Acute resetting of the carotid sinus baroreflex by aortic depressor nerve stimulation

1993 ◽  
Vol 264 (4) ◽  
pp. H1215-H1222 ◽  
Author(s):  
L. Hayward ◽  
M. Hay ◽  
R. B. Felder
Keyword(s):  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Renal Sympathetic Nerve Activity ◽  
Aortic Depressor Nerve ◽  
Central Neurons ◽  
Carotid Sinus Baroreflex ◽  
Before And After ◽  
The Right ◽  
Sinus Pressure ◽  
Renal Sympathetic

The effect of prolonged aortic depressor nerve (ADN) stimulation on carotid sinus baroreflex regulation of arterial pressure (AP) and renal sympathetic nerve activity (RSNA) was examined in anesthetized rabbits. Ramp increases in carotid sinus pressure (CSP) were repeated before and after 5 min of bilateral ADN stimulation. One minute after ADN stimulation the curve relating AP to CSP had shifted up and to the right, characterized by significant increases (P < 0.05) in the maximum (91 +/- 2 to 101 +/- 3 mmHg; mean +/- SE), midpoint (118 +/- 7 to 125 +/- 8 mmHg CSP), and minimum (45 +/- 3 to 53 +/- 4 mmHg) of the AP reflex curve. There was a parallel shift downward of the curve relating RSNA to CSP, characterized by significant decreases in the maximum [100 +/- 0 to 66 +/- 8% of maximum control RSNA value (%max)], the range (90 +/- 2 to 59 +/- 8%max), and the gain (-1.0 +/- 0.2 to -0.5 +/- 0.1%max/mmHg) of the RSNA reflex curve. Values returned to control within 10 min of cessation of ADN stimulation. These results suggest that central neurons processing baroreflex information from one set of mechanoreceptors can be reset by convergent signals arising from another baroreceptor site.

Bradykinin causes hypotension by activating pulmonary sympathetic afferents in the rabbit

2003 ◽  
Vol 95 (1) ◽  
pp. 233-240 ◽  
Author(s):  
Y. Wang ◽  
G. Soukhova ◽  
M. Proctor ◽  
J. Walker ◽  
J. Yu
Keyword(s):  
Sympathetic Nerve Activity ◽  
Lung Parenchyma ◽  
Systemic Circulation ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Before And After ◽  
Bilateral Vagotomy ◽  
The Right ◽  
Renal Sympathetic ◽  
Rule Out

Bradykinin (BK) activates sympathetic afferents in the heart, intestine, and kidney, and it alters hemodynamics. However, we know little about the influence of pulmonary sympathetic afferents on circulation. Activation of pulmonary afferents by directly injecting stimulants into the lung parenchyma permits examination of reflexes that originate in the lung without confounding effects from the systemic circulation. In the present study, we tested the hypothesis that pulmonary sympathetic afferents exert a significant influence on hemodynamics. We examined reflex effects of injecting BK (1 μg/kg in 0.1 ml) into the lung parenchyma on circulation in anesthetized, open-chest, artificially ventilated rabbits. BK significantly decreased mean arterial blood pressure (BP) (27 ± 3 mmHg) and heart rate (19 ± 4 beats/min). Both effects remained after bilateral vagotomy. To rule out possible direct systemic vasodilation by BK, we examined renal sympathetic nerve activity (RSNA) in response to BK injection and examined BP responses to injection of ACh (0.1 ml of 10-4 M). BK suppressed the RSNA before and after vagotomy. ACh did not change BP when injected into the lung parenchyma, but it decreased BP (31 ± 3 mmHg) when injected into the right atrium. Our data indicate that activating pulmonary sympathetic afferents reflexly suppresses hemodynamics.

