Despite extensive investigation, the biological mechanisms causing essential hypertension (EHT) remain unclear. To clarify the means by which hypotensive prostaglandins (Hypo-PGs, mainly PGE₁ and PGE₂) act in patients with EHT, the interaction between intravenously infused Hypo-PGs and pressor substances such as an adrenergic neurotransmitter, noradrenaline (NA) and angiotensin II (AII) was examined both in patients with EHT and in perfused isolated rabbit ear artery preparations. In patients with EHT, Hypo-PGs were shown to reduce the pressor responses to intravenously infused NA or AII, although no significant difference was found between the pressor responses to NA under basal conditions and the responses during intravenous infusion of Hypo-PGs. Animal studies were undertaken to investigate the inhibitory action of Hypo-PGs on the vasoconstrictive responses to electrical stimulation of the perivascular sympathetic nerves (VSNS) and to exogenous NA at pre- and postjunctional sites in blood vessel walls. The suppressive action of Hypo-PGs on the response to VSNS was shown to be more potent than that to their action on the response to exogenous NA. Thus, it was concluded that the hypotensive action of intravenously infused Hypo-PGs in patients with EHT may be more dependent on prejunctional sites than on the postjunctional sites in the walls of blood vessels.

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In order to study the structural changes in the intimal layer of varicose veins, we prospectively collected a total of 23 vein specimens from both the normal proximal thigh long saphenous (LSV) in 3 young trauma patients and from the unstripped proximal LSV near the sapheno-femoral junction and the distal calf blowouts in 10 primary varicose veins patients. Paraffin sections stained with hematoxylin and eosin were examined under the light microscope while ultra-thin sections were examined under the transmission electron microscope (TEM). Compared with the normal control LSV, varicose vein sections showed increase in the diameter of the lumen, hypertrophy of the wall and elongation and invagination of the intima. Along these invaginations, endothelial cells were compressed, elongated and thinned out. The cells also showed progressive degeneration and were finally lost into the lumen, leaving only the basal lamina to form the luminal surface. This invited blood components like platelets and red blood cells to stick to the bare intima and to penetrate through the wall. This may form the basis of the clinical condition of superficial thrombophlebitis, which sometimes complicates cases of varicose veins. In conclusion, varicose veins showed increased diameter of the lumen and hypertrophy, elongation and invagination of the intima. There was marked degeneration of the endothelial cells and desquamation of the endothelial layer.

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Complications in arteriovenous fistula (AVF) occur in up to 35% of renal failure patients on hemodialysis. The most frequent complication is thrombosis, usually from stenotic lesions in the venous outflow system. To study the pre-existing smooth muscle changes in the cephalic vein of these patients, we prospectively collected a total of 17 cephalic vein specimens from 3 normal controls and 14 renal failure patients undergoing primary AVF construction on the chosen limb. After preparation, ultrathin sections were stained with uranyl and lead acetate and were examined under the transmission electron microscope (TEM). Compared with the normal controls, abnormal fibrous infiltration of the intima and the media and varying degrees of smooth muscle degenerative changes were observed in all the cephalic vein sections of renal failure patients. Smooth muscle cells (SMCs) lost their normal fusiform shape and were widely separated by increased amount of irregularly disposed, extracellular collagen fibers. Other cellular abnormalities included irregular cell membrane, granular cytoplasm, Peri- and Para-nuclear vacuoles and mega mitochondria. SMCs also showed morphological expression of phagocytosis of collagen and elastic fibers as a sign of remodeling of the vein wall. In conclusion, pre-existing wall and smooth muscle changes were observed in all the cephalic vein sections of renal failure patients, which may contribute to the later complications of AVFs.

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