Using guinea-pig mesenteric arteries and arterioles, we investigated the membrane potential of endothelial cells at rest and during application of acetylcholine (ACh) with and without the smooth muscle layers attached. When smooth muscle and endothelial layers were in close apposition, the resting membrane potentials of the two types of cells were closely related and were slightly more negative in the smooth muscle cells than in the endothelial cells. Once the endothelial layer was separated from the smooth muscle layer, the endothelial cells depolarized (the average, -4.2 mV). In the isolated endothelial layer, ACh did not induce a membrane hyperpolarization as expected, but did induce a quick depolarization soon after conventional whole-cell recording was started. However, as the pipette solution (high K⁺) gradually diffused into the endothelial layer, the membrane response to ACh gradually changed toward hyperpolarization. ACh-induced hyperpolarization was also observed after incubating preparations in a high-potassium bath solution. Our results indicate that vascular smooth muscle cells and endothelial cells are influencing each other as a functional unit and that the endothelial cells rely on the smooth muscle cells for their intracellular ionic composition and resting membrane potential.

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The purpose of this study was to investigate the changes in vasocontractile responses in atherosclerosis, using abdominal aortic strips isolated from Watanabe heritable hyperlipidemic (WHHL) rabbits and Japanese White (control) rabbits. The aortic strips from WHHL rabbits showed a significantly lower contractile response to angiotensin II than that in strips from control rabbits. The contractile responses to phenylephrine and 5-hydroxytryptamine were not different in WHHL and control groups. The contractile response to angiotensin II was higher in endothelium-denuded aortic strips than in endothelium-intact strips, but to a greater extent in the control group than in the WHHL group. The contractile response to angiotensin II in the absence of the endothelium was also lower in the WHHL group than in the control group. Pretreatment with N^G-nitro-L-arginine significantly increased the contractile response to angiotensin II in the endothelium-intact aortic strips in both the WHHL and control groups, while pretreatment with diclofenac did not affects the aortic contractile response to angiotensin II. The contractile responses to angiotensin II in the presence of N^G-nitro-L-arginine and diclofenac were lower in the WHHL group than in the control group. The contractile response to angiotensin II in the presence of PD123319 was also lower in the WHHL group than in the control group. Endothelium-dependent relaxation by acetylcholine occurred to the some extent in the WHHL and control groups. These results suggest that the WHHL rabbit abdominal aorta displays attenuated angiotensin II-induced contraction, mainly due to an abnormality in the angiotensin II-specific contractile pathway of the medial smooth muscle.

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In order to characterize the motor activity of a surgically constructed gastric tube, several hours of ambulatory intraluminal pressure recordings were performed in 6 patients following esophagectomy and gastric tube construction. Whole pressure waves were spectrally analyzed by Fast Fourier Transform (FFT). Simultaneous abdominal and thoracic electrogastrograms (EGGs) were recorded for about 20 min both before and after meals during ambulatory pressure recording. The pressure waves and EGGs for each 20 min recording were analyzed by the maximal entropy method (MEM). While the motility index of the pressure waves decreased after a meal, the 3 cpm component of these waves (2.4-3.7 cpm) increased significantly (n=6, P<0.05). Both bradygastria (0-2.4 cpm) and the duodeno-respiratory component (10-15 cpm) decreased, while the tachygastria component (3.7-10 cpm) increased, although these differences were not significant. The peak power of the gastric tube abdominal EGGs was significantly larger than that of control abdominal or thoracic EGGs in each of the 1 cpm (0-2.4 cpm), 6 cpm (5.0-7.4) and 8 cpm components (7.5-9.9). The thoracic EGG consisted mainly of the 3 cpm component, while the spectral amplitudes of the 1, 6, 8 and 10 cpm components were below 6% of the 3 cpm component. The peak spectral frequency both of the intraluminal pressure waves by FFT and of the thoracic EGGs by MEM occurred within the 3 cpm component. A cross correlation of about 0.2-0.3 occurred between the thoracic EGGs and the intraluminal pressure waves. Thus the gastric tube seems to preserve most of the original gastric motor characteristics and to contribute as a substitute for the original esophagus and stomach.

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We investigated the effects of phorbol 12,13-dibutyrate (PDBu), a typical protein kinase C (PKC) activator, on smooth muscle tone in the rat stomach fundus. In 5-hydroxytriptamine (5-HT)-precontracted stomach fundus strips, PDBu induced dose-dependent relaxation, but 4α-phorbol 12,13-didecanoate, a phorbol ester that does not activate PKC, did not induce relaxation. A PDBu-induced dose-dependent relaxation was also observed in strips precontracted with platelet-activating factor (PAF), carbachol, or 60 mM K⁺. In stomach fundus strips pretreated with PDBu, the contractile responses to 5-HT and PAF were completely blocked, but those induced by carbachol and endothelin-1 (ET-1) were only partially inhibited. In stomach fundus strips preincubated with carbachol in Ca²⁺-free medium, the Ca²⁺-induced contraction was decreased by preincubation with PDBu. In strips preincubated with 5-HT, PAF, or ET-1 in Ca²⁺-free medium, Ca²⁺-induced contractions were greatly inhibited by pretreatment with PDBu. These results suggest that in rat stomach fundus strips, PDBu-induced relaxation is mediated by activation of PKC. We speculate that a major factor mediating the relaxant action of PDBu in rat stomach fundus smooth muscle is represented by a reduction in Ca²⁺ influx via an inhibition of Ca²⁺ channels.

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