scholarly journals Increased vascular α1-adrenergic receptor sensitivity in older adults with posttraumatic stress disorder

2020 ◽  
Vol 319 (6) ◽  
pp. R611-R616
Author(s):  
Cortnie L. Hartwig ◽  
Justin D. Sprick ◽  
Jinhee Jeong ◽  
Yingtian Hu ◽  
Doree G. Morison ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Sympathetic Nerve ◽  
Stress Disorder ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Blood Pressure Reactivity ◽  
Pressure Reactivity

Posttraumatic stress disorder (PTSD) is an independent risk factor for the development of hypertension and cardiovascular disease. Patients with PTSD have heightened blood pressure and sympathetic nervous system reactivity; however, it is unclear if patients with PTSD have exaggerated vasoconstriction in response to sympathetic nerve activation that could also contribute to increased blood pressure reactivity. Therefore, we hypothesized that patients with PTSD have increased sensitivity of vascular α1-adrenergic receptors (α1ARs), the major mediators of vasoconstriction in response to release of norepinephrine at sympathetic nerve terminals. To assess vascular α1AR sensitivity, we measured the degree of venoconstriction in a dorsal hand vein in response to exponentially increasing doses of the selective α1AR agonist, phenylephrine (PE), in 9 patients with PTSD (age = 59 ± 2 yr) and 10 age-matched controls (age = 60 ± 1 yr). Individual dose-response curves were generated to determine the dose of PE that induces 50% of maximal venoconstriction (i.e., PE ED50) reflective of vascular α1AR sensitivity. In support of our hypothesis, PE ED50 values were lower in PTSD compared with controls (245 ± 54 ng/min vs. 1,995 ± 459 ng/min, P = 0.012), indicating increased vascular α1AR sensitivity in PTSD. The PTSD group also had an increase in slope of rise in venoconstriction, indicative of an altered venoconstrictive reactivity to PE compared with controls (19.8% ± 1.2% vs. 15.1% ± 1.2%, P = 0.009). Heightened vascular α1AR sensitivity in PTSD may contribute to augmented vasoconstriction and blood pressure reactivity to sympathoexcitation and to increased cardiovascular disease risk in this patient population.

Current Posttraumatic Stress Disorder and Cardiovascular Disease Risk Factors in Dutch Resistance Veterans from World War II

1992 ◽  
Vol 57 (4) ◽  
pp. 164-171 ◽  
Author(s):  
Paul R.J. Falger ◽  
Wybrand Op den Velde ◽  
Johannes E. Hovens ◽  
Erik G.W. Schouten ◽  
Johannes H.M. De Groen ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Posttraumatic Stress Disorder ◽  
World War Ii ◽  
Posttraumatic Stress ◽  
Stress Disorder ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
World War ◽  
Resistance Veterans

scholarly journals Early onset neurocirculatory response to static handgrip is associated with greater blood pressure variability in women with posttraumatic stress disorder

2020 ◽  
Vol 318 (1) ◽  
pp. H49-H58 ◽  
Author(s):  
Jeung-Ki Yoo ◽  
Mark B. Badrov ◽  
Rosemary S. Parker ◽  
Elizabeth H. Anderson ◽  
Jessica L. Wiblin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Posttraumatic Stress Disorder ◽  
Muscle Contraction ◽  
Posttraumatic Stress ◽  
Early Onset ◽  
Stress Disorder ◽  
Muscle Sympathetic Nerve Activity ◽  
Pressor Responses ◽  
Increased Risk

