Effects of calcium channel blockers on isolated carotid baroreceptors and baroreflex

1983 ◽  
Vol 245 (4) ◽  
pp. H653-H661 ◽  
Author(s):  
C. M. Heesch ◽  
B. M. Miller ◽  
M. D. Thames ◽  
F. M. Abboud
Keyword(s):  
Carotid Sinus ◽  
Physiological Solution ◽  
Physiological Salt Solution ◽  
Channel Blockers ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Carotid Baroreceptors ◽  
Carotid Baroreflex ◽  
Bilateral Carotid

Our study determined the effects of the calcium antagonists, nifedipine and verapamil, on the carotid sinus baroreceptors and baroreflex. The left carotid sinus region in dogs was vascularly isolated and filled with oxygenated physiological salt solution. Steady-state multiunit activity was recorded from the carotid sinus nerve for sinus pressures of 50-200 mmHg after bathing the carotid sinus region in a solution containing no drug, 10 micrograms/ml nifedipine (n = 6), or 5 micrograms/ml verapamil (n = 5). The slopes of the curves relating carotid sinus nerve activity (% of maximum control) to carotid sinus pressure were control, 0.81 +/- 0.06; nifedipine, 1.29 +/- 0.14; and verapamil, 0.48 +/- 0.06%/mmHg, indicating that nifedipine increased and verapamil decreased the sensitivity of the carotid sinus baroreceptors. Additional studies with bilateral carotid sinus isolation (carotid sinus nerves intact) indicated that nifedipine enhanced and verapamil attenuated carotid baroreflex control of renal sympathetic nerve activity. Pressure-volume curves generated in the isolated carotid sinus showed that effects on smooth muscle do not account for the opposing effects of the two Ca2+ antagonists. Omitting Ca2+ from the physiological solution resulted in increased carotid sinus nerve activity, an effect blocked by verapamil but not nifedipine. Verapamil, but not nifedipine, inhibited veratrine-induced (Na+-dependent) excitation of carotid baroreceptors. Thus the excitatory effects of nifedipine on the carotid sinus baroreceptors are dependent on Ca2+ mechanisms, whereas the inhibitory effects of verapamil may be due mainly to interference with the inward Na+ current.

Time-dependent phrenic nerve responses to carotid afferent activation: intact vs. decerebellate rats

1993 ◽  
Vol 265 (4) ◽  
pp. R811-R819 ◽  
Author(s):  
F. Hayashi ◽  
S. K. Coles ◽  
K. B. Bach ◽  
G. S. Mitchell ◽  
D. R. McCrimmon
Keyword(s):  
Phrenic Nerve ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Short Term ◽  
Nerve Activity ◽  
A Value ◽  
Afferent Activation ◽  
Term Potentiation ◽  
Long Term Facilitation

The objectives were to determine 1) respiratory responses to carotid chemoreceptor inputs in anesthetized rats and 2) whether the cerebellar vermis plays a role in these responses. A carotid sinus nerve was stimulated (20 Hz) with five 2-min trains, each separated by approximately 3 min. During stimulation, respiratory frequency (f), peak amplitude of integrated phrenic nerve activity (integral of Phr), and their product (f x integral of Phr) immediately increased. As stimulation continued, integral of Phr progressively increased to a plateau [short-term potentiation (STP)], but f and f x integral of Phr decreased [short-term depression (STD)] to a value still above control. Upon stimulus termination, integral of Phr progressively decreased but remained above control; f and f x integral of Phr transiently decreased below baseline. After the final stimulation, integral of Phr remained above control for at least 30 min [long-term facilitation (LTF)]. Repeated 5-min episodes of isocapnic hypoxia also elicited STP, STD, and LTF. Vermalectomy lowered the CO2-apneic threshold and eliminated LTF. In conclusion, carotid chemoreceptor activation in rats elicits STP and LTF similar to that in cats; the vermis may play a role in LTF. A new response, STD, was observed.

