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We have recently segregated a new line of rabbit, named TGH, with severely high levels of plasma triglyceride and cholesterol. The aim of the present study was to investigate the progression of atherosclerosis and haemodynamic parameters in TGH rabbits. 2. Japanese white (JW) and TGH rabbits (24-27 months old) were anaesthetized with ketamine and xylazine. Plasma concentrations of triglyceride were 63.1 8.0 and 446.0 35.2 mg/dL in JW and TGH rabbits, respectively. Blood pressure was measured by a catheter implanted in the femoral artery. Histological examinations were performed using haematoxylin-eosin and elastica-Masson trichrome staining to detect atherosclerotic lesions. 3. The JW rabbits had no atherosclerotic lesions. In TGH rabbits, severe atherosclerotic lesions were observed throughout the aorta, especially in the aortic arch. Basal femoral arterial pressure was not significantly different between JW and TGH rabbits. However, the basal pulse pressure in TGH rabbits (48.3 4.5 mmHg) was significantly greater than that of JW rabbits (28.0 5.6 mmHg). Intravenous infusion of N(G)-nitro-L-arginine methyl ester (L-NAME; 26.9 mg/kg) increased the blood pressure of TGH and JW rabbits. There was no significant difference in the response to L-NAME between the two rabbit strains. 4. The present study shows that severe atherosclerotic changes develop in TGH rabbits and suggests that the hyperlipidaemia combined with hypercholesterolaemia and hypertriglyceridaemia is an important factor for promoting atherosclerosis in TGH rabbits. The greater pulse pressure in TGH rabbits may be due to the increased vascular stiffness with atherosclerosis. 5. This newly developed TGH rabbit line of heritable hypertriglyceridaemia with hypercholesterolaemia will become a useful animal model for studies on the role of hyperlipidaemia in the progression of atherosclerosis and in many atherosclerosis-related diseases.

The urinary bladder is innervated and functionally regulated by the autonomic nervous system. In order to elucidate the mechanism of functional changes in aged rat urinary bladder, we studied the influence of senescence on, 1) the α-adrenergic contractile response to phenylephrine in the urinary bladder body and trigone, 2) the muscarinic contractile response to carbachol in the body and trigone. The binding characteristics of [ 3 H]quinuclidinyl benzilate (QNB) to muscarinic cholinoceptors were compared in young and aged bladder. Bladders from young (2 -3 month-old) and aged (27 month-old) male Fischer 344 rats were isolated, cut into strips and mounted in the organ bath, then the developed tension was recorded. Histologically, the aged bladder did not show pathologic changes such as inflammation and hypertrophy. Carbachol-induced contraction in aged rat bladder was identical to that obtained in young rat. In the receptor binding assay, [ 3 H]QNB maximal binding capacity and Kd value were not significantly changed in aged bladder. In contrast, a selective α-adrenergic agonist phenylephrine, elicited greater contractions both in the aged body and trigone than those in young rats. The augmentation of α-adrenoceptor-mediated contractions in aged bladder may induce urinary dysfunction such as voiding difficulty.