Cardiovascular effects of posterior hypothalamic stimulation in baroreflex-denervated rats

1990 ◽  
Vol 259 (3) ◽  
pp. H720-H727 ◽  
Author(s):  
K. W. Barron ◽  
C. M. Heesch
Keyword(s):  
Electrical Stimulation ◽  
Vascular Resistance ◽  
Cardiovascular Effects ◽  
Posterior Hypothalamus ◽  
Intact Group ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Mesenteric Vascular Resistance ◽  
Posterior Hypothalamic Stimulation ◽  
Stimulation Of

The overall purpose of this study was to examine the effect of sinoaortic baroreceptor denervation (SAD) on the cardiovascular and sympathetic outflow responses to electrical stimulation of the posterior hypothalamus. In anesthetized rats that had undergone SAD 7-10 days before experimentation, electrical stimulation of the posterior hypothalamus elicited greater increases in mean arterial pressure, iliac vascular resistance, mesenteric vascular resistance, and lumbar sympathetic nerve activity than in sham-operated baroreceptor-intact animals. Similarly, the pressor effects of intravenous norepinephrine were also augmented in the baroreceptor-denervated group compared with the baroreceptor-intact group. When posterior hypothalamic and intravenous norepinephrine pressor stimuli, which produced equivalent pressor responses in sham-operated baroreceptor-intact animals, were compared in baroreceptor-denervated animals, the pressor effects of the central hypothalamic stimulus were enhanced to a greater degree than the norepinephrine pressor effects. These data provide evidence that arterial baroreceptor reflexes exert greater buffering of pressor stimuli initiated from the central nervous system compared with pressor responses due to peripheral vascular vasoconstrictor agents.

Hypothalamic stimulation induces acid secretion, hypoglycemia, and hyperinsulinemia

1975 ◽  
Vol 228 (4) ◽  
pp. 1206-1209 ◽  
Author(s):  
DN Stephens ◽  
SM Morrissey
Keyword(s):  
Electrical Stimulation ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Plasma Insulin ◽  
Posterior Hypothalamus ◽  
Hypothalamic Stimulation ◽  
Insulin Stimulation ◽  
Posterior Hypothalamic Stimulation ◽  
Stimulation Of

Electrical stimulation of the posterior hypothalamus brought about an increase in plasma insulin accompanied by a fall in blood glucose. If glucose fell below 55 mg/100 ml, gastric secretion of HCl ensued. The same relationship between acid secretion and glucose was observed when hypoglycemia was induced by intravenous injection of insulin. Stimulation outside the posterior hypothalamus did not give either a fall in glucose or an increase in gastric acid secretion. It is concluded that posterior hypothalamic stimulation causes gastric acid secretion by inducing insulin release and a consequent hypoglycemia.

Posterior hypothalamic influences on cardiovascular effects of aortic nerve stimulation

1989 ◽  
Vol 257 (6) ◽  
pp. H1994-H2000 ◽  
Author(s):  
J. K. Smith ◽  
K. W. Barron
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Posterior Hypothalamus ◽  
Hypothalamic Stimulation ◽  
Bipolar Electrode ◽  
Aortic Depressor Nerve ◽  
Aortic Nerve ◽  
Posterior Hypothalamic Stimulation ◽  
Stimulation Of

The purpose of this study was to examine the influence of stimulation of the posterior hypothalamus on the baroreflex responses produced by stimulation of the aortic depressor nerve. Animals were initially anesthetized and implanted with a bipolar electrode in the posterior hypothalamus. Three to 5 days later, animals were anesthetized with urethan, and the left aortic depressor nerve was dissected and placed on a bipolar platinum-iridium electrode. The effects of electrical stimulation of the posterior hypothalamus (0, 160, and 280 microA) were examined in baroreflex-intact and acutely sinoaortic baroreceptor-denervated animals, and the responses to aortic nerve stimulation (2, 8, 16, and 32 Hz) were examined during each level of hypothalamic stimulation. The first set of experiments was performed in baroreceptor-intact animals; e.g., in animals with arterial baroreceptor inputs intact from both carotid sinus regions in addition to intact right aortic baroreceptor afferent pathways. In that group, stimulation of the posterior hypothalamus attenuated the bradycardia and depressor effects of aortic nerve stimulation. When influences from other baroreceptor inputs were removed with acute sinoaortic baroreceptor denervation, posterior hypothalamic stimulation interrupted the reflex bradycardia due to aortic nerve stimulation; however, the depressor response to aortic nerve stimulation was not attenuated. Similar to the arterial pressure response, hypothalamic stimulation did not attenuate the decreases in mesenteric and iliac vascular resistance produced by aortic nerve stimulation in the baroreflex-denervated group. We conclude that posterior hypothalamic stimulation attenuates baroreflex-mediated bradycardia but does not alter baroreflex control of arterial pressure and peripheral vascular resistance.