Central and peripheral chemoreceptor inputs to phrenic and hypoglossal motoneurons

1982 ◽  
Vol 53 (6) ◽  
pp. 1504-1511 ◽  
Author(s):  
E. N. Bruce ◽  
J. Mitra ◽  
N. S. Cherniack
Keyword(s):  
Opposite Effect ◽  
Carotid Sinus ◽  
Ventral Surface ◽  
Carotid Sinus Nerve ◽  
Peripheral Chemoreceptor ◽  
Hypoglossal Motoneurons ◽  
Nerve Response ◽  
Bilateral Carotid ◽  
Hypoglossal Motoneuron ◽  
Before And After

We tested the hypothesis that phrenic and hypoglossal responses to progressive hypercapnia differ qualitatively because the CO2-related drive inputs to their respective motoneuron pools are different. The relative contributions of carotid sinus and central chemoreceptor inputs to hypoglossal and phrenic responses during hyperoxic hypercapnia were determined by comparing the two nerve activities during rebreathing runs done either before and after bilateral carotid sinus nerve (CSN) section, or without and with cooling of the intermediate, I(s), area on the ventral surface of the medulla. The studies were performed on chloralose-anesthetized, vagotomized, paralyzed cats. Cooling of the I(s) area impaired phrenic responsiveness to hypercapnia more than hypoglossal responsiveness, whereas CSN section had the opposite effect. Thus phrenic nerve response was more dependent on central chemoreceptor input than was the hypoglossal response, but hypoglossal response was more dependent on carotid sinus chemoreceptor input. We conclude that the phrenic and hypoglossal motoneuron pools each receive a different functional input from both the medullary and the carotid sinus chemoreceptors.

Respiratory responses to aortic and carotid chemoreceptor activation in the dog

1991 ◽  
Vol 70 (6) ◽  
pp. 2539-2550 ◽  
Author(s):  
F. A. Hopp ◽  
J. L. Seagard ◽  
J. Bajic ◽  
E. J. Zuperku
Keyword(s):  
Electrical Stimulation ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Chemical Stimulation ◽  
Respiratory Drive ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Respiratory Reflexes ◽  
Respiratory Responses ◽  
Stimulation Of

Respiratory responses arising from both chemical stimulation of vascularly isolated aortic body (AB) and carotid body (CB) chemoreceptors and electrical stimulation of aortic nerve (AN) and carotid sinus nerve (CSN) afferents were compared in the anesthetized dog. Respiratory reflexes were measured as changes in inspiratory duration (TI), expiratory duration (TE), and peak averaged phrenic nerve activity (PPNG). Tonic AN and AB stimulations shortened TI and TE with no change in PPNG, while tonic CSN and CB stimulations shortened TE, increased PPNG, and transiently lengthened TI. Phasic AB and AN stimulations throughout inspiration shortened TI with no changes in PPNG or the following TE; however, similar phasic stimulations of the CB and CSN increased both TI and PPNG and decreased the following TE. Phasic AN stimulation during expiration decreased TE and the following TI with no change in PPNG. Similar stimulations of the CB and CSN decreased TE; however, the following TI and PPNG were increased. These findings differ from those found in the cat and suggest that aortic chemoreceptors affect mainly phase timing, while carotid chemoreceptors affect both timing and respiratory drive.

Occlusive summation of carotid and aortic baroreflexes in control of renal nerve activity

1984 ◽  
Vol 246 (6) ◽  
pp. H851-H857 ◽  
Author(s):  
M. D. Thames ◽  
B. J. Ballon
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Baroreflex Control ◽  
Full Control ◽  
Carotid Baroreflex ◽  
Renal Nerve Activity ◽  
Vascular Beds ◽  
Alpha Chloralose

We recently reported that denervation of aortic or carotid baroreceptors impaired baroreflex control of heart rate but not of hindlimb vascular resistance or lumbar sympathetic nerve activity. Since baroreflex control of sympathetic outflow to different vascular beds is nonuniform, we determined whether carotid or aortic baroreceptor denervation would impair baroreflex control of renal nerve activity. Experiments were performed in 23 alpha-chloralose-anesthetized rabbits. Phenylephrine and nitroglycerin were infused to raise or lower arterial pressure. Pressure elevation inhibited and pressure reduction increased renal nerve activity. The linear regression relationships between changes in arterial pressure and percent change in renal nerve activity were determined with baroreflexes intact and after aortic or carotid denervation. Neither carotid nor aortic denervation alone impaired baroreflex control of renal nerve activity. In nine experiments responses were determined first with vagi sectioned. The results were comparable to those obtained without prior vagotomy. Our data indicate that one group of baroreceptors (aortic or carotid) exerts full control of renal nerve activity and that aortic and carotid baroreflex influences on renal nerve activity add by occlusive or mutual inhibitory summation.

