Role of alpha-adrenergic mechanisms on responses to area postrema stimulation and circulating vasopressin

1993 ◽  
Vol 265 (2) ◽  
pp. H530-H536 ◽  
Author(s):  
E. M. Hasser ◽  
V. S. Bishop
Keyword(s):  
Electrical Stimulation ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Adrenergic Antagonist ◽  
Renal Sympathetic ◽  
Catecholaminergic Mechanisms ◽  
Stimulation Of

This study evaluated the role of catecholamines in the nucleus tractus solitarius (NTS) on the inhibition of renal sympathetic nerve activity (RSNA) due to direct electrical stimulation of the area postrema. In addition, the effects of catecholaminergic mechanisms in the NTS on the ability of circulating arginine vasopressin (AVP) to modulate arterial baroreflex control of RSNA were evaluated. Electrical stimulation of the area postrema (15 microA, 0.3 ms, 5-80 Hz) produced progressive decreases in RSNA. Responses to area postrema activation were not altered by microinjection of the alpha 1-adrenergic antagonist, prazosin, or vehicle bilaterally into the NTS. Microinjection of the alpha 2-antagonist, yohimbine (4 injections of 20-40 nl, 1 ng/nl), unilaterally into the NTS significantly attenuated the RSNA response to area postrema stimulation. Bilateral injection of yohimbine into the NTS abolished the response to area postrema activation (P < 0.05). Baroreflex inhibition of RSNA was significantly greater during infusion of AVP than during infusion of phenylephrine (slopes = -5.18 +/- 0.39 and -2.64 +/- 0.27 for AVP and phenylephrine, respectively). Microinjection of yohimbine bilaterally into the NTS did not alter the slope of baroreflex control of RSNA for phenylephrine but normalized the slope for AVP (-2.85 +/- 0.54) to that of phenylephrine. Data are consistent with the hypothesis that AVP effects on baroreflex inhibition of RSNA and area postrema-mediated inhibition of RSNA require alpha 2-adrenergic signaling within the NTS.

Inhibition of renal sympathetic nervous activity by area postrema stimulation in rabbits

1987 ◽  
Vol 253 (1) ◽  
pp. H91-H99 ◽  
Author(s):  
E. M. Hasser ◽  
D. O. Nelson ◽  
J. R. Haywood ◽  
V. S. Bishop
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Consistent Change ◽  
Renal Sympathetic ◽  
Stimulation Of

This study investigated the effect of chemical and electrical stimulation of the area postrema on renal sympathetic nerve activity (RSNA), arterial pressure, and heart rate in urethan-anesthetized rabbits. Electrical stimulation of the area postrema at 2, 5, 10, 20, 40, and 80 Hz using constant currents of 7.5, 15, and 30 microA (pulse duration = 0.3 ms, train duration = 5 s) produced progressive decreases in RSNA and heart rate, with no consistent change in arterial pressure. To control for electrical activation of fibers of passage in or near the area postrema, L-glutamate was injected into the area postrema using glass micropipettes. Micropressure injection of L-glutamate (10 mM) in volumes of 5-10 nl produced rapid decreases in RSNA averaging 27 +/- 5% (P less than 0.05) accompanied by a small bradycardia. The effects of electrical stimulation of the area postrema, but not the adjacent nucleus tractus solitarius, were totally eliminated by micropressure injection of kainic acid (40 ng in 40 nl) into the area postrema. During continuous electrical stimulation of the area postrema using parameters that produced small decrements in RSNA and heart rate, the slope of the line relating baroreflex inhibition of RSNA to increases in arterial pressure during graded infusions of phenylephrine was significantly enhanced (-6.77 +/- 1.30 vs. -3.81 +/- 0.66% RSNA/mmHg). These data are consistent with the hypothesis that activation of neurons in the area postrema results in an inhibition of RSNA. Furthermore, stimulation of the area postrema augments baroreflex inhibition of RSNA during increases in arterial pressure with phenylephrine.

