Effect of paraventricular nucleus lesions on cardiovascular responses elicited by stimulation of the subfornical organ in the rat

1985 ◽  
Vol 63 (7) ◽  
pp. 816-824 ◽  
Author(s):  
Michael B. Gutman ◽  
John Ciriello ◽  
Gordon J. Mogenson
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Subfornical Organ ◽  
Short Latency ◽  
Peak Latency ◽  
Ganglionic Blockade ◽  
Stimulation Of

It has recently been reported that stimulation of the region of the subfornical organ (SFO) elicits an increase in arterial pressure. However, the mechanisms and forebrain neural circuitry that are involved in this cardiovascular response have not been elucidated. The present study was done in urethane-anaesthetized rats to determine whether selective activation of SFO neurons elicit cardiovascular responses and whether these responses were mediated by a pathway involving the paraventricular nucleus of the hypothalamus (PVH). Stimulation sites which required the lowest threshold current (30 μA) to elicit a pressor response and at which the largest rise in mean arterial pressure (MAP; 22 ± 2 mmHg) was elicited at a constant current intensity (150 μA) were histologically localized in the region of the SFO. Short (mean peak latency; 4 ± 2 s) and long (mean peak latency; 61 ± 8 s) latency increases in MAP were observed during and after electrical stimulation of the SFO, respectively. Cardiac slowing accompanied the short latency pressor response and cardioacceleration was observed in most (57%) of the cases to accompany the late pressor response. Microinjection of L-glutamate into the SFO consistently elicited cardiovascular responses qualitatively similar to those observed during electrical stimulation. Ganglionic blockade abolished the short latency increase in MAP and the accompanying bradycardia. However, the long latency pressor and cardioacceleratory responses were not altered by ganglionic blockade and adrenalectomy. Selective bilateral electrolytic or kainic acid lesions of the region of the PVH significantly attenuated the cardiovascular responses elicited by stimulation of the SFO. These data suggest that activation of neurons in the SFO elicit cardiovascular responses partially mediated by sympathetic outflow through a neural pathway involving the PVH.

Rebound cardiovascular responses following stimulation of canine vagosympathetic complexes or cardiopulmonary nerves

1985 ◽  
Vol 63 (9) ◽  
pp. 1122-1132 ◽  
Author(s):  
J. A. Armour ◽  
W. C. Randall
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Cardiovascular System ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Cardiac Responses ◽  
Stimulation Of

Electrical stimulation of a canine vagosympathetic complex or a cardiopulmonary nerve can elicit a variety of negative chronotropic and inotropic cardiac responses, with or without alterations in systemic arterial pressure. In the period immediately following cessation of such a stimulation "rebound" tachycardia, increased inotropism above control values in one or more regions of the heart, and (or) elevation in systemic arterial pressure can occur. These "rebound" phenomena are abolished by propranolol or ipsilateral chronic sympathectomy. It is proposed that "vagal" poststimulation "rebound" of the canine cardiovascular system is primarily the result of activation of sympathetic neural elements present in the vagosympathetic complexes or cardiopulmonary nerves.

Hypothalamic projections of renal afferent nerves in the cat

1980 ◽  
Vol 58 (5) ◽  
pp. 574-576 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Fluid Balance ◽  
Lateral Hypothalamus ◽  
Discharge Rate ◽  
Renal Nerves ◽  
Preoptic Nucleus ◽  
Afferent Nerves ◽  
Stimulation Of

In 10 cats anaesthetized with chloralose the electrical activity of spontaneously active hypothalamic units was recorded for changes in discharge rate during electrical stimulation of renal afferent nerves. The discharge rate of 141 single units was altered by stimulation of either the ipsilateral or contralateral renal nerves. Most of the responsive units were located in the regions of lateral preoptic nucleus, lateral hypothalamus, and paraventricular nucleus. These results demonstrate that renal afferent nerves provide information to hypothalamic structures known to be involved in the regulation of arterial pressure and fluid balance.

Functional identification of central pressor pathways originating in the subfornical organ

1991 ◽  
Vol 69 (7) ◽  
pp. 1035-1045 ◽  
Author(s):  
John Ciriello ◽  
Michael B. Gutman
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Paraventricular Nucleus ◽  
Supraoptic Nucleus ◽  
Subfornical Organ ◽  
Preoptic Nucleus ◽  
Thoracic Spinal Cord ◽  
Median Preoptic Nucleus ◽  
Pressor Responses ◽  
Stimulation Of

