摘要:

Yohimbine (10–8 to 10–4 M) produced a concentration-dependent contraction of the isolated dog basilar artery. The maximal amplitude of the contraction induced by yohimbine was approximately 50% of that induced by 5-hydroxytryptamine (5-HT) and twice as large as that of noradrenaline. This response to yohimbine (3 × 10–7 M) was attenuated by 5-HT receptor antagonists such as 5-methoxygramine, methysergide and ketanserin. Phentolamine also antagonized the yohimbine response but prazosin and DG-5128 did not. The 5-HT antagonists and phentolamine produced similar inhibition of the response to 5-HT. Propranolol, atropine and diphenhydramine did not modify the contractile responses to yohimbine and 5-HT. These results suggest that the contractile response to yohimbine is mediated through 5-HT receptors. In addition to the contractile action, yohimbine at concentrations over 10–6 M inhibited the contractile response to 5-HT. Thus, the possibility that yohimbine is a partial agonist on 5-HT receptors in the dog basilar artery has to be co

ISSN:1018-1172    

DOI:10.1159/000158612

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Microvascular pathology is one of the major problems associated with prolonged diabetes mellitus. The purpose of the present study was to determine if anatomical cellular pathology of the cerebral cortical microvessels could be detected very early after the onset of a streptozotocin-induced model of diabetes. Male rats at age 14–16 weeks were hyperglycemic &(>250 mg/dl) for 4 weeks prior to scanning and transmission electron microscopic analysis of the external and internal cell and vessel wall morphology of the arterioles. Scanning electron microscopic studies indicated that many processes of vascular smooth muscle cells changed their normal spindle shape to a branched or stellate configuration. The internal cellular changes included swollen mitochondria and cisternae of the endoplasmic reticulum and reduced cytoplasmic staining. Necrosis of arteriolar endothelial cells was evident in virtually every vessel section studied. These data indicate that vascular smooth muscle and endothelial cellular degeneration of cerebral cortical arterioles begins in the very early stages of the streptozotocin model of diabete

ISSN:1018-1172    

DOI:10.1159/000158613

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The distances between fibroblasts and adrenergic varicosities were measured in four distinct blood vessels of the dog, concomitantly with the measurement of corresponding distances between smooth muscle cells and adrenergic varicosities. The results showed a closer anatomical relationship between fibroblasts and adrenergic varicosities as compared to that of adrenergic varicosities and smooth muscle cells. These morphological results indicate that sympathetic neurotransmitter(s) may attain at the fibroblast membrane concentrations similar to those occurring at the smooth muscle cell membrane.

ISSN:1018-1172    

DOI:10.1159/000158614

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Cross-sections of rat mesenteric vessels were examined histologically after short-term perfusions of angiotensin II (AII), norepinephrine (NE), 5-hydroxytryptamine (5-HT), and histamine. Mesenteric veins (300–400 µm) and muscular venules (50–100 µm) exhibited dose-dependent constrictor responses to AII, but not to NE. Arterioles of comparable size (50–100 µm) did not constrict at low doses of AII or NE, but responded when higher pressor concentrations of each agonist were perfused. At equipressor doses, constriction of mesenteric arterioles was greater following NE when compared with AII. Short perfusions of 5-HT resulted in mild venoconstriction, while histamine induced dilation of the muscular venules. Ultrastructurally, vascular damage in response to AII was minimal and confined to the formation of small vacuoles in the endothelial cytoplasm. Endothelial integrity was preserved and no autonomous endothelial contraction was observed. Vacuolation induced by NE was far more extensive and particularly evident in arteries and ar

ISSN:1018-1172    

DOI:10.1159/000158615

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:1018-1172    

DOI:10.1159/000158616

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:1018-1172    

DOI:10.1159/000158617

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:1018-1172    

DOI:10.1159/000158618

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:1018-1172    

DOI:10.1159/000158611

出版商:S. Karger AG    

年代:1985

数据来源: Karger