cGMP release in rat mesenteric arterioles and in conduit mesenteric artery

Abstract

1. Relaxing factors were studied in two perfused preparations of the same vascular area in the rat: resistance mesenteric arterioles and conduit mesenteric artery. 2. In both preparations, an acetylcholine (ACh) infusion inhibited noradrenaline (NA) vasoconstrictor effects but at a ten-times greater concentration in conduit artery than in resistance arterioles. 3. Endothelium destruction with hypotonic Krebs solution did not change basal perfusion pressure, but increased NA responses and suppressed ACh inhibitory effects in arterioles and arteries. Likewise, L-NAME abolished the ACh effect in mesenteric arterioles but only reduced it in mesenteric artery. 4. Basal release of cyclic GMP was significantly greater in mesenteric artery than in resistance arterioles. By contrast, ACh-induced cGMP release was higher in mesenteric arterioles. Endothelium removal did not change basal release of cGMP in mesenteric arterioles but reduced it in mesenteric artery. 5. These results suggest that in basal conditions several relaxing factors are present in higher concentrations in conduit mesenteric artery than in resistance mesenteric arterioles. However, although it releases higher basal amount of cGMP, this vessel has a reduced role in vascular control than do smaller arteries.

Effects of exercise training on responsiveness of the mesenteric arterial bed to phenylephrine and KCl in male rats

“…On the other hand, training has been reported to increase basal NO in nontrained vascular beds, and the mesenteric vascular beds are analogous to non‐exercised forearm muscle of cycling training ( Kingwell et al ., 1997 ). In order to prove these possibilities, we perfused the mesenteric arterial beds with flow rate of 2 ml min −1 ( Dubois‐Aubecq et al ., 1996 ; Hendriks et al ., 1992 ; Randall et al ., 1988 ) versus 5 ml min −1 ( Kamata & Makino, 1997 ; Parsons et al ., 1994 ; Ralevic & Burnstock, 1996 ), and the D‐R curves to KCl were obtained in the absence or presence of L ‐NOARG for the arterial beds from both exercise‐trained and sedentary control rats. It would be expected that if there had been a structural adaptation, the basal perfusion pressure and the responses to KCl of those from exercise‐trained animals would be greater than those of control.…”

“…On the other hand, training has been reported to increase basal NO in nontrained vascular beds, and the mesenteric vascular beds are analogous to non-exercised forearm muscle of cycling training (Kingwell et al, 1997). In order to prove these possibilities, we perfused the mesenteric arterial beds with¯ow rate of 2 ml min 71 (Dubois-Aubecq et al, 1996;Hendriks et al, 1992;Randall et al, 1988) versus 5 ml min 71 (Kamata & Figure 5 Eects of N G -nitro-L-arginine, LN, 300 mM (left) and indomethacin, IDM, 1 mM (right) on the increase in perfusion pressure responses to phenylephrine of the mesenteric arterial beds of sedentary control (con) and exercise-trained (sw) rats. Each point represents mean+s.e.mean of 5 ± 11 experiments.…”

Human C-reactive protein induces endothelial dysfunction and uncoupling of eNOS in vivo

“…After vessels obtained stable basal tone (~60 min), the concentration-dependent responses to acetylcholine (ACh, 0.1 nM to 0.1 mM) and sodium nitroprusside (SNP, 0.1 nM to 10 μM) were examined. In vessels from control rats without HuSA or CRP treatment, vasodilations to ACh and SNP were evaluated before and after incubation with NOS inhibitor L-NAME (10 μM) (5,23,24) for 30 min or following intraluminal incubation with CRP (7 μg/ml) or boiled CRP (7 μg/ml) for 60 min. Mesenteric arterioles were exposed to each dose of the vasodilator agents for 1–2 min until a stable diameter was established.…”