The functional projections from pressor sites in the subfornical organ (SFO) were identified using the 2-deoxyglucose (2-DG) autoradiographic method in urethane-anesthetized, sinoaortic-denervated rats. Autoradiographs of brain and spinal cord sections taken from rats whose SFO was continuously stimulated electrically for 45 min with stereotaxically placed monopolar electrodes (150 μA, 1.5-ms pulse duration, 15 Hz) following injection of tritiated 2-DG were compared with control rats that received intravenous infusions of pressor doses of phenylephrine to mimic the increase in arterial pressure observed during SFO stimulation. Comparisons were also made to autoradiographs from rats in which the ventral fornical commissure (CFV), just dorsal to the SFO, was electrically stimulated. The pressor responses during either electrical stimulation of the SFO or intravenous infusion of phenylephrine were similar in magnitude. On the other hand, stimulation of the CFV did not elicit a significant pressor response. Electrical stimulation of the SFO increased 2-DG uptake, in comparison to the phenylephrine-infused rats, in the nucleus triangularis, septofimbrial nucleus, lateral septal nucleus, nucleus accumbens, bed nucleus of the stria terminalis, dorsal and ventral nucleus medianus (median preoptic nucleus), paraventricular nucleus of the thalamus, hippocampus, supraoptic nucleus, suprachiasmatic nucleus, paraventricular nucleus of the hypothalamus, and the intermediolateral nucleus of and central autonomic area of the thoracic spinal cord. In contrast, in rats whose CFV was stimulated, these nuclei did not demonstrate changes in 2-DG uptake compared with control animals that received pressor doses of phenylephrine. These data have demonstrated some of the components of the neural circuitry likely involved in mediating the pressor responses to stimulation of the SFO and the corrective responses to activation of the SFO by disturbances to circulatory and fluid balance homeostasis.Key words: cardiovascular reflex pathways, drinking, median preoptic nucleus, osmoreceptors, paraventricular nucleus of the hypothalamus, supraoptic nucleus.

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.

Group III muscle afferents evoke reflex depressor responses to repetitive muscle contractions in rabbits

2000 ◽  
Vol 278 (3) ◽  
pp. H871-H877 ◽  
Author(s):  
J. M. Legramante ◽  
G. Raimondi ◽  
C. M. Adreani ◽  
S. Sacco ◽  
F. Iellamo ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Muscle Twitch ◽  
Group Iii ◽  
Twitch Contraction ◽  
Depressor Response ◽  
Stimulation Of

Repetitive-twitch contraction of the hindlimb muscles in anesthetized rabbits consistently evokes a reflex depressor response, whereas this type of contraction in anesthetized cats evokes a reflex pressor response in about one-half of the preparations tested. Rapidly conducting group III fibers appear to comprise the afferent arm of the reflex arc, evoking the depressor response to twitch contraction in rabbits because electrical stimulation of their axons reflexly decreases arterial pressure. In contrast, electrical stimulation of the axons of slowly conducting group III and group IV afferents reflexly increases arterial pressure in rabbits. In the present study, we examined the discharge properties of group III and IV muscle afferents and found that the former (i.e., 13 of 20), but not the latter (i.e., 0 of 10), were stimulated by 5 min of repetitive-twitch contraction (1 Hz) of the rabbit triceps surae muscles. Moreover, most of the group III afferents responding to contraction appeared to be mechanically sensitive, discharging in synchrony with the muscle twitch. On average, rapidly conducting group III afferents responded for the 5-min duration of 1-Hz repetitive-twitch contraction, whereas slowly conducting group III afferents responded only for the first 2 min of contraction. We conclude that rapidly conducting group III afferents, which are mechanically sensitive, are primarily responsible for evoking the reflex depressor response to repetitive-twitch contractions in anesthetized rabbits.

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.

Imidazoline receptors of the paraventricular nucleus on the pressor response induced by stimulation of the subfornical organ

1998 ◽  
Vol 92 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Wilson Abrão Saad ◽  
Luiz Antonio de Arruda Camargo ◽  
José Eduardo Nogueira Silveira ◽  
Roberta Saad ◽  
Gabriela Maria Pavan de Arruda Camargo
Keyword(s):  
Paraventricular Nucleus ◽  
Pressor Response ◽  
Subfornical Organ ◽  
Imidazoline Receptors ◽  
Stimulation Of

Mechanisms of hemodynamic responses to electrical stimulation of subfornical organ

1986 ◽  
Vol 250 (6) ◽  
pp. R1117-R1122 ◽  
Author(s):  
M. L. Mangiapane ◽  
M. J. Brody
Keyword(s):  
Electrical Stimulation ◽  
Pressor Response ◽  
Subfornical Organ ◽  
Constant Current ◽  
Pulsed Doppler ◽  
Mesenteric Circulation ◽  
Pressor Responses ◽  
Constant Current Stimulation ◽  
Vascular Beds ◽  
Stimulation Of

