scholarly journals Acute blood pressure elevation during repetitive hypocapnic and eucapnic hypoxia in rats

1997 ◽  
Vol 82 (4) ◽  
pp. 1071-1078 ◽  
Author(s):  
Gang Bao ◽  
Preet M. Randhawa ◽  
Eugene C. Fletcher
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Parasympathetic Nervous System ◽  
Cardiovascular Response ◽  
Nerve Activity ◽  
Blood Pressure Elevation ◽  
Wky Rats ◽  
Pressure Elevation ◽  
Adrenergic Blocker

Bao, Gang, Preet M. Randhawa, and Eugene C. Fletcher.Acute blood pressure elevation during repetitive hypocapnic and eucapnic hypoxia in rats. J. Appl. Physiol. 82(4): 1071–1078, 1997.—Using a rat model, we investigated whether episodic eucapnic hypoxia was a more potent stimulus to acute blood pressure (BP) elevation and bradycardia than episodic hypocapnic hypoxia. We also investigated the role of sympathetic and parasympathetic nervous system in this cardiovascular response. Sprague-Dawley (SD) and Wistar Kyoto (WKY) rats were exposed to repetitive 30-s cycles of hypocapnic or eucapnic hypoxia before and after intravenous injection of the α1-adrenergic blocker prazosin, α2-adrenergic blocker yohimbine, or atropine. Eucapnic hypoxia caused a threefold elevation in systolic BP from baseline (83.5 ± 3.5 mmHg in WKY, 70.6 ± 4.6 mmHg in SD) and greater bradycardia (−178 ± 20 beats/min in WKY, −178 ± 21 beats/min in SD) compared with hypocapnic hypoxia (29.8 ± 3.6 mmHg and −43 ± 15 beats/min in WKY, 19.0 ± 4.1 mmHg and −45 ± 12 beats/min in SD). After prazosin, the BP increase from eucapnic hypoxia was blunted, yohimbine showed no effect, and atropine blocked the bradycardia. Direct measurement of sympathetic nerve activity confirmed that adding CO2 to the hypoxic gas mixture caused a 61% increase in sympathetic nerve activity. WKY rats seem more vulnerable than SD rats to both hypoxia exposures in terms of the elevation in BP. We conclude that, in the rat, eucapnic hypoxia is a more potent stimulus to acute BP elevation and bradycardia than is hypocapnic hypoxia. An increased sympathetic tone appears to be involved in the BP response to acute episodic hypoxia.

The effect of aging on blood pressure elevation in response to muscle sympathetic nerve activity

1995 ◽  
Vol 56 (1-2) ◽  
pp. 130
Author(s):  
Yoshiki Sugiyama ◽  
Hisashi Okada ◽  
Takemasa Watanabe ◽  
Toshiyoshi Matsukawa ◽  
Satoshi Iwase ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Blood Pressure Elevation ◽  
Pressure Elevation

scholarly journals Chronic intermittent hypoxia in humans during 28 nights results in blood pressure elevation and increased muscle sympathetic nerve activity

2010 ◽  
Vol 299 (3) ◽  
pp. H925-H931 ◽  
Author(s):  
G. S. Gilmartin ◽  
M. Lynch ◽  
R. Tamisier ◽  
J. W. Weiss
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Intermittent Hypoxia ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Chronic Intermittent Hypoxia ◽  
Sympathetic Activation ◽  
Nerve Activity ◽  
Blood Pressure Elevation ◽  
Healthy Humans

