VISCOELASTIC BEHAVIOR OF IN-SITU AORTIC-WALL DURING HEMORRHAGIC HYPOTENSION

Viscoelastic and electrophysiological mechanisms have been implicated in resetting of baroreceptors in hypertension, but resetting in respon se to hypotension has been less exhaustively studied. To assess the im portance of viscoelastic mechanisms in hypotension, we examined the be havior of the ''in situ'' aorta during hemorrhage. Fifteen minutes of hemorrhage in anesthetized Wistar rats produced stable hypotension (30 mmHg) and a progressive contraction of the mean aortic caliber (-93.8 +/- 18.0 mu m, P < 0.05) compared with control measurements. Contract ion was not altered by sinoaortic denervation, vagotomy, nephrectomy, adrenalectomy, hexamethonium (30 mg/kg), losartan (10 mg/kg), V-1 anta gonist (10 mu g/kg), arterial pH and blood gas control, or indomethaci n (3.0 mg/kg). Aortic contraction was greater in rats treated with N-o mega-nitro-L-arginine (-164.0 +/- 43.0 mu m, P < 0.05) than in those t reated with sodium nitroprusside (-54.1 +/- 7.5 mu m, P < 0.05). The r esults indicate that aortic contraction is compatible with viscoelasti c contraction and suggest that shortening of viscoelastic elements in series with baroreceptor endings increases stress at the baroreceptor membrane and contributes to the development of baroreceptor resetting to hypotension.