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 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.

Electrical stimulation of the carotid sinus lowers arterial pressure and improves heart rate variability in l-NAME hypertensive conscious rats

2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Conscious Rats ◽  
Stimulation Of

Stimulation of parabrachial neurons elicits a sympathetically mediated pressor response in cats

1988 ◽  
Vol 255 (6) ◽  
pp. H1349-H1358 ◽  
Author(s):  
J. S. Hade ◽  
S. W. Mifflin ◽  
T. S. Donta ◽  
R. B. Felder
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Electrical Stimulus ◽  
Respiratory Drive ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Low Intensity ◽  
Stimulation Of

We examined the role of the parabrachial neuronal mass in mediating the pressor response to electrical stimulation of parabrachial nucleus (PBN). In anesthetized cats, 100 mM L-glutamate (L-glu) was microinjected into PBN at sites from which low-intensity (25 microA) electrical stimulation evoked a pressor response. Arterial pressure, heart rate, and, in some animals, renal or phrenic nerve activity were monitored. Microinjection of L-glu caused an increase in arterial pressure that was comparable with that elicited by low-intensity electrical stimulation. Electrical stimulation, and to a lesser extent L-glu microinjection, caused an increase in renal sympathetic nerve activity but no significant change in heart rate. No consistent change in central respiratory drive accompanied the pressor response. These responses were preserved after baroreceptor denervation but were blocked by intravenous administration of the alpha-adrenergic receptor antagonist phentolamine. Microinjection into PBN of 2 mM kainic acid, which selectively depolarizes neurons but spares axons, reversibly blocked the arterial pressure and renal nerve responses to the 25-microA electrical stimulus. We conclude that the pressor response elicited by electrical stimulation of PBN in the anesthetized cat is mediated by cellular elements in PBN, not by fibers of passage. Because phentolamine completely blocked the pressor response, we suggest that it is subserved peripherally by sympathetic alpha-adrenergic rather than humoral (e.g., angiotensin, vasopressin) vasoconstrictor mechanisms. Finally, our data indirectly suggest that PBN stimulation may differentially engage efferent components of the sympathetic nervous system to elicit the pressor response.

Fastigial stimulation releases vasopressin in amounts that elevate arterial pressure

1983 ◽  
Vol 244 (5) ◽  
pp. H687-H694 ◽  
Author(s):  
A. Del Bo ◽  
A. F. Sved ◽  
D. J. Reis
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Stimulus Train ◽  
Specific Antagonist ◽  
6 Hydroxydopamine ◽  
Stimulation Of ◽  
Intact Rats

Electrical stimulation of the cerebellar fastigial nucleus (FN) in anesthetized, paralyzed, and artificially ventilated rat with a 10-s stimulus train (50 Hz) resulted in a stimulus-locked elevation in arterial pressure (AP) and heart rate, the fastigial pressor response (FPR). Blockade of autonomic effectors by chemosympathectomy (produced by treatment with 6-hydroxydopamine) combined with adrenalectomy, or by spinal cord transection at C1, abolished the FPR but unmasked an elevation of AP with longer latency (10-12 s) and duration (2-4 min), termed the residual FPR. The residual FPR was 1) abolished by midbrain transection, 2) blocked by administration of a specific antagonist of the vasopressor response to arginine vasopressin (AVP) [1,d(CH2)5Tyr(Me)AVP], and 3) was absent in homozygous and attenuated in heterozygous rats of the Brattleboro strain. FN stimulation elevated AVP threefold (from 13 +/- 1 to 38 +/- 8 pg/ml, P less than 0.02; n = 6) in intact rats and sevenfold in rats with combined chemosympathectomy and adrenalectomy (from 14 +/- 1 to 96 +/- 11 pg/ml, P less than 0.001; n = 9). Stimulation of the cerebellar FN can release AVP. In the absence of sympathoadrenal effectors, the amount so released is enhanced and capable of elevating AP.

Localization of sites within dorsal motor nucleus of vagus that affect gastric motility

1985 ◽  
Vol 249 (1) ◽  
pp. G73-G84 ◽  
Author(s):  
F. D. Pagani ◽  
W. P. Norman ◽  
D. K. Kasbekar ◽  
R. A. Gillis
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Gastric Motility ◽  
Motor Nucleus ◽  
Fast Blue ◽  
Medial Nucleus ◽  
Dorsal Motor Nucleus ◽  
Propantheline Bromide ◽  
Stimulation Of