Interaction of right and left carotid sinus baroreflexes in the dog

1986 ◽  
Vol 250 (1) ◽  
pp. H96-H107 ◽  
Author(s):  
A. S. Greene ◽  
M. J. Brunner ◽  
A. A. Shoukas
Keyword(s):  
Heart Rate ◽  
Tidal Volume ◽  
Carotid Sinus ◽  
The Other ◽  
Reflex Response ◽  
Pentobarbital Sodium ◽  
Simultaneous Excitation ◽  
Carotid Sinus Baroreflex ◽  
The Right ◽  
Sinus Pressure

Carotid sinus reflex interactions were studied in 10 dogs anesthetized with pentobarbital sodium. The right and left carotid sinus regions were isolated and perfused at controlled pressures. Pressure in the right and left carotid sinuses were independently varied, and the resulting steady-state reflex changes in arterial pressure, heart rate, respiratory frequency, tidal volume, and total ventilation were measured. Reflex changes when carotid sinus pressure was changed on one side were strongly influenced by pressure in the contralateral carotid sinus (P less than 0.05). Right carotid sinus gain was found to be 0.628 +/- 0.058 at a left carotid sinus pressure of 50 mmHg and 0.148 +/- 0.027 when left carotid sinus pressure was 200 mmHg. Similar results were found for left carotid sinus gain. Suppression was also found for heart rate, respiratory rate, tidal volume, and total ventilation. The hypothesis that rapid resetting of one carotid sinus baroreflex might influence responses from the other side was also tested. Although ipsilateral resetting was consistently observed, no contralateral component of the resetting was detected. An additional inhibitory summation between the right and left carotid sinuses was found such that simultaneous excitation of both receptors resulted in a smaller reflex response than did the sum of individual responses. Sympathetic denervation of the carotid sinus region had no effect.

Central sympathoinhibition and peripheral neuronal uptake blockade after desipramine in rabbits

1991 ◽  
Vol 260 (4) ◽  
pp. R824-R832 ◽  
Author(s):  
G. Eisenhofer ◽  
T. Saigusa ◽  
M. D. Esler ◽  
H. S. Cox ◽  
J. A. Angus ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Nerves ◽  
Neuronal Uptake ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Mediated Effects ◽  
Before And After ◽  
Peripheral Effect ◽  
Renal Sympathetic

Peripheral- and central nervous system (CNS)-mediated effects of desipramine (Des) on sympathetic nerves and the contribution of alpha 2-adrenoceptors to these effects were studied in conscious rabbits. Blood pressure, renal sympathetic nerve activity (SNA), and norepinephrine (NE) reuptake and spillover into plasma were measured before and after intracisternal (ic) or intravenous (i.v.) administration of Des. In other animals, NE spillover responses to i.v. Des were examined before and after alpha 2-adrenoceptor blockade with i.v. idazoxan. Treatment with i.v. Des blocked neuronal reuptake and decreased renal SNA but did not alter blood pressure or NE spillover. Decreased NE release by sympathetic nerves after i.v. Des was reflected by a decrease in the combined rate of NE reuptake and spillover. Treatment with ic Des (at 1.7% of the i.v. dose) decreased blood pressure and renal SNA and produced equivalent falls in NE reuptake and spillover, indicating little peripheral effect of centrally administered Des on the efficiency of neuronal reuptake. Thus Des had two distinct actions: the drug blocked neuronal reuptake by direct actions on nerve endings and reduced SNA by actions within the CNS. After ic Des, decreased SNA produced parallel falls in NE reuptake, spillover, and blood pressure. After i.v. Des, blockade of neurotransmitter reuptake increased NE concentrations at sympathoeffector junctions offsetting the fall in SNA, so that there was little change in NE spillover or blood pressure. However, after alpha 2-adrenoceptor blockade with i.v. idazoxan, NE spillover increased in response to i.v. Des. Thus the Des-induced decrease in NE release was partly mediated by an action of raised intrasynaptic NE concentrations on inhibitory alpha 2-adrenoceptors.

