The roles of cGMP and cAMP in active thermoregulatory vasodilation

Farrell, Daniel; Bishop, Vernon S.

doi:10.1152/ajpregu.1997.272.3.r975

Cited by 17 publications

(15 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In human skin, NO is capable of mediating cutaneous vasodilation synergistically with sympathetic cotransmitters, resulting in a combined vasodilation that is greater than the sum of the individual contributions (36). The synergistic effect may occur downstream through cross-talk between NO-mediated cGMP-dependent and sympathetic neurotransmitter(s)-mediated cAMP-dependent mechanisms (8,9), or NO may prejunctionally enhance the release of sympathetic neurotransmitter(s) (12).…”

Section: Discussionmentioning

confidence: 99%

Local ascorbate administration augments NO- and non-NO-dependent reflex cutaneous vasodilation in hypertensive humans

Holowatz¹,

Kenney²

2007

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Full expression of reflex cutaneous vasodilation (VD) is dependent on nitric oxide (NO) and is attenuated with essential hypertension. Decreased NO-dependent VD may be due to 1) increased oxidant stress and/or 2) decreased L-arginine availability through upregulated arginase activity, potentially leading to increased superoxide production through uncoupled NO synthase (NOS). The purpose of this study was to determine the effect of antioxidant supplementation (alone and combined with arginase inhibition) on attenuated NO-dependent reflex cutaneous VD in hypertensive subjects. Nine unmedicated hypertensive [HT; mean arterial pressure (MAP) = 112 +/- 1 mmHg] and nine age-matched normotensive (NT; MAP = 81 +/- 10 mmHg) men and women were instrumented with four intradermal microdialysis (MD) fibers: control (Ringer), NOS inhibited (NOS-I; 10 mM N(G)-nitro-L-arginine), L-ascorbate supplemented (Asc; 10 mM L-ascorbate), and Asc + arginase inhibited [Asc+A-I; 10 mM L-ascorbate + 5 mM (S)-(2-boronoethyl)-L-cysteine-HCl + 5 mM N(omega)-hydroxy-nor-L-arginine]. Oral temperature was increased by 0.8 degrees C via a water-perfused suit. N(G)-nitro-L-arginine was then ultimately perfused through all MD sites to quantify the change in VD due to NO. Red blood cell flux was measured by laser-Doppler flowmetry over each skin MD site, and cutaneous vascular conductance (CVC) was calculated (CVC = flux/MAP) and normalized to maximal CVC (%CVC(max); 28 mM sodium nitroprusside + local heating to 43 degrees C). During the plateau in skin blood flow (Delta T(or) = 0.8 degrees C), cutaneous VD was attenuated in HT skin (NT: 42 +/- 4, HT: 35 +/- 3 %CVC(max); P < 0.05). Asc and Asc+A-I augmented cutaneous VD in HT (Asc: 57 +/- 5, Asc+A-I: 53 +/- 6 %CVC(max); P < 0.05 vs. control) but not in NT. %CVC(max) after NOS-I in the Asc- and Asc+A-I-treated sites was increased in HT (Asc: 41 +/- 4, Asc+A-I: 40 +/- 4, control: 29 +/- 4; P < 0.05). Compared with the control site, the change in %CVC(max) within each site after NOS-I was greater in HT (Asc: -19 +/- 4, Asc+A-I: -17 +/- 4, control: -9 +/- 2; P < 0.05) than in NT. Antioxidant supplementation alone or combined with arginase inhibition augments attenuated reflex cutaneous VD in hypertensive skin through NO- and non-NO-dependent mechanisms.

show abstract

Section: Discussionmentioning

confidence: 99%

Local ascorbate administration augments NO- and non-NO-dependent reflex cutaneous vasodilation in hypertensive humans

Holowatz¹,

Kenney²

2007

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…First, bradykinin B 2 receptors are constitutively expressed, in contrast to bradykinin B 1 receptors that are induced by inflammation (30). In addition, Warren and Loi (31) found that B 2 -receptor antagonists abolished the cutaneous vasodilation induced by intradermal injections of bradykinin, whereas B 1 -receptor antagonists did not alter the response in the rabbit, a species frequently used to model the human cutaneous active vasodilator system (5,6). Bradykinin B 2 receptors effect vasodilation by stimulating nitric oxide or eicosanoid production (29,31), and cutaneous active vasodilation in humans is also known to involve nitric oxide (14,28), thus suggesting a possible role for the B 2 -receptor subtype in cutaneous active vasodilation.…”

