SUMMARY1. Intracellular potentials and measurements of contractions were recorded in adjacent veins and arteries in the colonic mesentery of the guinea-pig in vitro during stimulation of post-ganglionic nerve trunks.2. Repetitive stimulation (0'S5-Hz) of lumbar colonic nerve trunks produced frequency-dependent slow depolarizations in all venous and in 92 % ofarterial smooth muscle cells. Excitatory junction potentials were observed for each nerve shock in arteries, but not in veins.3. Low-frequency stimulations produced slow depolarizations of greater amplitude and longer duration in veins than in arteries. The frequencies at which half-maximal depolarizations and contractions occurred were always lower for veins than for arteries.4. The az-adrenergic antagonist prazosin (5 x 10-7 M) reduced the mean arterial slow depolarizations by 82 % and reduced mean venous slow depolarizations by 58 % for 5 Hz stimulations. Arterial contractions were completely inhibited by prazosin but venous contractions were incompletely reduced in a frequency-dependent manner.5. These findings suggest that functional differences in activation between mesenteric veins and arteries during sympathetic stimulation are a result of differences in neuromuscular transmission.

SUMMARY1. The present study examined the effects of repetitive nerve stimulation on membrane potential and on contractile responses to noradrenaline in the guinea-pig inferior mesenteric artery and its distal branches.2. Repetitive stimulation of perivascular nerves evoked slow inhibitory junction potentials (IJPs) and dilator responses. Individual nerve shocks elicited excitatory junction potentials (EJP)s.3. Stimulation-evoked IJPs were abolished in the presence of tetrodotoxin 6. Pre-treatment of arteries with guanethidine (30 ,M) or 6-hydroxydopamine (0 4 mM) abolished stimulation-evoked EJPs but had no effect on stimulation-evoked IJPs. 7. In a similar manner to repetitive nerve stimulation, capsaicin (10 4uM

We investigated mechanisms mediating bradykinin (BK)-induced anterior mesenteric artery (AMA) vasodilation in anesthetized rats. The velocity of blood flowing (VBF) in the AMA was measured with pulsed Doppler velocimetry, and arterial pressure (BP) was measured with a pressure transducer. Drugs were infused through an intra-aortic catheter positioned proximal to the AMA origin. AMA conductance (C) was calculated from mean VBF/BP and expressed as percent of control C. BK infusion (10-1,000 ng.kg-1.min-1) increased C significantly (Cmax = 201 +/- 18%, ED50 = 100 ng.kg-1.min-1, P < 0.01 for all doses). A B2-subtype receptor antagonist, D-Arg,[Hyp3,Thi5.8,D-Phe7]BK, administered at 10(5) ng.kg-1.min-1 before or during BK infusion, inhibited the vasodilation by 73 +/- 7 and 103 +/- 7%, respectively. A nitric oxide (NO) synthesis inhibitor, NG-nitro-L-arginine, administered at 5.0 mg/kg 15 min before BK, inhibited the hyperemia by 61 +/- 8%. Neither a B1-receptor antagonist nor intrajejunal capsaicin inhibited BK-induced vasodilation. BK-evoked, dose-dependent, mesenteric vasodilation in rats appears to be mediated partly by B2-receptors and endogenous NO generation.

To determine the effects of exercise and high altitude on the contributions of shunt, ventilation-perfusion (V/Q) nonhomogeneity, and diffusion limitation to the alveolar-arterial O2 gradient (AaDo2), we measured pulmonary exchange of O2, CO2, and six inert gases (SF6, ethane, cyclopropane, halothane, diethyl ether, and acetone) during rest and exercise in unanesthetized dogs at sea level and after acute exposure to an altitude of 6,096 m in a hypobaric chamber. Shunt and dead-space fractions, calculated from inert gas measurements, did not change. High altitude decreased the inert gas partial pressure gradients between mixed alveolar gas and mixed end-capillary blood, indicating that V/Q relationships became more homogeneous. Exercise had no effect on these gradients. At sea level, AaDo2 was mainly due to V/Q nonhomogeneity, with a small portion due to shunt. At high altitude, the contribution of shunt became negligible and that of V/Q nonhomogeneity diminished. These improvements were partially offset, however, by a gradient due to diffusion limitation. Exercise had no effect on AaDo2 or any of its components. At high altitude, estimated pulmonary O2 diffusing capacity averaged 20.8 ml.min-1 at rest and 35.3 ml-min-1.Torr-1 during exercise.

We investigated the involvement of primary sensory nerves in intestinal autoregulatory escape induced by postganglionic nerve stimulation (NS) in anesthetized rats. Anterior mesenteric artery (AMA) blood flow velocity (BF) was measured with a pulsed Doppler flowmeter. Periarterial NS elicited an abrupt fall in BF, which was followed by a recovery in BF toward the basal value, despite sustained NS. This recovery from NS constituted the neurogenic escape phenomenon. Vasoconstrictor responses to NS were abolished by periarterial application of tetrodotoxin. Acute, surgical interruption of proximal periarterial nerves had no effect on BF responses to distal NS, suggesting a peripheral rather than a central nervous mechanism for the escape phenomenon. Escape from NS-induced vasoconstriction was significantly inhibited by prior administration of the selective sensory neurotoxin capsaicin as either subcutaneous injection in neonatal life, acute application to periarterial nerves, or acute injection into the jejunal lumen. In rats pretreated 24 h with reserpine, NS provoked a vasodilator response that was inhibited by intrajejunal capsaicin. Increases in arterial blood pressure (BP) and heart rate observed during NS were blocked by periarterial (but not intrajejunal) application of capsaicin. Transmural electrical field stimulation elicited significantly greater nerve-induced contractions in AMA rings from control rats. Our findings support the hypothesis that postganglionic NS activates both vasoconstrictor sympathetic nerve branches and vasodilator afferent C-fibers. The latter nerves release vasodilator peptides in the periphery during continuous low frequency NS that appear to be essential for autoregulatory escaped in our model.