The purpose of our study was to determine the localization of sites within the dorsal motor nucleus of the vagus (DMV) of the cat that when stimulated would increase gastric motility. To do this, two types of experiments were performed. First, the retrograde tracer fast blue was injected into the antrum and pylorus, and labeled neurons in the DMV were identified. Second, electrical stimulation was performed in areas of the DMV labeled with fast blue as well as in nearby areas with no labeling while monitoring gastric motility, arterial pressure, and heart rate. Results from the first type of studies revealed that peak labeling in the DMV occurred between 0.56 and 1.56 mm rostral to obex. Electrical stimulation in this area using 100 microA, 0.2 ms duration pulses, and 50 Hz resulted in increases in antral and pyloric contractions in 20 animals. The magnitude of pyloric and antral responses elicited by stimulation of the DMV generally correlated to the number of cell bodies labeled with fast blue within the DMV. No changes in arterial pressure occurred, and only a slight (-4%) decrease in heart rate was observed. Maximal increases in motility occurred with 20 Hz (antrum) or 100 Hz (pylorus). These increases in motility were maintained even at 200- and 400-Hz stimulation. Ipsilateral vagotomy or pretreatment with propantheline bromide prevented the increases in gastric motility produced by electrical stimulation of the DMV. Electrical stimulation of more rostral sites in the DMV, the medial nucleus of the solitary tract (NTS), and an area within 1.0 mm medial to the DMV resulted in attenuated or no motility responses. Stimulation of the medial nucleus of the NTS did result in pronounced slowing in heart rate (-61 +/- 21 beats/min). These results suggest that there is a localization of a “stomach area” within the DMV and that electrical stimulation of this area results in gastric motility responses that are mediated by vagal fibers projecting directly to the stomach. In addition, electrical stimulation of the DMV results in selective effects on the gastrointestinal tract in that no pronounced changes in heart rate and arterial pressure occur.

Area postrema stimulation induced cardiovascular changes in the rat

1988 ◽  
Vol 255 (5) ◽  
pp. R855-R860 ◽  
Author(s):  
A. V. Ferguson ◽  
P. Marcus
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Cardiovascular Control ◽  
Control Mechanisms ◽  
Arterial Blood

The studies described here have utilized electrical stimulation techniques to examine the effects of activation of neural elements within the area postrema (AP) on cardiovascular control mechanisms. A total of 45 urethananesthetized male Sprague-Dawley rats were used in these experiments. Low-frequency electrical stimulation (10 Hz, 200 microA) in the AP resulted in rapid onset (less than 2 s), short-lasting (less than 5 s after end of stimulation) decreases in mean arterial blood pressure (-34.8 +/- 2.7 mmHg, n = 17 rats). In contrast, similar stimulation in the adjacent nucleus tractus solitarius (NTS) caused similarly timed increases in blood pressure (+43.1 +/- 6.7 mmHg, n = 5 rats). Activation of neural elements within the AP was found to significantly (Student's t test, P less than 0.01) reduce heart rate, an effect that was also specific to the AP site as similar stimulation in the NTS was without effect. These data support an important role for AP in cardiovascular control mechanisms. They demonstrate that stimulation in AP results in rapid reversible decreases in mean arterial blood pressure and heart rate. Such findings further emphasise the potential roles of this circumventricular structure in autonomic control mechanisms.

Effects of vasoactive intestinal peptide on canine prostatic contraction and secretion

1984 ◽  
Vol 247 (4) ◽  
pp. R701-R708 ◽  
Author(s):  
E. R. Smith ◽  
T. B. Miller ◽  
M. M. Wilson ◽  
M. C. Appel
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Vasoactive Intestinal Peptide ◽  
Ganglion Cells ◽  
Nerve Fibers ◽  
Hypogastric Nerve ◽  
Autonomic Ganglion ◽  
Anesthetized Dogs ◽  
Stimulation Of

Vasoactive intestinal peptide (VIP)-like immunoreactivity was found in intrinsic autonomic ganglion cells and nerve fibers located at the surface and within the canine prostate. In anesthetized dogs, porcine VIP (100–3,000 ng/kg iv) decreased arterial pressure and increased heart rate but did not result in the release of fluid from the prostate, indicating that VIP neither contracted glandular smooth muscle to expel fluid nor provoked secretion. Intravenous infusions of VIP at 10, 50, 100, and/or 200 ng X kg-1 X min-1 produced dose-related decreases in arterial pressure, increases in heart rate, and potentiation of the secretory response to the intravenous administration of pilocarpine and to electrical stimulation of the hypogastric nerves at 2 but not at 20 Hz. VIP at 1 microgram/ml neither contracted isolated strips of prostate nor modified their contraction by norepinephrine. It is unlikely that VIP mediates hypogastric nerve-induced prostatic contraction or secretion in the dog, but VIP may serve as a neuromodulator of nerve-induced secretion.

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