The effect of time of electrical stimulation of the carotid sinus on the amount of reduction in arterial pressure

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.

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Treatment of Paroxysmal Supraventricular Tachycardia by Electrical Stimulation of the Carotid-Sinus Nerves

New England Journal of Medicine ◽

10.1056/nejm196910162811607 ◽

1969 ◽

Vol 281 (16) ◽

pp. 885-887 ◽

Cited By ~ 28

Author(s):

Eugene Braunwald ◽

Burton E. Sobel ◽

Nina S. Braunwald

Keyword(s):

Electrical Stimulation ◽

Supraventricular Tachycardia ◽

Carotid Sinus ◽

Paroxysmal Supraventricular Tachycardia ◽

Stimulation Of

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Hypothalamic projections of renal afferent nerves in the cat

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y80-095 ◽

1980 ◽

Vol 58 (5) ◽

pp. 574-576 ◽

Cited By ~ 47

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.

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Vasoconstrictor and vasodilator sites within anteroventral third ventricle region

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1987.253.6.r827 ◽

1987 ◽

Vol 253 (6) ◽

pp. R827-R831 ◽

Cited By ~ 7

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.

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Respiratory responses to aortic and carotid chemoreceptor activation in the dog

Journal of Applied Physiology ◽

10.1152/jappl.1991.70.6.2539 ◽

1991 ◽

Vol 70 (6) ◽

pp. 2539-2550 ◽

Cited By ~ 12

Author(s):

F. A. Hopp ◽

J. L. Seagard ◽

J. Bajic ◽

E. J. Zuperku

Keyword(s):

Electrical Stimulation ◽

Carotid Body ◽

Carotid Sinus ◽

Chemical Stimulation ◽

Respiratory Drive ◽

Carotid Sinus Nerve ◽

Nerve Activity ◽

Respiratory Reflexes ◽

Respiratory Responses ◽

Stimulation Of

Respiratory responses arising from both chemical stimulation of vascularly isolated aortic body (AB) and carotid body (CB) chemoreceptors and electrical stimulation of aortic nerve (AN) and carotid sinus nerve (CSN) afferents were compared in the anesthetized dog. Respiratory reflexes were measured as changes in inspiratory duration (TI), expiratory duration (TE), and peak averaged phrenic nerve activity (PPNG). Tonic AN and AB stimulations shortened TI and TE with no change in PPNG, while tonic CSN and CB stimulations shortened TE, increased PPNG, and transiently lengthened TI. Phasic AB and AN stimulations throughout inspiration shortened TI with no changes in PPNG or the following TE; however, similar phasic stimulations of the CB and CSN increased both TI and PPNG and decreased the following TE. Phasic AN stimulation during expiration decreased TE and the following TI with no change in PPNG. Similar stimulations of the CB and CSN decreased TE; however, the following TI and PPNG were increased. These findings differ from those found in the cat and suggest that aortic chemoreceptors affect mainly phase timing, while carotid chemoreceptors affect both timing and respiratory drive.

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Effect of baroreceptor denervation on stimulation of drinking by angiotensin II in conscious dogs

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1991.260.3.e333 ◽

1991 ◽

Vol 260 (3) ◽

pp. E333-E337 ◽

Cited By ~ 7

Author(s):

C. K. Klingbeil ◽

V. L. Brooks ◽

E. W. Quillen ◽

I. A. Reid

Keyword(s):

Blood Pressure ◽

Drinking Water ◽

Angiotensin Ii ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Carotid Sinus ◽

Plasma Osmolality ◽

Plasma Angiotensin ◽

High Doses ◽

Stimulation Of

Angiotensin II causes marked stimulation of drinking when it is injected centrally but is a relatively weak dipsogen when administered intravenously. However, it has been proposed that the dipsogenic action of systemically administered angiotensin II may be counteracted by the pressor action of the peptide. To test this hypothesis, the dipsogenic action of angiotensin II was investigated in dogs, in which low and high baroreceptor influences had been eliminated by denervation of the carotid sinus, aortic arch, and heart. In five sham-operated dogs, infusion of angiotensin II at 10 and 20 ng.kg-1.min-1 increased plasma angiotensin II concentration to 109.2 +/- 6.9 and 219.2 +/- 38.5 pg/ml and mean arterial pressure by 20 and 29 mmHg, respectively, but did not induce drinking. In four baroreceptor-denervated dogs, the angiotensin II infusions produced similar increases in plasma angiotensin II concentration and mean arterial pressure but, in contrast to the results in the sham-operated dogs, produced a dose-related stimulation of drinking. Water intake with the low and high doses of angiotensin II was 111 +/- 44 and 255 +/- 36 ml, respectively. The drinking responses to an increase in plasma osmolality produced by infusion of hypertonic sodium chloride were not different in the sham-operated and baroreceptor-denervated dogs. These results demonstrate that baroreceptor denervation increases the dipsogenic potency of intravenous angiotensin II and provides further support for the hypothesis that the dipsogenic action of intravenous angiotensin II is counteracted by the rise in blood pressure.

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