The rat subfornical organ (SFO) is involved in the pressor response to circulating angiotensin II, and recent evidence indicates that SFO electrical stimulation also produces a pressor response. In the present experiments we examined the hemodynamic, neural, and humoral mechanisms that underlie the pressor response to electrical stimulation of the SFO. Rats were anesthetized with urethan and instrumented with femoral arterial catheters and with pulsed Doppler flow probes on the superior mesenteric and renal arteries and on the abdominal aorta. Constant-current stimulation, delivered to the SFO via tungsten microelectrodes, resulted in stimulus-locked frequency-dependent pressor responses and vasoconstriction in all vascular beds tested. The stimulation-evoked increases in vascular resistance were greatest in the mesenteric circulation and least in the renal. Movement of the electrode away from the SFO produced significantly smaller responses. Ganglionic blockade abolished the responses to electrical stimulation, whereas vasopressin blockade significantly attenuated the responses. The responses of baroreceptor-denervated rats were qualitatively similar to but approximately double in magnitude of those of normal rats. We conclude that electrical stimulation of the SFO elicits widespread regional vasoconstriction that is most pronounced in the mesenteric circulation. The sympathetic nervous system appears responsible for these effects, but there may be facilitation of the responses by vasopressin.

scholarly journals Stimulation of the paraventricular nucleus modulates firing of neurons in the nucleus of the solitary tract

1999 ◽  
Vol 277 (2) ◽  
pp. R403-R411 ◽  
Author(s):  
Yu-Fei Duan ◽  
Irwin J. Kopin ◽  
David S. Goldstein
Keyword(s):  
Electrical Stimulation ◽  
Paraventricular Nucleus ◽  
Pressor Response ◽  
Hypothalamic Paraventricular Nucleus ◽  
Solitary Tract ◽  
Defense Reaction ◽  
Neuronal Inhibition ◽  
Pressor Responses ◽  
Baroreceptor Stimulation ◽  
Stimulation Of

The present study assessed whether the baroreflex inhibition elicited by electrical stimulation of the hypothalamic paraventricular nucleus (PVN) involves altered activity in the nucleus of the solitary tract (NTS). Unit recordings were made from 107 neurons in the NTS in anesthetized rabbits. Intravenous phenylephrine was used to induce a pressor response and to activate baroreflexes. Of the neurons that responded to pressor responses, two-thirds were excited and one-third was inhibited. Stimulation of the PVN inhibited 70% of the phenylephrine-responsive NTS neurons, with or without concurrent baroreceptor stimulation. When PVN stimulation was delivered concurrently with phenylephrine injection, more NTS neuronal inhibition and less excitation occurred than with phenylephrine alone. Usually PVN stimulation inhibited NTS neurons that were excited by pressor responses; less commonly, PVN stimulation excited NTS neurons that were inhibited by pressor responses. The findings are consistent with the view that PVN activation during the defense reaction inhibits baroreflexes by altering firing of NTS neurons.

Electrical stimulation of the aortic depressor nerve in conscious rats overcomes the attenuation of the baroreflex in chronic heart failure

2016 ◽  
Vol 310 (7) ◽  
pp. R612-R618 ◽  
Author(s):  
Tomás O. C. Teixeira Pinto ◽  
Renata M. Lataro ◽  
Jaci A. Castania ◽  
Marina T. Durand ◽  
Carlos A. A. Silva ◽  
...  
Keyword(s):  
Heart Failure ◽  
Electrical Stimulation ◽  
Chronic Heart Failure ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Control Male ◽  
Aortic Depressor Nerve ◽  
Male Wistar Rats ◽  
Parasympathetic Function ◽  
Stimulation Of

Chronic heart failure (CHF) is characterized by autonomic dysfunction combined with baroreflex attenuation. The hypotensive and bradycardic responses produced by electrical stimulation of the aortic depressor nerve (ADN) were examined in conscious CHF and control male Wistar rats (12–13 wk old). Furthermore, the role of parasympathetic and sympathetic nervous system in mediating the cardiovascular responses to baroreflex activation was evaluated by selective β1-adrenergic and muscarinic receptor antagonists. CHF was induced by myocardial infarction. After 6 wk, the subjects were implanted with electrodes for ADN stimulation. Twenty-four hours later, electrical stimulation of the ADN was applied for 20 s using five different frequencies (5, 15, 30, 60, and 90 Hz), while the arterial pressure was recorded by a catheter implanted into the femoral artery. Electrical stimulation of the ADN elicited progressive and similar hypotensive and bradycardic responses in control ( n = 12) and CHF ( n = 11) rats, while the hypotensive response was not affected by methylatropine. Nevertheless, the reflex bradycardia was attenuated by methylatropine in control, but not in CHF rats. Atenolol did not affect the hypotensive or bradycardic response in either group. The ADN function was examined under anesthesia through electroneurographic recordings. The arterial pressure-ADN activity relationship was attenuated in CHF rats. In conclusion, despite the attenuation of baroreceptor function in CHF rats, the electrical stimulation of the ADN elicited a stimulus-dependent hypotension and bradycardia of similar magnitude as observed in control rats. Therefore, electrical activation of the aortic baroreflex overcomes both the attenuation of parasympathetic function and the sympathetic overdrive.

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