Non-uniform effects of neurohumoral agents on the internal diameter in parallel and series arranged small arteries in rabbit hindlimb.

Abstract

Using X-ray angiography, the internal diameter (ID) of 31 sites of arteries in the hindlimb, i.e., the iliac, main femoral, profundal femoral, circumflex femoral, saphenous, and popliteal arteries, was measured in anesthetized rabbits. ID under the control condition was 294-1,796 µm, but was changed to 376-1,828 µm, 127-1,914 µm, and 423-2,098 ,um with administration of hexamethonium bromide, noradrenaline, and phentolamine, respectively. The constrictor effects of noradrenaline and plasma catecholamine were larger in the femoral artery than in the iliac artery. At the transition site from the iliac to the femoral artery, ID per unit length increased from 190 µm/10 mm in the control to 320 ,um/10 mm with noradrenaline. The constrictor effects of sympathetic nerve activity (SNA) on the profundal femoral, circumflex femoral, saphenous, and popliteal arteries varied among 19 out of 20 sites. Plasma catecholamine constricted ID at 18 sites but dilated it at 2 sites. Noradrenaline constricted ID at all 20 sites, particularly in the popliteal and saphenous arteries. It was concluded that the effects of SNA and plasma catecholamine on ID of rabbit hindlimb arteries were qualitatively and quantitatively non-uniform among different arteries and at different sites of the given artery.

Selective Prostacyclin Receptor Agonist Selexipag, in Contrast to Prostacyclin Analogs, Does Not Evoke Paradoxical Vasoconstriction of the Rat Femoral Artery

“…The contractile synergy between femoral EP 3 receptors and a 1 ARs described here and by others (Hung et al, 2006) may contribute to the well documented peripheral muscle pain (myalgia) reported in patients with PAH receiving treatment with PGI 2 analogs (Tapson et al, 2012(Tapson et al, , 2013Pagani-Estévez et al, 2017). Involvement of other lower limb arteries that are under adrenergic control (e.g., the popliteal artery) (Sada et al, 1985) cannot be excluded. Although the development of pain is considered to arise from IP and EP 3 receptor-dependent sensitization of sensory afferent neurons (Nakae et al, 2005;Southall and Vasko, 2001), our data support an additional vascular mechanism.…”