Posttraumatic stress disorder (PTSD) is a psychiatric illness that is more prevalent in women, and accumulating evidence suggests a link between PTSD and future development of cardiovascular disease. The underlying mechanisms are unclear, but augmented sympathetic reactivity to daily stressors may be involved. We measured muscle sympathetic nerve activity (MSNA), blood pressure (BP), and heart rate responses in 14 women with PTSD and 14 healthy women (controls) during static handgrip (SHG) exercise to fatigue at 40% of maximal voluntary contraction (MVC). Two minutes of postexercise circulatory arrest (PECA) was followed immediately after SHG to fatigue. MVC and the time to fatigue during SHG did not differ between groups (both P > 0.05). At the first 30 s of SHG, women with PTSD showed augmented sympathetic neural [mean ± SD, ∆MSNA burst frequency (BF): 5 ± 4 vs. 2 ± 3 bursts/30 s, P = 0.02 and ∆MSNA total activity (TA): 82 ± 58 vs. 25 ± 38 arbitrary units/30 s, P = 0.004] and pressor (∆systolic BP: 10 ± 5 vs. 4 ± 3 mmHg, P = 0.003) responses compared with controls. However, MSNA and BP responses at fatigue and during PECA were not different between groups. More interestingly, the augmented initial neural and pressor responses to SHG were associated with greater awake systolic BP variability during ambulation in women with PTSD (MSNA BF: r = 0.55, MSNA TA: r = 0.62, and SBP: r = 0.69, all P < 0.05). These results suggest that early onset exercise pressor response in women with PTSD may be attributed to enhanced mechano- rather than metaboreflexes, which might contribute to the mechanisms underlying the link between PTSD and cardiovascular risk. NEW & NOTEWORTHY The novel findings of the current study are that women with posttraumatic stress disorder (PTSD) exhibited augmented sympathetic neural and pressor responses at the first 30 s of submaximal isometric muscle contraction. More interestingly, exaggerated neurocirculatory responses at the onset of muscle contraction were associated with greater ambulatory awake systolic blood pressure fluctuations in women with PTSD. Our findings expand the knowledge on the physiological mechanisms that perhaps contribute to increased risk of cardiovascular disease in such a population.

Is stressor-evoked cardiovascular reactivity a pathway linking positive and negative emotionality to carotid intima-media thickness?

2020 ◽  
Author(s):  
Caitlin Marie DuPont ◽  
Aidan G.C. Wright ◽  
Stephen N. Manuck ◽  
Matthew Muldoon ◽  
J. Richard Jennings ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Heart Rate ◽  
Cardiovascular Reactivity ◽  
Disease Risk ◽  
Negative Emotionality ◽  
Heart Rate Reactivity ◽  
Positive Emotionality ◽  
Blood Pressure Reactivity ◽  
Pressure Reactivity

Stressor-evoked cardiovascular reactivity, trait positive emotionality, and negative emotionality are all associated with cardiovascular disease. It is unknown, however, whether cardiovascular reactivity may constitute a pathway by which trait positive or negative emotionality relates to disease risk. Accordingly, this study modeled the cross-sectional relationships between trait positive and negative emotionality, stressor-evoked cardiovascular reactivity, and severity of a subclinical vascular marker of cardiovascular risk, carotid artery intima-media thickness (CA-IMT). The sample consisted of healthy, midlife adults free from clinical cardiovascular disease (N = 286; ages 30-54; 50% female). Trait positive and negative emotionality were measured by three questionnaires. Heart rate and blood pressure reactivity were assessed across three stressor tasks. CA-IMT was assessed by ultrasonography. Latent factors of positive and negative emotionality, blood pressure reactivity, heart rate reactivity, and CA-IMT were created using structural equation modeling. Greater negative emotionality was marginally associated with more CA-IMT (β = .21; p = .049), but lower blood pressure reactivity (β = -.19; p = .03). However, heightened blood pressure (β = .21; p = .03), but not heart rate reactivity (β = -.05; p = .75), associated with greater CA-IMT. Positive emotionality was uncorrelated with cardiovascular reactivity (blood pressure: β = -.04; p = .61; heart rate: β = .16; p = .11) and CA-IMT (β = .16; p = .07). Although trait negative emotionality associates with a known marker of cardiovascular disease risk, independent of positive emotionality, it is unlikely via a stressor-evoked cardiovascular reactivity pathway.

scholarly journals Age modification of ozone associations with cardiovascular disease risk in adults: a potential role for soluble P-selectin and blood pressure

2018 ◽  
Vol 10 (7) ◽  
pp. 4643-4652 ◽  
Author(s):  
Drew B. Day ◽  
Merlise A. Clyde ◽  
Jianbang Xiang ◽  
Feng Li ◽  
Xiaoxing Cui ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Potential Role ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Soluble P
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