Vagal inhibition of respiratory-linked efferent activity in the carotid sinus nerve

1984 ◽  
Vol 247 (4) ◽  
pp. R681-R686
Author(s):  
D. R. Kostreva ◽  
G. L. Palotas ◽  
J. P. Kampine
Keyword(s):  
Carotid Body ◽  
Carotid Sinus ◽  
Respiratory Rhythm ◽  
Systemic Blood Pressure ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Efferent Activity ◽  
Central Origin ◽  
Spontaneously Breathing

The hypothesis tested in this study was that glossopharyngeal efferent nerve activity coursing through the carotid sinus nerve has a central origin. Efferent activity in the carotid sinus nerve exhibited a respiratory rhythm in spontaneously breathing, closed-chest, mongrel dogs anesthetized with pentobarbital sodium (30 mg/kg iv). Carotid sinus nerve activity was recorded from the intact or cut central end of the carotid sinus nerve. Diaphragm electromyogram (D-EMG), carotid sinus pressure, systemic blood pressure, and electrocardiogram were also recorded. Before vagotomy, small increases in carotid sinus efferent nerve activity (CSENA) synchronous with increases in the D-EMG were observed during spontaneous inspiration. Section of the contralateral cervical vagosympathetic trunk markedly potentiated the increases in CSENA. Bilateral superior cervical ganglionectomy or nodose ganglionectomy failed to alter the increases in CSENA. Section of the ipsilateral glossopharyngeal nerve near the skull abolished the CSENA. This study demonstrates that respiratory-modulated glossopharyngeal efferents course through the carotid sinus nerve to the carotid sinus or carotid body. These efferents may be part of a central respiratory regulatory mechanism that may rapidly alter the sensitivity of the carotid sinus baroreceptors and/or carotid body receptors on a breath-to-breath basis.

Dynamics of sympathetic baroreflex control of arterial pressure in rats

2003 ◽  
Vol 285 (1) ◽  
pp. R262-R270 ◽  
Author(s):  
Takayuki Sato ◽  
Toru Kawada ◽  
Masashi Inagaki ◽  
Toshiaki Shishido ◽  
Masaru Sugimachi ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Transfer Functions ◽  
Carotid Sinus ◽  
Quantitative Estimation ◽  
Systemic Arterial Pressure ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Low Pass ◽  
Compensatory Effect

By a white noise approach, we characterized the dynamics of the sympathetic baroreflex system in 11 halothane-anesthetized rats. We measured sympathetic nerve activity (SNA) and systemic arterial pressure (SAP), while carotid sinus baroreceptor pressure (BRP) was altered randomly. We estimated the transfer functions from BRP to SNA (mechanoneural arc), from SNA to SAP (neuromechanical arc), and from BRP to SAP (total arc). The gain of the mechanoneural arc gradually increased about threefold as the frequency of BRP change increased from 0.01 to 0.8 Hz. In contrast, the gain of the neuromechanical arc rapidly decreased to 0.4% of the steady-state gain as the frequency increased from 0.01 to 1 Hz. Although the total arc also had low-pass characteristics, the rate of attenuation in its gain was significantly slower than that of the neuromechanical arc, reflecting the compensatory effect of the mechanoneural arc for the sluggish response of the neuromechanical arc. We conclude that the quantitative estimation of the baroreflex dynamics is vital for an integrative understanding of baroreflex function in rats.