Baroreflex dysfunction in diabetes mellitus. II. Site of baroreflex impairment in diabetic rabbits

1994 ◽  
Vol 266 (1) ◽  
pp. H244-H249 ◽  
Author(s):  
T. S. McDowell ◽  
G. Hajduczok ◽  
F. M. Abboud ◽  
M. W. Chapleau
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Companion Paper ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Diabetic Rabbits ◽  
The Right ◽  
Alpha Chloralose ◽  
Induced Changes ◽  
Renal Sympathetic

In our companion paper [T. S. McDowell, M. W. Chapleau, G. Hajduczok, and F. M. Abboud, Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H235-H243, 1994] we report that baroreflex-mediated bradycardia is impaired in diabetic rabbits. The purpose of the present study was to identify the site of impairment. Diabetes was induced in rabbits by alloxan (90–100 mg/kg iv; n = 7). Alloxan-treated rabbits that remained normoglycemic (n = 8) and rabbits given saline instead of alloxan (n = 4) served as controls. Twenty-four weeks after administration of alloxan or saline, rabbits were anesthetized with alpha-chloralose. Aortic baroreceptor and renal sympathetic nerve activity (RSNA) were recorded during phenylephrine- and nitroglycerin-induced changes in arterial pressure. The slope of the baroreceptor pressure-activity relation was not significantly different in diabetic rabbits (1.3 +/- 0.3%/mmHg, n = 7) compared with either alloxan-treated (1.3 +/- 0.1%/mmHg) or saline-treated normoglycemic rabbits (1.2 +/- 0.2%/mmHg). The slope of the arterial pressure-RSNA relation was not significantly different in diabetic rabbits (-3.5 +/- 0.3%/mmHg, n = 7) compared with the alloxan-treated normoglycemic rabbits (-3.0 +/- 0.4%/mmHg, n = 8) and was greater than that in saline-treated normoglycemic rabbits (-1.9 +/- 0.3%/mmHg, n = 4; P < 0.05). The decreases in heart rate in response to electrical stimulation (10 V, 2 ms, 0.5–16 Hz) of the cut peripheral end of the right cervical vagus were similar in diabetic and alloxan-treated normoglycemic rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Baroreflex regulation of renal sympathetic nerve activity and heart rate in renal wrap hypertensive rats

2005 ◽  
Vol 288 (4) ◽  
pp. R856-R862 ◽  
Author(s):  
M. Vitela ◽  
M. Herrera-Rosales ◽  
J. R. Haywood ◽  
S. W. Mifflin
Keyword(s):  
Heart Rate ◽  
Sodium Nitroprusside ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sigmoid Function ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
The Right ◽  
Renal Sympathetic

Despite its usefulness as a nongenetic model of hypertension, little information is available regarding baroreflex function in the Grollman, renal wrap model of hypertension in the rat. Baroreflex regulation of renal sympathetic nerve activity (RSNA) and heart rate (HR) were studied in male, Sprague-Dawley rats hypertensive (HT) for 1 or 4–6 wk after unilateral nephrectomy and figure-8 ligature around the remaining kidney or normotensive (NT) after sham surgery. Rats were anesthetized with Inactin and RSNA, and HR was recorded during intravenous infusions of sodium nitroprusside or phenylephrine to lower or raise mean arterial pressure (MAP). Response curves were analyzed using a logistic sigmoid function. In 1- and 4-wk HT rats the midpoints of RSNA and HR reflex curves were shifted to the right ( P < 0.05). Comparing NT to 1- or 4-wk HT rats, the gain of RSNA-MAP curves was no different; however, gain was reduced in the HR-MAP curves at both 1 and 4 wk in HT rats ( P < 0.05). In anesthetized rats the HR range was small; therefore, MAP and HR were measured in conscious rats during intravenous injections of three doses of phenylephrine and three doses of sodium nitroprusside. Linear regressions revealed a reduced slope in both 1- and 4-wk HT rats compared with NT rats ( P < 0.05). The results indicate that baroreflex curves are shifted to the right, to higher pressures, in hypertension. After 1–4 wk of hypertension the gain of baroreflex regulation of RSNA is not altered; however, the gain of HR regulation is reduced.

