Reflex responses of arterial pressure to electrical stimulation of the muscle are enhanced in the ovariectomized rats

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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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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DECREASES IN ARTERIAL PRESSURE AND HEART RATE ELICITED BY ELECTRICAL STIMULATION OF THE ANTERIOR HYPOTHALAMUS OF PENTOBARBITAL ANESTHETIZED DOGS

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)52732-9 ◽

1982 ◽

Vol 32 (1) ◽

pp. 195-197

Author(s):

Kazuo NUNOKI ◽

Toshihiko IUIMA

Keyword(s):

Heart Rate ◽

Electrical Stimulation ◽

Arterial Pressure ◽

Anterior Hypothalamus ◽

Anesthetized Dogs ◽

Stimulation Of

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.253.1.h91 ◽

1987 ◽

Vol 253 (1) ◽

pp. H91-H99 ◽

Cited By ~ 2

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.

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Hemodynamic effects of electrical stimulation of forebrain angiotensin and osmosensitive sites

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1978.235.4.h445 ◽

1978 ◽

Vol 235 (4) ◽

pp. H445-H451 ◽

Cited By ~ 5

Keyword(s):

Blood Flow ◽

Electrical Stimulation ◽

Arterial Pressure ◽

Median Eminence ◽

Regional Blood Flow ◽

Renal Hypertension ◽

Brain Structures ◽

Ventromedial Hypothalamus ◽

Pressure Changes ◽

Stimulation Of

Previous studies from this laboratory have indicated an important role for angiotensin-sensitive anteroventral third ventricular (AV3V) brain structures in normal regulation of arterial pressure and development of renal hypertension. The present experiments examined the effects of electrical stimulation of these periventricular areas on arterial pressure and regional blood flow in the anesthetized rat. Electrodes were placed in the AV3V region 3–10 days prior to acute studies. Blood flow was measured in extracorporeal blood flow circuits. Electrical stimulation produced only small changes in arterial pressure. Despite the small pressure changes, stimulation caused marked frequency-dependent alterations in regional blood flow. Renal and splanchnic flows were reduced while hindlimb flow was increased. Resistance changes were abolished by surgical denervation or ganglionic blockade but were unaffected by adrenalectomy. Hemodynamic responses to AV3V stimulation were abolished by a lesion in the area of the median eminence. It may be concluded that AV3V stimulation, through activation of pathways descending through the ventromedial hypothalamus-median eminence region, produces profound regional blood flow shifts without greatly altering arterial pressure.

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