Abstract 032: Carotid Chemoreceptor Activation Blunts The Hypotensive Response Caused By The Electrical Stimulation Of The Carotid Sinus In Conscious Rats

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Pedro L Katayama ◽  
Jaci A Castania ◽  
Rubens Fazan ◽  
Helio C Salgado
Keyword(s):  
Electrical Stimulation ◽  
Resistant Hypertension ◽  
Carotid Sinus ◽  
Hemodynamic Responses ◽  
Carotid Chemoreceptors ◽  
Conscious Rats ◽  
Carotid Baroreceptors ◽  
Bilateral Carotid ◽  
Hypotensive Response ◽  
Stimulation Of

The mechanisms involved in Baroreflex Activation Therapy (BAT) in patients with resistant hypertension require better understanding. It was shown that electrical stimulation of the carotid sinus (ESCS), in conscious carotid body-denervated rats, caused bradycardia and greater hypotensive response when compared with intact control rats. In the current study the activation of the chemoreceptors due to ESCS, in conscious rats, was examined in the absence of the carotid baroreceptors. Wistar rats with unilateral denervation of the right carotid chemoreceptors were divided into three groups: 1) control (CONT, n=7); 2) bilateral carotid chemoreceptor denervation (CD, n=7); 3) unilateral denervation of the left carotid baroreceptors (BD, n=4). Under ketamine/xylazine anesthesia bipolar electrodes were implanted around the left carotid sinus combined with arterial and venous catheters into the femoral vessels. On the next day, after basal hemodynamic recordings, the animals received three ESCS (5V, 1 ms) with 15 Hz, 30 Hz and 60 Hz, applied randomly for 20s. Carotid chemoreceptors denervation was confirmed by the lack of hemodynamic responses after the administration of KCN (40 μg iv). The efficacy of left carotid baroreceptor denervation was confirmed by the absence of hemodynamic responses to changes in the left carotid sinus pressure ranging from 60 mmHg to 180 mmHg. The results showed that ESCS was efficient to cause greater hypotensive responses in the CD as compared with the CONT group at 60 Hz (-37 ± 6 vs -19 ± 3 mmHg) and to cause hypertensive responses in the BD group at 30 Hz and 60 Hz (15 ± 2 and 19 ± 2 mmHg). ESCS caused no alteration of the heart rate in the CONT but caused significant bradycardia in the CD group at 30 Hz and 60 Hz (-31 ± 11 and -35 ± 12 bpm) and in the BD group at 15 Hz, 30 Hz and 60 Hz (-38 ± 6, -37 ± 6 and -34 ± 4 bpm). These data demonstrated that carotid chemoreceptor activation in the absence of the carotid baroreceptors caused hypertension and bradycardia, indicating that when the baroreceptors are intact, the chemoreceptors blunt the hypotensive response caused by ESCS. These findings provide important information for the clinical studies using BAT in patients with resistant hypertension and/or heart failure.

Pulsatile activation of baroreceptors causes central facilitation of baroreflex

1989 ◽  
Vol 256 (6) ◽  
pp. H1735-H1741 ◽  
Author(s):  
M. W. Chapleau ◽  
G. Hajduczok ◽  
F. M. Abboud
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Static Pressure ◽  
Carotid Sinus ◽  
Pulse Frequency ◽  
The Other ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Pulsatile Pressure ◽  
Sinus Pressure

The reflex decrease in arterial pressure is greater and more sustained with elevated pulsatile than with elevated static carotid sinus pressure. The purpose of this study was to relate afferent baroreceptor activity (BRA) and efferent sympathetic nerve activity (SNA) during static and pulsatile pressure to evaluate the influence of pulsatile pressure on the central mediation of the baroreflex. The carotid sinuses were isolated in 11 dogs anesthetized with chloralose. Both vagosympathetic trunks were cut and both carotid sinuses exposed to static and pulsatile pressures over a range of mean carotid sinus pressures (40-180 mmHg). BRA was recorded from one carotid sinus nerve, and the other intact carotid sinus served to initiate reflex changes in lumbar or renal SNA and arterial pressure. For the same mean carotid sinus pressure, pulsatile pressure caused significantly greater inhibition of SNA than static pressure. More importantly, for the same or lesser levels of baroreceptor activity per second, pulsatile pressure caused significantly greater inhibition of SNA than static pressure. The inhibition of SNA was not sustained (i.e., there was "adaptation") with continuous baroreceptor input during static pressure, whereas the inhibition of SNA was sustained (i.e., there was no significant adaptation) with the phasic input during pulsatile pressure. Increases in pulse frequency from 1.4 to 2.5 and 3.7 Hz caused progressively less inhibition of SNA.(ABSTRACT TRUNCATED AT 250 WORDS)

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