Section: Discussionmentioning

confidence: 99%

Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans

Kellogg

Liu

McAllister

et al. 2002

Journal of Applied Physiology

View full text Add to dashboard Cite

To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B(2) receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 microM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 +/- 2% maximal CVC, P < 0.01) and untreated sites (65 +/- 2% maximal CVC, P < 0.01). These responses did not differ between sites (P > 0.05). Because the bradykinin B(2)-receptor antagonist HOE-140 did not alter SkBF responses to heat stress, we conclude that bradykinin does not mediate cutaneous active vasodilation.

show abstract

“…Our findings at 30°C may have some physiological relevance as this temperature is reached during moderate cooling that in some circumstances may occur physiologically in the rabbit ear artery [11], which is a superficial artery involved in thermoregulation [25] and has perivascular sympathetic endings containing NPY [28]. Therefore, NPY, by facilitating the cutaneous vasoconstriction in response to sympathetic stimulation at low ambient temperatures, might participate in the regulation of body temperature by reducing cutaneous blood flow and preventing body heat losses.…”

Section: Discussionmentioning

confidence: 61%

“…The temperature of the bath was adjusted from the beginning of the experiment to 37°C or 30°C (cooling), and the arteries remained at the chosen temperature for the duration of the experiment. This temperature of 30°C was chosen to study the effects of cooling, because previous studies have shown that it produces clear differences in the vascular response compared with 37°C [24], and it is a temperature that may occur in the skin of the rabbit ear in physiological conditions [11].…”

Section: Methodsmentioning

confidence: 99%

Effect of neuropeptide Y on the sympathetic contraction of the rabbit central ear artery during cooling

Garcı́a-Villalón

Padilla

Fernández

et al. 2000

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

In order to analyse the effect of neuropeptide Y (NPY) on the cutaneous vascular response to sympathetic nerve stimulation during cooling, the isometric response of isolated 2-mm segments of the rabbit central ear (cutaneous) artery was recorded at 37 degrees C and during cooling (30 degrees C). Electrical field stimulation (4-16 Hz) at 37 degrees C produced a frequency-dependent contraction, which was reduced during cooling (45% for 16 Hz) and potentiated by NPY (10(-8), 3x10(-8) and 10(-7) M), this potentiation being greater at 30 degrees C than at 37 degrees C. The NPY-induced potentiation of the contraction elicited by electrical field stimulation (8 Hz) was abolished by an antagonist of Y1 subtype NPY receptors, BIBP3226 (10(-6) M), at 37 degrees C and 30 degrees C, reduced by phentolamine (10(-6) M) at 30 degrees C but not at 37 degrees C, was not modified by the purinoceptor antagonist PPADS (3x10(-5) M) and was reduced by application of both phentolamine and PPADS at both temperatures. Both NiCl2 (10(-3) M) and verapamil (10(-5) M) abolished the potentiating effect of NPY at 37 degrees C and reduced it at 30 degrees C. Neither application of an inhibitor of nitric oxide synthesis, L-Nomega-nitro-arginine (L-NOARG, 10(-4) M), nor endothelium removal modified the potentiating effect of NPY at 37 degrees C or 30 degrees C. NPY (10(-8), 3x10(-8) and 10(-7) M) potentiated in a concentration-dependent way the arterial contraction in response to exogenous noradrenaline (10(-8)-10(-4) M) at 30 degrees C but not at 37 degrees C, and it increased the response to ATP (10(-4)-10(-2) M) at both temperatures. Therefore, in cutaneous (ear) arteries: (1) NPY potentiates the sympathetic response at 37 degrees C and at 30 degrees C, (2) this potentiating effect of NPY was more marked at 30 degrees C than at 37 degrees C, probably because of greater potentiation of the alpha-adrenoceptor response during cooling, and (3) the potentiating effect of NPY at both temperatures is mediated by NPY receptors of the Y1 subtype, is dependent of Ca2+ channels and is independent of the release of endothelial nitric oxide.

show abstract

The roles of cGMP and cAMP in active thermoregulatory vasodilation

Cited by 17 publications

References 0 publications

Local ascorbate administration augments NO- and non-NO-dependent reflex cutaneous vasodilation in hypertensive humans

Local ascorbate administration augments NO- and non-NO-dependent reflex cutaneous vasodilation in hypertensive humans

Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans

Effect of neuropeptide Y on the sympathetic contraction of the rabbit central ear artery during cooling

Contact Info

Product

Resources

About