Abstract P195: Hypertension is Associated With an Abnormal Pressor Response to Voluntary Apnea

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Noah Jouett ◽  
Ryan Mason ◽  
Dorene Niv ◽  
Donald E Watenpaugh ◽  
Michael L Smith

Background: Cardiovascular diseases are commonly associated with elevated sympathetic nerve activity (SNA). Previously, we have shown that the blood pressure response to a voluntary apnea is closely correlated with the SNA response in patients with sleep disordered breathing (SDB) and thus may serve as an index of SNA responsiveness. In the current study, we hypothesized that the pressor response to apnea is 1) reduced with effective treatment of SDB in SDB patients, and 2) that it is exaggerated in hypertensive patients (HTN) when compared to healthy control subjects. Methods: 22 OSA patients (14 treated and 8 untreated), 19 treated hypertensive patients and 23 healthy normotensive control subjects were recruited from the UNTHSC Primary Care Center and Sleep Consultants of Texas. Subjects completed a medical history questionnaire and Epworth Sleepiness survey. Blood pressure was measured by standard auscultatory assessment in the seated position. Baseline blood pressure was obtained in triplicate during quiet rest. Then after practicing a voluntary breath hold, subjects repeated three voluntary 20-second breath holds each beginning at end-expiration. Comparisons were made 1) between treated and untreated SDB patients, and 2) between HTN patients and healthy control subjects using a Student t test. Results: Importantly, as in prior studies the pressor response to apnea was not different from zero in the healthy control subjects (-1.0 ± 4.2 mmHg, p>0.05). In the SDB patients, the pressor response was significantly greater than zero in both treated (11.4 ± 3.9 mm Hg) and untreated (24.5 ± 9.8 mm Hg) SDB patients (p<0.001), and was significantly reduced in the treated SDB patients (p<0.001). In addition, the pressor response was significantly greater in the HTN patients (10.5 ± 5.3 mmHg, p<0.001) compared to the healthy control subjects. Conclusions: These data support our hypotheses that the pressor response to voluntary apnea is exaggerated in both untreated SDB and treated HTN patients and that effective treatment of SDB reduces this response, but does not normalize the response. These data suggest that the pressor response to apnea may be a simple physiologic index of exaggerated sympathetic responsiveness.

2009 ◽  
Vol 3 (3) ◽  
pp. 94
Author(s):  
Kyungdon Ryu ◽  
Young-Sub Byun ◽  
Byoung Kwon Lee ◽  
Choong-Won Goh ◽  
Kun-Joo Rhee

1994 ◽  
Vol 267 (6) ◽  
pp. E921-E926 ◽  
Author(s):  
D. T. Van den Berg ◽  
W. de Jong ◽  
E. R. de Kloet

We report here that with a direct method for measurement of cardiovascular parameters in conscious rats, intracerebroventricular administration of the mineralocorticoid receptor (MR) antagonist RU-28318 (100 ng) reduces the blood pressure, heart rate, and the corticosterone response to a brief restraint stress, provided the rats were previously subjected to a daily 30-min exposure to 32 degrees C for 2 wk. The daily exposure to warming and restraint stress are applied identically to the training procedure required for indirect blood pressure measurement using the tail-cuff method. The basal arterial pressure is not affected by the MR antagonist. The effect of the MR antagonist on the stress-induced pressor response develops with a delay of several hours in the normotensive rats. The corticosterone response to daily warming and stress is also attenuated by the intracerebroventricular infusion of MR antagonist but with shorter onset and shorter duration. The findings suggest that conditioning to daily warming and stress imposes mineralocorticoid dependency of the pressor response, which involves MR functioning in brain.


1994 ◽  
Vol 77 (6) ◽  
pp. 2761-2766 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
P. S. Clifford

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.


Diabetologia ◽  
2010 ◽  
Vol 53 (7) ◽  
pp. 1295-1303 ◽  
Author(s):  
E. I. Ekinci ◽  
G. Thomas ◽  
R. J. MacIsaac ◽  
C. Johnson ◽  
C. Houlihan ◽  
...  

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