Excitatory amino acid receptors within NTS mediate arterial chemoreceptor reflexes in rats

1993 ◽  
Vol 265 (2) ◽  
pp. H770-H773 ◽  
Author(s):  
W. Zhang ◽  
S. W. Mifflin
Keyword(s):  
Electrical Stimulation ◽  
Amino Acid ◽  
Receptor Antagonist ◽  
Carotid Body ◽  
Excitatory Amino Acid ◽  
Pressor Responses ◽  
Carotid Body Chemoreceptors ◽  
Arterial Chemoreceptor ◽  
Stimulation Of ◽  
Arterial Baroreceptor

The nucleus tractus solitarius (NTS) is the primary site of termination of arterial baroreceptor and chemoreceptor afferent fibers. Excitatory amino acid (EAA) receptors within NTS have been shown to play an important role in the mediation of arterial baroreceptor reflexes; however, the importance of EAA receptors within NTS in the mediation of arterial chemoreceptor reflexes remains controversial. Therefore, in chloralose-urethan-anesthetized, mechanically ventilated, paralyzed rats, 4 nmol of the broad-spectrum EAA receptor antagonist kynurenic acid (Kyn) was injected into the NTS to observe the effects of EAA receptor blockade on the pressor responses evoked by either activation of ipsilateral carotid body chemoreceptors (by close arterial injection of CO2-saturated bicarbonate) or electrical stimulation of ipsilateral carotid sinus nerve (CSN). Under control conditions, activation of carotid body chemoreceptors and CSN stimulation evoked increases in arterial pressure of 27 +/- 2 (n = 24 sites) and 28 +/- 3% (n = 8), respectively. Kyn microinjection into NTS significantly reduced the pressor responses evoked by activation of carotid body chemoreceptors and electrical stimulation of the CSN for 20 and 25 min, respectively. Attenuation of pressor responses evoked by chemoreceptor activation were maximal at 20 min post-Kyn injection (13 +/- 2%), whereas CSN-evoked pressor responses were maximally attenuated at 15 min (6 +/- 4%). Microinjection into NTS of 4 nmol of xanthurenic acid, a structural analogue of Kyn with no EAA receptor antagonist properties, had no effect on chemoreceptor reflexes. We conclude that EAA receptors within NTS play an important role in the mediation of arterial chemoreceptor reflexes.

scholarly journals Global Cerebral Vasodilatation Elicited by Focal Electrical Stimulation within the Dorsal Medullary Reticular Formation in Anesthetized Rat

1983 ◽  
Vol 3 (3) ◽  
pp. 270-279 ◽  
Author(s):  
Costantino Iadecola ◽  
Masatsugu Nakai ◽  
Ehud Arbit ◽  
Donald J. Reis
Keyword(s):  
Electrical Stimulation ◽  
Reticular Formation ◽  
Medial Longitudinal Fasciculus ◽  
Medullary Reticular Formation ◽  
Tissue Samples ◽  
The Central Nervous System ◽  
Cerebral Vasodilatation ◽  
Cervical Sympathetic ◽  
Global Increase ◽  
Stimulation Of

We examined the effects of electrical stimulation of a restricted area of the dorsal medullary reticular formation (DMRF) on regional cerebral blood flow (CBF) in anesthetized (by chloralose), paralyzed (by curare) rats. CBF was measured in tissue samples by the Kety principle, with 14C-iodoantipyrine as indicator. Stimulation of DMRF elicited a widespread, significant increase in CBF in 12 of 13 areas. The increase in flow was greatest in cerebral cortex, up to 240% of control. However, it was also substantially increased in selected regions of telencephalon, diencephalon, mesencephalon, and lower brainstem, but not cerebellum. In contrast, electrical stimulation of the midline (interstitial nucleus of the medial longitudinal fasciculus) 1 mm medial to the DMRF did not change CBF. The increase in CBF evoked by DMRF stimulation persisted after transection of the spinal cord at C1 or cervical sympathetic trunk. We conclude that excitation of neurons originating in or passing through the DMRF can elicit a potent and virtually global increase of CBF. The effect appears to be mediated by intrinsic pathways of the central nervous system.

Vasoconstrictor and vasodilator sites within anteroventral third ventricle region

1987 ◽  
Vol 253 (6) ◽  
pp. R827-R831 ◽  
Author(s):  
M. L. Mangiapane ◽  
M. J. Brody
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Third Ventricle ◽  
Renal Vascular Resistance ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Tungsten Microelectrode ◽  
Renal Vascular ◽  
Stimulation Of

Previous studies have shown that electrical stimulation of the rat anteroventral third ventricle (AV3V) region produces a characteristic pattern of hemodynamic effects, i.e., renal and mesenteric vasoconstriction, and hindquarters vasodilation. In the present study, we localized the vasoconstrictor and vasodilator effects to specific subregions of the AV3V. In urethan-anesthetized rats prepared with arterial catheters and pulsed Doppler flow probes, we assessed the effects of electrical stimulation of four nuclei within AV3V on mean arterial pressure and renal, mesenteric, and hindquarters resistance. These nuclei were the organum vasculosum lamina terminalis (OVLT), ventral nucleus medianus (median preoptic nucleus), anterior (precommissural) nucleus medianus (median preoptic nucleus), and periventricular preoptic nuclei. Stimulation was carried out by use of a tungsten microelectrode. Stimulation of the OVLT consistently provoked stimulus-locked increases in arterial pressure coupled with increases in mesenteric and renal vascular resistance. Ganglionic blockade with chlorisondamine prevented these responses, demonstrating that they were mediated neurogenically. Stimulation of the three remaining nuclei produced decreases in arterial pressure, hindquarters vasodilation, and little change in mesenteric and renal vascular resistance. No changes in heart rate were observed with stimulation of any of the four nuclei. These results suggest that the vasoconstrictor and pressor functions of the AV3V region are localized in or near the OVLT region, whereas the remaining nuclei of the AV3V region mediate vasodilator and depressor responses.

