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

Abstract

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.

Experimental Physiology –Research Paper: The effect of cooling on the contractility of equine digital small lamellar arteries: modulating role of the endothelium

“…Therefore, the use of 30 • C as a control condition represents a suitable temperature to analyse the effect of a moderate reduction of temperature on this cutaneous superficial A B vasculature. Furthermore, in other cutaneous vascular beds, such as the rabbit ear artery, in vitro experiments have been conducted using the superficial skin temperature as a closer physiological temperature for this superficial artery (Garcia-Villalon et al 2000). Indeed, other researchers have also chosen a similar temperature (31 • C) to conduct in vitro experiments on the same vascular bed in pigs (Blaylock & Wilson, 1995).…”

Role of α2C‐adrenoceptors in the reduction of skin blood flow induced by local cooling in mice

“…Unlike in rats, about half of the cooling‐induced response in mice was insensitive to phentolamine. Several mediators other than catecholamines and ATP, such as NO (Hodges et al , 2006; Yamazaki et al , 2006), vasopressin (García‐Villalón et al , 1999), endothelin‐1 (García‐Villalón et al , 1997), neuropeptide Y (García‐Villalón et al , 2000), 5‐hydroxytryptamine and angiotensin II (Furspan et al , 2004), have also been suggested to participate in cooling‐induced vasoconstriction. Further investigations are needed to elucidate the mechanism for the cooling‐induced response that is not affected by α ‐adrenoceptor antagonists in mice.…”

Altered neurotransmitter control of reflex vasoconstriction in aged human skin

“…ATP is commonly costored with NA in small vesicles (compared to NA–NPY costorage in large, dense‐core vesicles) in many sympathetic adrenergic nerves (Lundberg, 1996; Burnstock, 1999). ATP participates in VC responses to low‐frequency electrical nerve stimulation (Ralevic & Burnstock, 1991; Racchi et al 1999; García‐Villalón et al 2000; Bradley et al 2003) and lower body negative pressure (Taddei et al 1990) in thermoregulatory cutaneous circulations; this VC is mediated by P 2X purinoceptors, which are found on vascular smooth muscle. Together, these studies suggest that NPY and/or ATP may actively function as cotransmitters in young human skin.…”