Angiotensin II type 1 receptor blockade corrects cutaneous nitric oxide deficit in postural tachycardia syndrome

To reheat, or to not reheat: that is the question: The efficacy of a local reheating protocol on mechanisms of cutaneous vasodilatation

“…Additionally, Cracowski et al (2007) following a similar heat-reheat protocol, raising skin temperature at a rate of 0.09°C·s − 1 , also noted no differences in the thermal hyperemia response to a local heating stimulus (Cracowski et al, 2007). Thus, it seems as though the rapid rate of heating employed in the studies by Ciplak et al and Frantz et al may explain the conflicting results compared to those of protocols 1 and 2 of the present study and those previously published by others (Cracowski et al, 2007;Medow et al, 2011;Shastry and Joyner, 2002;Stewart et al, 2007a;Stewart et al, 2009;Stewart et al, 2011;Stewart et al, 2008a).…”

“…After 10 min, and confirmation that the recordings were stable, baseline measurements were recorded at 33°C for 10 min, local skin temperature was then increased to 42°C at 0.5°C·10 s −1 .No sensation of pain was reported by any participant as a result of the local skin heating protocol. All skin sites were maintained at 42°C until a stable plateau in skin blood flow had been achieved, after which, all skin heaters were returned to 33°C and the skin was allowed to passively cool for 60 min (Stewart et al, 2008a;Stewart et al, 2008b), though some sites did take longer to return to stable baseline skin blood flow. After a second 10 min baseline was recorded at 33°C, the reheat protocol was initiated, increasing local skin temperature as per the first heating protocol.…”

“…In protocol 1, we examined the effect of a heat-reheat protocol on cutaneous vasodilatation at forearm and leg skin sites. Based on the work of Stewart and coworkers (Medow et al, 2011;Stewart et al, 2007a;Stewart et al, 2009;Stewart et al, 2011;Stewart et al, 2008a) we hypothesized that the vasodilator response to the second bout of heating would be the same as the first. In protocol 2, we examined the effect of NOS inhibition combined with the same (protocol 1) heat-reheating procedure.…”

The Dermatological Manifestations of Postural Tachycardia Syndrome: A Review with Illustrated Cases

“…It lasts a few minutes or less, involves the jaw and neck, and does not cause warmth, pain, or pruritus. It was previously described by a case study in a patient with POTS [11]; it is proposed that EH results from focal, unevenly distributed [31][32][33][34]. This is further supported by improvement in EH with the administration of losartan, an angiotensin-II receptor blocker.…”

“…Ang-(1-7) is a product of angiotensin-II metabolism catalyzed by angiotensin-converting enzyme (ACE)-2 [32], and the study suggests that Ang-(1-7) mediates vasodilation independent of nitric oxide (NO) or angiotensin 1 receptor. In patients with POTS, ACE2 activity seems to be blunted, and the result is an increase in angiotensin-II and a decrease in Ang- (1)(2)(3)(4)(5)(6)(7) and NO [33,34].…”