Mechanisms of pressor response produced by stimulation of nucleus ambiguus

1990 ◽  
Vol 259 (5) ◽  
pp. R955-R962
Author(s):  
B. H. Machado ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Pressor Responses ◽  
Regional Vascular Resistance ◽  
Parasympathetic Control ◽  
Renal Vascular ◽  
Stimulation Of

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

Evidence for a central role for vasopressin in cardiovascular regulation

1983 ◽  
Vol 244 (6) ◽  
pp. H852-H859 ◽  
Author(s):  
K. H. Berecek ◽  
R. L. Webb ◽  
M. J. Brody
Keyword(s):  
Vascular Resistance ◽  
Third Ventricle ◽  
Cardiovascular Responses ◽  
Cardiovascular Regulation ◽  
Brattleboro Rats ◽  
Vascular Responses ◽  
The Third ◽  
Neuronal Systems ◽  
Mesenteric Vascular Resistance ◽  
Stimulation Of

Central vasopressin (VP) may modulate the functional activity of specific neuronal systems involved in cardiovascular regulation. To test this hypothesis we compared cardiovascular (CV) responses to electrical stimulation of the anteroventral region of the third ventricle (AV3V) in Brattleboro rats homozygous for diabetes insipidus (DI), in heterozygous DI rats (DI-HZ) and in normal Long-Evans rats (LE). We also studied the effects of peripheral and intracerebroventricular (ivt) treatment of DI rats with VP and treatment of LE rats with an antipressor blocker of VP on cardiovascular responses to AV3V stimulation. Stimulation of the AV3V region in anesthetized LE rats produced a frequency-dependent increase in renal (RVR) and mesenteric vascular resistance (MVR), a decrease in hindquarter vascular resistance (HQVR), and a decrease in arterial pressure (AP) and heart rate (HR). DI and DI-HZ rats showed significantly greater decreases in AP and HR and lesser changes in RVR, MVR, and HQVR. The deficiency in vasoconstriction in DI rats appeared to be centrally mediated inasmuch as vascular responses to peripherally administered phenylephrine and nerve stimulation were comparable in LE and DI rats. Treatment of DI rats with VP peripherally improved CV responses to AV3V stimulation. An even greater improvement in CV responses to AV3V stimulation was obtained when DI were given ivt infusion of VP. Finally, following intravenous administration of an antipressor VP blocker LE rats showed a greater decrease in AP and HR and lesser resistance changes in response to AV3V stimulation. Our data suggest that cardiovascular responses elicited from stimulation of the AV3V region may depend, in part, on a central vasopressin mechanism.

Cardiovascular responses to exercise in the rat: role of corticotropin-releasing factor

1990 ◽  
Vol 68 (2) ◽  
pp. 561-567 ◽  
Author(s):  
K. C. Kregel ◽  
J. M. Overton ◽  
D. R. Seals ◽  
C. M. Tipton ◽  
L. A. Fisher
Keyword(s):  
Heart Rate ◽  
Vascular Resistance ◽  
Treadmill Exercise ◽  
Cardiovascular Responses ◽  
Corticotropin Releasing Factor ◽  
Receptor Blockade ◽  
Conscious Rat ◽  
The Central Nervous System ◽  
Mesenteric Vascular Resistance

The effects of intracerebroventricular (icv) administration of a corticotropin-releasing factor (CRF) receptor antagonist, alpha-helical CRF, on systemic and regional hemodynamic adjustments to exercise were studied in conscious rats. On consecutive days, rats received saline icv, alpha-helical CRF icv, and no treatment 30 min before treadmill exercise (TMX). Increases in heart rate (HR) and mean arterial pressure (MAP) in response to TMX (16.1-28.6 m/min) were similar after icv administration of saline or no treatment. In rats receiving saline icv or no treatment, estimated vascular resistance increased in the mesenteric and renal regions and declined in the iliac (hindlimb) region. After icv administration of alpha-helical CRF9-41, HR and MAP responses during TMX were significantly attenuated. In addition, TMX-induced elevations of estimated mesenteric vascular resistance and iliac blood flow velocity were blunted after CRF receptor blockade. These altered cardiovascular and hemodynamic responses were ultimately reflected in the animals' compromised ability to run. The results suggest that the central nervous system actions of endogenous CRF are necessary for the full expression of the cardiovascular adjustments to TMX in the conscious rat.

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