Acute response of aortic nerve activity to free drop-induced microgravity in anesthetized rats

Endothelin is a peptide with potent, long-lasting pressor effects characterized by increases in mesenteric and hindquarters vascular resistance and bradycardia following an initial, transient depressor response. This study examined the mechanisms of action of endothelin on regional hemodynamics in conscious, freely moving rats and on baroreflex sensitivity both in conscious and chloralose-anesthetized rats. The pressor response to endothelin (0.67 nmol/kg) was attenuated by nifedipine (25 micrograms/kg) and augmented by chloralose anesthesia. The bradycardia was attenuated by pentolinium (10 mg/kg), atropine methyl sulfate (0.5 mg/kg), or chloralose anesthesia. Hindquarter vaso-constriction was attenuated by nifedipine, pentolinium, and atropine, whereas mesenteric vasoconstriction was less sensitive to blockade. The vasopressin V1 antagonist, [d(CH2)5Tyr(Me)]-AVP (20 micrograms/kg), indomethacin (5 mg/kg), or verapamil (150 micrograms/kg) did not affect any of these cardiovascular responses. Renal sympathetic nerve activity was reduced similarly in chloralose-anesthetized rats to pressor responses elicited by either phenylephrine or endothelin, and the slope of the baro-reflex function curve after endothelin was similar to that of phenylephrine. These results suggest that endothelin is a potent vasoconstrictor in which its action on visceral and skeletal muscle vasculature is mediated by somewhat different mechanisms. Endothelin does not alter baroreceptor reflex control of sympathetic nerve activity or heart rate.

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Effect of Bunazosin on Cardiac Sympathetic Nerve Activity in Anesthetized Rats

Clinical and Experimental Hypertension Part A Theory and Practice ◽

10.3109/10641968909035296 ◽

1989 ◽

Vol 11 (1) ◽

pp. 137-147 ◽

Cited By ~ 1

Author(s):

Mitsuhiro Yoshioka ◽

Hiroko Togashi ◽

Machiko Matsumoto ◽

Masaru Minami ◽

Hideya Saito

Keyword(s):

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Cardiac Sympathetic Nerve ◽

Nerve Activity ◽

Cardiac Sympathetic Nerve Activity ◽

Anesthetized Rats

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Is there a central nervous system component to acute baroreflex resetting in rats?

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.2.h503 ◽

1992 ◽

Vol 262 (2) ◽

pp. H503-H510 ◽

Cited By ~ 2

Author(s):

C. M. Heesch ◽

K. W. Barron

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Nerve Stimulation ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

System Component ◽

Nerve Activity ◽

Linear Portion ◽

Aortic Nerve ◽

Maximum Inhibition

This study was designed to evaluate a possible central nervous system (CNS) component to acute baroreflex resetting. In nine arterial baroreceptor-denervated, chloralose-urethan-anesthetized rats, a control (C) aortic nerve stimulation curve (3-5 V, 1 ms, 0-64 Hz) was obtained. Next, a constant "baroreceptor" input was delivered to the CNS (left aortic nerve stimulation, 10 min, 10.2 +/- 1.5 Hz). Within the first 13 s of aortic nerve stimulation, maximum inhibition of lumbar sympathetic nerve activity (LSNA) was 60 +/- 7.8% of baseline and at 1 min it increased to 68 +/- 5.6% of baseline. At the end of the 10-min aortic nerve stimulation, LSNA was not different from the response at 1 min (68 +/- 5.6% = 74 +/- 4.1%). Immediately after the constant stimulation (within 30 s), a test or reset (RS) curve was obtained (0-64 Hz). A recovery (RC) curve was obtained 10-20 min later. The slope of the linear portion of the curve and the stimulation frequency that produced 50% maximum inhibition (ES50) were compared among the three baroreflex curves (C, RS, RC,) and no significant differences were found. Thus, although a CNS component to baroreflex adaptation was evident during the first minute of aortic nerve stimulation, a longer term acute resetting of the baroreflex curve did not occur.

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Effect of an antihypertensive drug, budralaziie, on sympathetic nerve activity in anesthetized rats

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)58237-3 ◽

1987 ◽

Vol 43 ◽

pp. 144

Author(s):

Mitsuhiro Yoshioka ◽

Haruhisa Yahagi ◽

Masaru Minami ◽

Hiroko Togashi ◽

Hideya Saito

Keyword(s):

Antihypertensive Drug ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Nerve Activity ◽

Anesthetized Rats

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Role of nitrosyl factors in the hemodynamic adjustments to heat stress in the rat

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.273.3.h1537 ◽

1997 ◽

Vol 273 (3) ◽

pp. H1537-H1543 ◽

Cited By ~ 9

Author(s):

K. C. Kregel ◽

M. J. Kenney ◽

M. P. Massett ◽

D. A. Morgan ◽

S. J. Lewis

Keyword(s):

Methyl Ester ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Nerve Activity ◽

Adrenoceptor Antagonist ◽

Arterial Blood ◽

Anesthetized Rats ◽

Colonic Temperature ◽

Alpha Chloralose ◽

Oxide Synthase

The present study examined the mechanisms responsible for the hindlimb vasodilation produced by elevating core body (colonic) temperature (Tco) of alpha-chloralose-anesthetized rats from 37 to 39 degrees C. Elevating Tco to 39 degrees C produced equivalent decreases in hindlimb vascular resistance in sham-operated (-48 +/- 2%) and sinoaortic baroreceptor-denervated rats (-44 +/- 3%) rats. There were no changes in mean arterial blood pressure, heart rate, or lumbar sympathetic nerve activity in either group. The prior administration of the alpha 1-adrenoceptor antagonist prazosin (100 micrograms/kg i.v.) did not prevent the heat-induced decrease in hindlimb resistance in sham-operated rats (-52 +/- 7% vs. baseline). In contrast, the fall in hindlimb resistance was markedly attenuated (-20 +/- 5% vs. baseline) in sham-operated rats that had received a prior injection of the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (100 mumol/kg i.v.). Dexamethasone (1 mg/kg i.v.), administered to prevent the possible induction of inducible NOS, did not modify the heat-induced hindlimb vasodilation in sham-operated rats (-41 +/- 5%). These results demonstrate that the elevation of Tco to 39 degrees C in alpha-chloralose-anesthetized rats produces a relative vasodilation in the hindlimb that is not obviously linked to an alteration in lumbar sympathetic nerve activity. Because the vasodilation occurred in the presence of prazosin, it is unlikely that the decline in resistance is due to the loss of the vasoconstrictor potency of neurally derived catecholamines. The findings that NG-nitro-L-arginine methyl ester, but not dexamethasone, diminished the heat-induced hindlimb vasodilation suggests that the fall in resistance is due in part to constitutive NOS and supports a role for NOS as a mediator of thermoregulatory active vasodilation.

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