid sinus with ouabain (0.01 micrograms/ml) caused a significant decrease in threshold pressure and a significant increase in peak discharge frequency, as well as an increase in slope of the CSP-discharge curve [25].
• Surgical carotid sinus denervation or A-V sequential DDD pacing were ineffective in completely controlling symptoms [31].
• In this study, we investigated whether the C1 area of the RVL mediates the vasodepressor responses (VDR) induced by either electrical stimulation of the vagus nerve or carotid sinus stretch [21].
• Central and regional cardiovascular responses to step changes in carotid sinus pressure were evaluated in dogs before and after increasing carotid sinus reflex set point pressure, by approximately 30%, via an intravenous infusion of angiotensin II at three anesthetic levels (isoflurane) [32].
• Vagotomy or carotid sinus sectioning had no significant effect on anandamide- or capsaicin-induced responses [33].

References