Role of baroreceptor afferents on area postrema-induced inhibition of sympathetic activity

1991 ◽  
Vol 260 (4) ◽  
pp. H1353-H1358
Author(s):  
M. Hay ◽  
E. M. Hasser ◽  
K. P. Undesser ◽  
V. S. Bishop
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Activity ◽  
Area Postrema ◽  
Afferent Input ◽  
Dependent Manner ◽  
Chemical Application ◽  
Renal Sympathetic Nerve Activity ◽  
Before And After ◽  
Stimulation Of

Activation of the area postrema by either electrical stimulation or chemical application of L-glutamate has been shown to result in an enhancement of cardiovascular baroreflexes similar to that seen with systemic infusions of arginine vasopressin (AVP). In addition, it has been found that the effects of AVP on baroreflex inhibition of renal sympathetic nerve activity (RSNA) are similar to those observed with phenylephrine following lesions of the area postrema or after partial denervation of baroreceptor afferents. The present study was undertaken to determine the role of baroreceptor afferent input on area postrema stimulation-induced decreases in sympathetic activity. In anesthetized rabbits, the responses of arterial pressure, heart rate, and RSNA to area postrema electrical stimulation were obtained before and after progressive sinoaortic denervation and vagotomy. Stimulation of the area postrema in carotid sinus-denervated animals consistently decreased RSNA in a frequency-dependent manner. However, following bilateral removal of both the aortic nerves and the vagi, electrical stimulation of the area postrema had no effect on RSNA. These results suggest that the ability of area postrema stimulation to inhibit RSNA is dependent on the presence of baroreceptor afferent input.

AT1 receptor block does not affect arterial baroreflex during pregnancy in rabbits

2001 ◽  
Vol 280 (5) ◽  
pp. H1996-H2005 ◽  
Author(s):  
Kathleen P. O'Hagan ◽  
Kara A. Skogg ◽  
Jennifer B. Stevenson
Keyword(s):  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Sympathetic Response ◽  
Reflex Gain ◽  
Receptor Block ◽  
Renal Sympathetic

The role of ANG II in the arterial baroreflex control of renal sympathetic nerve activity (RSNA) in eight term-pregnant (P) and eight nonpregnant (NP) conscious rabbits was assessed using sequential intracerebroventricular and intravenous infusions of losartan, an AT1 receptor antagonist. The blood pressure (BP)-RSNA relationship was generated by sequential inflations of aortic and vena caval perivascular occluders. Pregnant rabbits exhibited a lower maximal RSNA reflex gain (−44%) that was primarily due to a reduction in the maximal sympathetic response to hypotension (P, 248 ± 20% vs. NP, 357 ± 41% of rest RSNA, P < 0.05). Intracerebroventricular losartan decreased resting BP in P (by 9 ± 3 mmHg, P < 0.05) but not NP rabbits, and had no effect on the RSNA baroreflex in either group. Subsequent intravenous losartan decreased resting BP in NP and further decreased BP in P rabbits, but had no significant effect on the maximal RSNA reflex gain. ANG II may have an enhanced role in the tonic support of BP in pregnancy, but does not mediate the gestational depression in the arterial baroreflex control of RSNA in rabbits.

Sympathetic responses to stimulation of area postrema in decerebrate and anesthetized rats

1995 ◽  
Vol 268 (3) ◽  
pp. H1086-H1095 ◽  
Author(s):  
A. A. Hegarty ◽  
L. F. Hayward ◽  
R. B. Felder
Keyword(s):  
Electrical Stimulation ◽  
Excitatory Amino Acid ◽  
Area Postrema ◽  
Neuronal Cell ◽  
Renal Sympathetic Nerve Activity ◽  
Pentobarbital Sodium ◽  
Anesthetized Rats ◽  
Neuronal Cell Bodies ◽  
Decerebrate Rat ◽  
Stimulation Of

The effects of electrical and chemical stimulation of the area postrema (AP) on mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were examined in urethan- and pentobarbital sodium-anesthetized rats and in unanesthetized decerebrate rats. The AP was electrically stimulated over a range of frequencies (10–100 Hz) and intensities (10–80 microA) with a pulse duration of 0.2 or 1.0 ms. The excitatory amino acid L-glutamate (100 or 200 mM) was microinjected into the AP to preferentially stimulate neuronal cell bodies. In urethan-anesthetized rats, electrical stimulation of the AP decreased MAP and RSNA. In pentobarbital sodium-anesthetized rats, MAP and RSNA were markedly increased by AP stimulation. In unanesthetized decerebrate rats, increases in MAP and RSNA were also observed during electrical AP stimulation. Microinjection of L-glutamate had no effect on MAP and RSNA in anesthetized or in unanesthetized rats. These results indicate that electrical AP stimulation increases sympathetic output in the unanesthetized decerebrate rat and that anesthesia modifies this sympathetic response. The findings also suggest that peripheral responses to L-glutamate and electrical stimulation of the AP are mediated over different central pathways.