scholarly journals Perfusion of Isolated Carotid Sinus With Hydrogen Sulfide Attenuated the Renal Sympathetic Nerve Activity in Anesthetized Male Rats

2016 ◽  
pp. 413-423 ◽  
Author(s):  
Q. GUO ◽  
Y. WU ◽  
H. XUE ◽  
L. XIAO ◽  
S. JIN ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Calcium Channels ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Male Rats ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

The purpose of the present study was to define the indirect central effect of hydrogen sulfide (H2S) on baroreflex control of sympathetic outflow. Perfusing the isolated carotid sinus with sodium hydrosulfide (NaHS), a H2S donor, the effect of H2S was measured by recording changes of renal sympathetic nerve activity (RSNA) in anesthetized male rats. Perfusion of isolated carotid sinus with NaHS (25, 50, 100 μmol/l) dose and time-dependently inhibited sympathetic outflow. Preconditioning of glibenclamide (20 µmol/l), a ATP-sensitive K+ channels (KATP) blocker, the above effect of NaHS was removed. With 1, 4-dihydro-2, 6-dimethyl-5-nitro-4-(2-[trifluoromethyl] phenyl) pyridine-3-carboxylic acid methyl ester (Bay K8644, 500 nmol/l) pretreatment, which is an agonist of L-calcium channels, the effect of NaHS was eliminated. Perfusion of cystathionine γ-lyase (CSE) inhibitor, DL-propargylglycine (PPG, 200 μmol/l), increased sympathetic outflow. The results show that exogenous H2S in the carotid sinus inhibits sympathetic outflow. The effect of H2S is attributed to opening KATP channels and closing the L-calcium channels.

Effect of sympathetic sensitization of baroreceptors on renal nerve activity

1987 ◽  
Vol 252 (2) ◽  
pp. R328-R335 ◽  
Author(s):  
J. L. Seagard ◽  
F. A. Hopp ◽  
J. P. Kampine
Keyword(s):  
Sympathetic Activity ◽  
Carotid Sinus ◽  
Baroreceptor Sensitivity ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Efferent Nerve ◽  
Before And After ◽  
Renal Nerve Activity ◽  
Sinus Pressure ◽  
Renal Sympathetic

The role of sympathetic efferent innervation of the carotid sinus on the regulation of baroreceptor sensitivity was examined in thiopental-sodium anesthetized dogs (5 mg X kg-1 X h-1 infusion). Baroreflex sensitivity was defined as the slope of renal sympathetic efferent nerve activity vs. carotid sinus pressure in an isolated, perfused carotid sinus. Slopes were obtained before and after sinus sympathectomy performed by section of the cervical sympathetic trunk. There was no significant differences between baroreflex decreases in renal sympathetic activity due to increases in carotid sinus pressure before and after sympathectomy, but the responses to decreases in carotid sinus pressure after sympathectomy were significantly greater than control. Base-line level of renal sympathetic activity, obtained at a constant perfusion pressure of 115 mmHg, abruptly increased by 11% in response to sinus sympathectomy. The response of baroreceptors to sympathomimetic stimulation was examined by recording carotid baroreceptor afferent nerve activity during ramp changes in carotid sinus pressure after addition of epinephrine (10(-8) to 10(-6) M) to the perfusate of the sympathetically denervated sinus. The slopes of the sinus nerve activity vs. carotid sinus pressure were used as direct indexes of baroreceptor sensitivity. Lower levels of epinephrine (10(-8), 10(-7) M) increased the sensitivity of the baroreceptors and reduced renal nerve activity back toward presympathectomy levels. A higher dose of epinephrine (10(-6) M) did not significantly increase baroreceptor sensitivity. The results of this study suggest that sinus sympathetic fibers produce a tonic sensitization of the baroreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

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