Nitric oxide modulates arteriolar responses to increased sympathetic nerve activity

1996 ◽  
Vol 271 (3) ◽  
pp. H860-H869 ◽  
Author(s):  
G. P. Nase ◽  
M. A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Nitric Oxide Synthase Inhibitor ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Endogenous Nitric Oxide ◽  
Synthase Inhibitor ◽  
Oxide Synthase

The purpose of this study was to determine whether arteriolar responses to increased sympathetic nerve activity are limited by the actions of endogenous nitric oxide. Intravital microscopy was used to examine diameter responses of small feed arteries (SFA), first-order arterioles (1A) and second-order arterioles (2A) to perivascular sympathetic nerve stimulation in the superfused rat small intestine. Stimulation induced a frequency-dependent constriction in all vessel types that was completely abolished by the alpha-adrenoceptor antagonist phentolamine (10(-6) M). In SFA and 1A, the magnitude of sympathetic constriction was increased significantly in the presence of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine(L-NMMA, 10(-4) M). In SFA (n = 7), stimulation at 3, 8, and 16 Hz induced constrictions of 11 +/- 1, 28 +/- 4, and 42 +/- 3%, respectively, under the normal superfusate vs. 28 +/- 3, 46 +/- 5, and 76 +/- 3% in the presence of L-NMMA. For 1A (n = 7), stimulation induced constrictions of 10 +/- 1, 27 +/- 4, and 37 +/- 3% under the normal superfusate vs. 24 +/- 2, 47 +/- 3, and 72 +/- 4% in the presence of L-NMMA. The effect of L-NMMA on sympathetic constriction in SFA (n = 7) was completely reversed by the additional presence of 5 x 10(-3) M L-arginine in the superfusate. These results suggest that endogenous nitric oxide activity can attenuate sympathetic neurogenic constriction in the intestinal microvasculature.

Nitric oxide-independent effects of tempol on sympathetic nerve activity and blood pressure in normotensive rats

2001 ◽  
Vol 281 (2) ◽  
pp. H975-H980 ◽  
Author(s):  
Hui Xu ◽  
Gregory D. Fink ◽  
Alex Chen ◽  
Stephanie Watts ◽  
James J. Galligan
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Nerve Activity ◽  
Nitric Oxide Synthase Inhibitor ◽  
Arterial Blood ◽  
Independent Effects ◽  
Synthase Inhibitor

The role of the sympathetic nervous system in 4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl (tempol)-induced cardiovascular responses in urethane-anesthetized, normotensive rats was evaluated. Tempol caused dose-dependent (30–300 μmol/kg iv) decreases in renal sympathetic nerve activity (RSNA), mean arterial blood pressure (MAP), and heart rate (HR). Similar responses were obtained after sinoaortic denervation and cervical vagotomy. These responses were not blocked following treatment with the nitric oxide synthase inhibitor N G-nitro-l-arginine (2.6 mg · kg−1 · min−1 iv for 5 min) or the α2-adrenergic receptor antagonist idazoxan (0.3 mg/kg iv bolus). Idazoxan blocked the effects of clonidine (10 μg/kg iv) on HR, MAP, and RSNA. Hexamethonium (30 mg/kg iv) inhibited RSNA, and tempol did not decrease RSNA after hexamethonium. The effects of tempol on HR and MAP were reduced by hexamethonium. In conclusion, depressor responses caused by tempol are mediated, partly, by sympathoinhibition in urethane-anesthetized, normotensive rats. Nitric oxide does not contribute to this response, and the sympathoinhibitory effect of tempol is not mediated via α2-adrenergic receptors. Finally, tempol directly decreases HR, which may contribute to the MAP decrease.

scholarly journals Endogenous Nitric Oxide Synthase Inhibitor in Human Atheromatous Lesion

1997 ◽  
Vol 75 ◽  
pp. 55
Author(s):  
Hidehiro Matsuoka ◽  
Hiroshi Miyazaki ◽  
Seiya Katoh ◽  
Hideo Yasukawa ◽  
Michiaki Usui ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nitric Oxide Synthase Inhibitor ◽  
Endogenous Nitric Oxide ◽  
Synthase Inhibitor ◽  
Oxide Synthase

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

1997 ◽  
Vol 273 (3) ◽  
pp. H1537-H1543 ◽  
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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