Chronic intermittent hypoxia (CIH) is thought to be responsible for the cardiovascular disease associated with obstructive sleep apnea (OSA). Increased sympathetic activation, altered vascular function, and inflammation are all putative mechanisms. We recently reported (Tamisier R, Gilmartin GS, Launois SH, Pepin JL, Nespoulet H, Thomas RJ, Levy P, Weiss JW. J Appl Physiol 107: 17–24, 2009) a new model of CIH in healthy humans that is associated with both increases in blood pressure and augmented peripheral chemosensitivity. We tested the hypothesis that exposure to CIH would also result in augmented muscle sympathetic nerve activity (MSNA) and altered vascular reactivity contributing to blood pressure elevation. We therefore exposed healthy subjects between the ages of 20 and 34 yr ( n = 7) to 9 h of nocturnal intermittent hypoxia for 28 consecutive nights. Cardiovascular and hemodynamic variables were recorded at three time points; MSNA was collected before and after exposure. Diastolic blood pressure (71 ± 1.3 vs. 74 ± 1.7 mmHg, P < 0.01), MSNA [9.94 ± 2.0 to 14.63 ± 1.5 bursts/min ( P < 0.05); 16.89 ± 3.2 to 26.97 ± 3.3 bursts/100 heartbeats (hb) ( P = 0.01)], and forearm vascular resistance (FVR) (35.3 ± 5.8 vs. 55.3 ± 6.5 mmHg·ml−1·min·100 g tissue, P = 0.01) all increased significantly after 4 wk of exposure. Forearm blood flow response following ischemia of 15 min (reactive hyperemia) fell below baseline values after 4 wk, following an initial increase after 2 wk of exposure. From these results we conclude that the increased blood pressure following prolonged exposure to CIH in healthy humans is associated with sympathetic activation and augmented FVR.

Sympathetic nerve activity: role in regulation of blood pressure in the spontaenously hypertensive rat.

1976 ◽  
Vol 38 (6) ◽  
pp. 21-29 ◽  
Author(s):  
W V Judy ◽  
A M Watanabe ◽  
D P Henry ◽  
H R Besch ◽  
W R Murphy ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Hypertensive Rat ◽  
Regulation Of Blood Pressure

scholarly journals Effects of bunazosin on blood pressure, sympathetic nerve activity, urinary catecholamines and urinary electrolytes in rats

1986 ◽  
Vol 40 ◽  
pp. 71
Author(s):  
Hiroko Togashi ◽  
Masaru Minami ◽  
Machiko Sano ◽  
Mitsuhiro Yoshioka ◽  
Iwao Saito ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Urinary Catecholamines

scholarly journals Chronic femoral artery ligation exaggerates the pressor and sympathetic nerve responses during dynamic skeletal muscle stretch in decerebrate rats

2018 ◽  
Vol 314 (2) ◽  
pp. H246-H254 ◽  
Author(s):  
Evan A. Kempf ◽  
Korynne S. Rollins ◽  
Tyler D. Hopkins ◽  
Alec L. Butenas ◽  
Joseph M. Santin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Peripheral Artery Disease ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Peripheral Artery ◽  
Nerve Activity ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Artery Disease ◽  
Dynamic Stretch

Mechanical and metabolic signals arising during skeletal muscle contraction reflexly increase sympathetic nerve activity and blood pressure (i.e., the exercise pressor reflex). In a rat model of simulated peripheral artery disease in which a femoral artery is chronically (~72 h) ligated, the mechanically sensitive component of the exercise pressor reflex during 1-Hz dynamic contraction is exaggerated compared with that found in normal rats. Whether this is due to an enhanced acute sensitization of mechanoreceptors by metabolites produced during contraction or involves a chronic sensitization of mechanoreceptors is unknown. To investigate this issue, in decerebrate, unanesthetized rats, we tested the hypothesis that the increases in mean arterial blood pressure and renal sympathetic nerve activity during 1-Hz dynamic stretch are larger when evoked from a previously “ligated” hindlimb compared with those evoked from the contralateral “freely perfused” hindlimb. Dynamic stretch provided a mechanical stimulus in the absence of contraction-induced metabolite production that closely replicated the pattern of the mechanical stimulus present during dynamic contraction. We found that the increases in mean arterial blood pressure (freely perfused: 14 ± 1 and ligated: 23 ± 3 mmHg, P = 0.02) and renal sympathetic nerve activity were significantly greater during dynamic stretch of the ligated hindlimb compared with the increases during dynamic stretch of the freely perfused hindlimb. These findings suggest that the exaggerated mechanically sensitive component of the exercise pressor reflex found during dynamic muscle contraction in this rat model of simulated peripheral artery disease involves a chronic sensitizing effect of ligation on muscle mechanoreceptors and cannot be attributed solely to acute contraction-induced metabolite sensitization. NEW & NOTEWORTHY We found that the pressor and sympathetic nerve responses during dynamic stretch were exaggerated in rats with a ligated femoral artery (a model of peripheral artery disease). Our findings provide mechanistic insights into the exaggerated exercise pressor reflex in this model and may have important implications for peripheral artery disease patients.

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