摘要:

The effects of chronic treatment of young rats (initially 8 weeks old) with the collagen cross-linking inhibitor, beta-aminoproprionitrile (BAPN), on arterial wall properties were studied. BAPN was added to the drinking water for 8 weeks to produce intakes of 0, 100, 200 and 400 mg/kg/day. Systolic pressure of treated animals did not increase with age as rapidly as that of untreated controls. Weight gain of treated animals was inhibited at the highest (BAPN) treatment level. Passive stiffness of isolated, cylindrical segments of carotid arteries was decreased in BAPN-treated animals in a dose-dependent manner. BAPN treatment had no significant effect on the total collagen or elastin content (hydroxyproline) of carotid arteries. Values of maximum active force development to 10 µM norepinephrine plus 75 mM K+ were decreased by BAPN treatment in a dose-dependent manner. There was no significant effect of BAPN treatment on total water content or its cellular and extracellular components in the carotid artery. The relative cell volume of carotid arteries was not altered by BAPN treatment, suggesting that the decreased force development was a characteristic of individual cells. These results suggest that BAPN treatment may decrease stiffness by altering secondary characteristics of the connective tissue matrix without affecting connective tissue content. The decreased maximum smooth muscle force development may be responsible for the blood pressure-lowering effects of BAPN

ISSN:1018-1172    

DOI:10.1159/000158719

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

We isolated the elastic network from the bifurcation region of guinea pig carotid arteries by treatment with hot alkali and examined its adventitial and adluminal components by SEM. The thickness of networks from common and external carotid arteries averaged 87.5 µm (±6.9 SD) and from the carotid sinus averaged 46.8 µm (±2.4 SD). The networks consisted of a mesh of elastic tissue that became a continuous sheet, 2 µm thick, which formed the internal elastic lamina (IEL). The IEL was fenestrated; the perforations varied in number among the vessels (occipital > carotid sinus > common = external carotid), and some were spanned by delicate elastic fibers. The IEL’s adluminal surface was a smooth membranous sheet, which in some specimens bore unidirectional loose fibers, or was composed of tightly fused bundles of uni- or multidirectional fibers. The interior region of the cranial carotid sinus contained unique blister-like structures and dense clusters of fenestrations, together with a honeycomb-like mesh near the ascending pharyngeal artery. The outer, adventitial elastic layer consisted of a network of loose elastic fibers that were fused with the inner layers. We conclude that the structural differences noted among the common and external carotid arteries and carotid sinus are related to the sinus’s unique pressure-sensing f

ISSN:1018-1172    

DOI:10.1159/000158720

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The purpose of this study was to determine whether heterogeneity in endothelium-dependent responses to acetylcholine between canine blood vessels of different anatomical origin reflects variations in endothelial function or in responsiveness of vascular smooth muscle cells. Experiments were conducted in a bioassay system, where segments of femoral artery or vein with endothelium were perfused intraluminally and the perfusate used to superfuse rings of femoral arteries or veins without endothelium. Indomethacin was present in all experiments to prevent the synthesis of prostanoids. The blood vessels were contracted by phenylephrine. Measurement of wall tension in both the perfused segment and bioassay ring allowed simultaneous detection of endothelium-derived relaxing factor(s) released abluminally (segment) and intraluminally (ring). Intraluminal infusion of acetylcholine (ACh) induced relaxations in the perfused artery but not in vein segments. During arterial superfusion ACh induced relaxation in femoral arterial rings but contraction in venous rings. After treatment with atropine the arterial perfusate evoked relaxations in venous rings. Infusion of ACh through the femoral vein evoked only moderate relaxations in arterial rings. These data demonstrate that depressed endothelium-dependent relaxation to ACh in femoral veins compared to femoral arteries is due to a masking effect of the direct stimulating action of ACh and decreased release of the same mediator or the release of a different relaxing factor from venous endothelium.

ISSN:1018-1172    

DOI:10.1159/000158721

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

In spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY), we have examined both the endogenous norepinephrine (NE) contents of caudal arteries, mesenteric arteries and cardiac tissue as well as the rates of decline of NE in these tissues after inhibition of NE synthesis. The endogenous NE contents of caudal and mesenteric arteries from SHR rats were greater than those from WKY rats. In contrast, the NE contents of hearts from SHR and WKY rats were similar. After synthesis inhibition with α-methy -p-tyrosine (300 mg/kg i.p.), the NE contents of hearts and mesenteric arteries decreased in a monoexponential fashion. The rates of decline of NE were similar for corresponding tissues from SHR and WKY rats. Cold stress, reported to selectively activate sympathetic discharge, did not influence the rates of decline of NE in mesenteric arteries of either SHR or WKY animals. In contrast, cold exposure dramatically accelerated the rate of decline of NE in cardiac tissue from both SHR and WKY rats. It is concluded that in mesenteric arteries from SHR rats there is a larger pool of NE with turnover characteristics not dissimilar from that prevailing in vessels from normotensive animals. The failure of cold stress to modify the rates of decline of NE in mesenteric and caudal arteries of SHR and WKY rats suggests that these arteries are under considerable sympathetic influence at ambient temperature. The results support the view that the hypernoradrenergic innervation found in SHR blood vessels, together with normal functioning of the sympathetic nervous system, may have the potential for producing a heightened peripheral vascular resistance in this model

ISSN:1018-1172    

DOI:10.1159/000158722

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The ploidy of smooth muscle cells (SMCs) enzymatically isolated from the aorta and superior mesenteric artery (elastic arteries), caudal artery (small muscular artery) and the small mesenteric arteries and arterioles (mesenteric resistance vessels) of the spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats at ages 12, 26, 32 and 40 weeks was determined by flow cytometric DNA analysis and Feulgen-DNA photometric measurements. Frequency of polyploid cells in the aorta and superior mesenteric artery of the SHR increased from 4.43 ± 1.35 and 7.58 ± 1.69%, respectively, at 12 weeks to 31.26 ± 3.00 and 14.13 ± 1.30% at 40 weeks. There was a smaller increase in the percentage of polyploid cells in these two vessels of the WKY from 4.73 ± 0.74 and 5.82 ± 0.33%, respectively, at 12 weeks to 10.64 ± 0.17 and 7.68 ± 0.64% at 40 weeks. The caudal artery and mesenteric resistance vessels showed no significant increase in the percentage of 4N (tetraploid) cells in the SHR from 12 weeks (6.80 ± 0.92 and 6.10 ± 0.75%) to 40 weeks (7.83 ± 0.67 and 7.57 ± 0.07%). Similarly, there was no significant change in ploidy in these arteries of the WKY. Hence, while polyploidy of SMCs increases in the aorta and superior mesenteric artery of the rat with increasing age and with duration of hypertension, there is no significant change in the number of polyploid cells in smaller vessels such as the caudal artery or mesenteric resistance vessels. Since it is the resistance vessels that are involved in the development and maintenance of hypertension, polyploidy of SMCs in the blood vessel wall appears to hold little relevance to the etiology of this disease. As well, increased incidence of polyploidy is not directly attributable to increases in blood pressure as the caudal artery has a high systolic pressure in the SHR yet the incidence of polyploid cells in this artery does not

ISSN:1018-1172    

DOI:10.1159/000158723

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:1018-1172    

DOI:10.1159/000158724

出版商:S. Karger AG    

年代:1988

数据来源: Karger