Key result
Posttraumatic stress disorder was associated with increased vascular α1-adrenergic receptor sensitivity compared to controls (PE ED50 245 vs. 1,995 ng/min; P=0.012).
Why the study?
It was unclear whether patients with PTSD have exaggerated vasoconstriction in response to sympathetic nerve activation contributing to heightened blood pressure reactivity.
Do older adults with PTSD have increased vascular α1-adrenergic receptor sensitivity compared to age-matched controls?
Case-Control (n=19)
Do older adults with PTSD have increased vascular α1-adrenergic receptor sensitivity compared to age-matched controls?
Absolute Event Rate: 245% vs 1995%
p-value: p=0.012
Older adults with PTSD exhibit heightened vascular α1-adrenergic receptor sensitivity, which may contribute to augmented blood pressure reactivity and increased cardiovascular risk.
May augment vasoconstriction and BP reactivity in PTSD; hypothesis-generating for mechanisms, needs prospective trials before practice change.
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 ED50values 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.
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Hartwig et al. (2020) conducted a case-control in Posttraumatic stress disorder (n=19). Posttraumatic stress disorder vs. Age-matched controls was evaluated on Dose of phenylephrine (PE) that induces 50% of maximal venoconstriction (PE ED50) (p=0.012). Posttraumatic stress disorder was associated with increased vascular α1-adrenergic receptor sensitivity compared to controls (PE ED50 245 vs. 1,995 ng/min; P=0.012).