Anandamide content and interaction of endocannabinoid/GABA modulatory effects in the NTS on baroreflex-evoked sympathoinhibition

2004 ◽  
Vol 286 (3) ◽  
pp. H992-H1000 ◽  
Author(s):  
Jeanne L. Seagard ◽  
Caron Dean ◽  
Sachin Patel ◽  
David J. Rademacher ◽  
Francis A. Hopp ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Baroreflex Sensitivity ◽  
Nucleus Tractus Solitarius ◽  
Glutamate Release ◽  
Physiological Role ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Afferent Projections ◽  
Pressure Changes ◽  
Renal Sympathetic

Cannabinoids have been shown to modulate central autonomic regulation and baroreflex control of blood pressure (BP). The presence of cannabinoid CB1 receptors on fibers in the nucleus tractus solitarius (NTS) suggests that some presynaptic modulation of transmitter release could occur in this region, which receives direct afferent projections from arterial baroreceptors and cardiac mechanoreceptors. This study, therefore, was performed to determine the mechanism(s) of effects of microinjection of an endocannabinoid, arachidonylethanolamide (anandamide, AEA), into the NTS on baroreflex sympathetic nerve responses produced by phenylephrine-induced pressure changes in anesthetized rats. AEA prolonged reflex inhibition of renal sympathetic nerve activity (RSNA), suggesting an increase in baroreflex sensitivity. This effect of AEA was blocked by prior microinjection of SR-141716 to block cannabinoid CB1 receptors. To determine whether this baroreflex enhancement by AEA involved a GABAA mechanism, the baroreflex response to AEA was tested after prior blockade of postsynaptic GABAA receptors by bicuculline, which would eliminate any effects due to modulation of GABA activity. After bicuculline, which alone prolonged the baroreflex inhibition of RSNA, AEA shortened the duration of RSNA inhibition, suggesting a possible presynaptic inhibition of glutamate release previously obscured by a more dominant GABAA effect. To support a possible physiological role for AEA, AEA concentration in the NTS was measured after a phenylephrine-induced increase in BP. AEA content in the NTS was increased significantly over that in normotensive animals. These results support the hypothesis that AEA content is increased by brief periods of hypertension and suggest that AEA can modulate the baroreflex through activation of CB1 receptors within the NTS, possibly modulating effectiveness of GABA and/or glutamate neurotransmission.

Increase in sympathetic activity with age. II. Role of impairment of cardiopulmonary baroreflexes

1991 ◽  
Vol 260 (4) ◽  
pp. H1121-H1127 ◽  
Author(s):  
G. Hajduczok ◽  
M. W. Chapleau ◽  
F. M. Abboud
Keyword(s):  
Carotid Sinus ◽  
Young Group ◽  
Left Ventricular ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Carotid Sinus Baroreflex ◽  
Cardiopulmonary Baroreflex ◽  
Bilateral Vagotomy ◽  
Renal Sympathetic

We have previously shown that arterial baroreflex function is significantly impaired in a group of old beagles [G. Hajduczok, M. W. Chapleau, S. L. Johnson, and F. M. Abboud. Am. J. Physiol. 260 (Heart Circ. Physiol. 29): H1113-H1120, 1991]. In the present study, we determined whether the neural limb of the cardiopulmonary baroreflex control of renal sympathetic nerve activity (RSNA) and the interaction between the arterial and cardiopulmonary reflexes is also impaired with senescence. In the anesthetized state, the aortic nerves were sectioned and carotid sinuses were isolated bilaterally with carotid sinus pressures held at 50 mmHg in both young (1 yr) and old animals (11 yr). In response to graded volume expansion (VE) with 3% dextran (0 to 30 ml/kg iv), the gain of cardiopulmonary baroreflex control of RSNA was significantly lower in the old (5.1 +/- 3%/mmHg) compared with the young (13.4 +/- 3%/mmHg) animals. There were no significant differences in systemic vascular compliance or left ventricular mass index between the two groups. The gain of the carotid sinus baroreflex inhibition of RSNA was significantly attenuated by VE in the young group but was not affected in the old group. Bilateral vagotomy (VX) resulted in a 182 +/- 74% increase in RSNA in the young (P less than 0.05), but VX did not significantly increase RSNA in the old (12 +/- 17%). After VX, the carotid sinus baroreflex gain markedly increased by nearly eightfold in the young group (P less than 0.05) but was not altered in the old dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Glucocorticoid modulation of cardiovascular and autonomic function in preterm lambs: role of ANG II

2001 ◽  
Vol 280 (3) ◽  
pp. R646-R654 ◽  
Author(s):  
Jeffrey L. Segar ◽  
Kurt A. Bedell ◽  
Oliva J. Smith
Keyword(s):  
Renin Angiotensin System ◽  
Glucocorticoid Treatment ◽  
Baroreflex Control ◽  
Angiotensin System ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Before And After ◽  
Maternal Administration ◽  
Renal Sympathetic

The mechanisms by which antenatal glucocorticoids facilitate postnatal circulatory function in preterm infants are uncertain but may be related to augmented angiotensinergic functions. To test the hypothesis that the effects of glucocorticoids on postnatal cardiovascular and sympathetic activity are mediated via the renin-angiotensin system, we studied the effects of AT1 receptor blockade on postnatal changes in heart rate (HR), mean arterial blood pressure (MABP), renal sympathetic nerve activity (RSNA), and baroreflex control of HR in prematurely delivered lambs. After maternal administration of betamethasone (12 mg im 48 and 24 h before delivery), chronically instrumented preterm lambs (118- to 123-day gestation, term 145 days) were studied before and after delivery by cesarean section; fetuses received either the AT1 receptor antagonist losartan (10 mg iv, n = 6) or saline ( n = 6) 1 h before delivery. A third group of animals ( n = 6) received losartan without prior exposure to betamethasone. Compared with fetal values, betamethasone-treated animals demonstrated significant increases ( P < 0.05) in MABP (47 ± 2 to 58 ± 2 mmHg) and RSNA (181 ± 80% of fetal value) 1 h after delivery. Betamethasone + losartan-treated lambs also displayed increases in MABP (48 ± 1 to 55 ± 3 mmHg) and RSNA (198 ± 96% of fetal value) 60 min after birth, similar to betamethasone alone lambs. Losartan alone treated animals had no postnatal increase in either MABP or RSNA, responses similar to those seen in nontreated sheep delivered at the same gestational age. The sensitivity of baroreflex-mediated changes in HR in response to increases in MABP was less in both groups of betamethasone-treated animals; no effect was seen with losartan. These results suggest the postnatal increases in MABP and RSNA seen with antenatal glucocorticoid treatment are not mediated by stimulation of peripherally accessible AT1 receptors. We speculate that augmented cardiovascular function in glucocorticoid-treated premature lambs is dependent, in part, on a generalized sympathoexcitatory response and that this effect of glucocorticoids is mediated by central mechanisms.

Interaction of vasopressin with area postrema during volume expansion

1987 ◽  
Vol 253 (4) ◽  
pp. R605-R610 ◽  
Author(s):  
E. M. Hasser ◽  
K. P. Undesser ◽  
V. S. Bishop
Keyword(s):  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Area Postrema ◽  
Right Atrial ◽  
Reflex Inhibition ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Maximum Inhibition ◽  
Renal Sympathetic

Effects of arginine vasopressin (AVP) on inhibition of renal sympathetic nerve activity (RSNA) during activation of cardiopulmonary reflexes by volume expansion were examined in conscious sinoaortic-denervated rabbits. The role of the area postrema in mediating these effects was also evaluated in rabbits subjected to area postrema lesion. Animals were subjected to 12% volume expansion with whole blood alone or during infusion of AVP (0.6 mU . kg-1 . min-1). Volume expansion in area postrema-intact animals caused a progressive reflex inhibition of RSNA (maximum = -36.5 +/- 3.3% delta RSNA). Vasopressin infusion did not significantly alter resting arterial pressure, right atrial pressure, heart rate, or RSNA. However, maximum inhibition of RSNA during volume expansion (-62.6 +/- 3.2% delta RSNA) was significantly augmented during AVP infusion, and the augmentation was reversed by a specific vascular (V1) AVP receptor antagonist. Vagotomy eliminated RSNA responses to volume expansion with or without AVP. In area postrema-lesioned animals, the RSNA response to volume expansion was similar to that of intact animals (-31.8 +/- 2.3% delta RSNA). However, AVP did not augment the RSNA response to volume expansion in lesioned animals (-30.4 +/- 2.5% delta RSNA). Thus exogenous AVP augmented cardiopulmonary reflex-mediated inhibition of RSNA due to volume expansion. This effect appeared to be mediated by the V1 AVP receptor and to require the presence of an intact area postrema.

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