摘要:

Experiments were performed to determine the conditions in which norepinephrine release from adrenergic nerve terminals in smooth muscle from canine blood vessels and spleen might be inhibited by prejunctional α-adrenergic receptor activation. Strips of aorta, mesenteric and splenic arteries, splenic capsule and portal and saphenous veins were labeled with 7-3H-norepinephrine and mounted for superfusion. In the portal vein, an inhibitory effect of prejunctional receptor activation with exogenous norepinephrine (1.2 × 10–6 M) on transmitter efflux could be demonstrated during electrical stimulation (9 V, 2 Hz) of the nerve terminals. By contrast, in the other tissues, inhibition of transmitter release during electrical stimulation or depolarization of the nerve terminals with K+ (40 mEq/l) could only be demonstrated after blockade of the neuronal uptake mechanism. That activation of prejunctional α-adrenergic receptors in blood vessels inhibits the exocytotic process is suggested by the failure of exogenous norepinephrine to affect either the basal efflux of 3H-norepinephrine or the displacement of 3H-norepinephrine by tyra

ISSN:1018-1172    

DOI:10.1159/000158198

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

In order to study the action of serotonin (5-HT), noradrenaline (NA), hypertensin (HT), prostaglandins A1, B1 and E2 (PGA1, PGB1 and PGE2) and vasopressin (VP), internal carotid arteries were isolated in situ PGE2 PGB1 NA. The relative duration of the constrictor effects was: 5-HT < PGA1- < HT and PGE2 < PGB1 and NA < VP. The relaxation index of these substances on the vascular wall was: 5-HT < PGE2 < HT < PGB1- < NA < PGA1 < VP. Some of these substances, specifically PGB1 PGE2 and VP, frequently caused a residual constriction of the smooth muscle following their dilator effect. The role of these vasoactive substances in the development of vasospasm is discusse

ISSN:1018-1172    

DOI:10.1159/000158199

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

The rates of onset and offset of α-adrenoreceptor blockade by phentolamine (5 × 10-7 M) have been studied on the normal and denervated rabbit aorta and rat vas deferens. Removal of the adventitia with its accompanying sympathetic nerve component results in an approximately threefold increase in the rate of onset of α-adrenoreceptor blockade by phentolamine in the rabbit aorta. The rate of offset of blockade by the antagonist on the aorta is likewise faster after the adventitia has been removed (approximately threefold faster for loss of 90% of the antagonist from the region of the receptors). This effect is not likely to be attributed to the absence of sympathetic nerve terminals since surgical denervation of the rat vas deferens has no effect on the kinetics of receptor blockade in this densely innervated organ. These data suggest that the adventitia of the rabbit aorta may serve as a diffusion barrier which limits the antagonist’s access to, and efflux from, the region of the receptors. The dissociation constant of phentolamine (calculated from the equilibrium dose ratio) on the α-adrenoreceptor is unaltered by denervation in either tissue and is identical in both tissues. It is suggested that α-adrenoreceptors in the rabbit aorta and rat vas deferens are of a single type and are not significantly affected, with respect to antagonist affinity, by dener

ISSN:1018-1172    

DOI:10.1159/000158200

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

Controversy exists regarding the mechanism by which prazosin lowers blood pressure without a marked increase in heart rate; a mechanism involving both sympatholytic activity and direct smooth muscle relaxation has been suggested. α-Adrenergic receptor blockade by prazosin is well documented and occurred to exogenous norepinephrine and to field stimulation in vitro in rat arteries and veins. A parallel shift of the norepinephrine concentration response curves in the aorta and mesenteric artery contrasted with a nonparallel shift and a marked depression of maximal norepinephrine responses in the inferior vena cava, portal, iliac and femoral veins. Nonspecific direct acting vasodilators will antagonize contractile responses to all agonists. However, prazosin (10–8 M) specifically antagonized norepinephrine-induced responses. Concentration response curves to potassium chloride or to serotonin were not affected in these rat tissues. In addition, prazosin (up to 10–6M) did not significantly relax aortic tissue previously contracted with potassium chloride or serotonin, whereas the vasodilator, nitroglycerin, produced a clear relaxation. Prazosin only reduced the tone of vessels contracted with norepinephrine. These data indicate that prazosin exhibits minimal, if any, direct smooth muscle relaxant properties in concentrations higher than those producing α-adrenergic receptor blockade, and relaxes rat veins by a mechanism involving α-adrenergic receptor bl

ISSN:1018-1172    

DOI:10.1159/000158201

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

The innervation of three embryologically distinct segments of the canine inferior vena cava was investigated. These segments were termed A (supradiaphragm), B-C (intrahepatic and that between liver and renal veins), and D (infrarenal). Strips were cut from these segments, and their isometric tensions were recorded. Transmural electrical stimulation induced contractile responses in circular strips from segment B-C (66.5% of the maximum norepinephrine-induced response) and in those from D (14.4%), but not in A. These responses almost completely disappeared in the presence of phenoxybenzamine. In segment B-C, however, the remaining small contraction was markedly enhanced by neostigmine and abolished by atropine. The same phenomenon was also observed in the contraction remaining after reserpinization. Longitudinal strips from segment C responded similarly. Concentration-response curves of circular strips for acetylcholine were shifted by neostigmine markedly to the left only in segment B-C, while no significant shift occurred in A and D. It was concluded that the adrenergic innervation is remarkably dense in B-C, sparse in D, and probably lacking in A. In addition, a cholinergic excitatory innervation is present in segment B-C.

ISSN:1018-1172    

DOI:10.1159/000158202

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

The effect of atropine on the electrical-field stimulation-evoked overflow of tritium from isolated rabbit pulmonary arteries preincubated with 3H-noradrenaline was studied. Atropine (10–4M) and phentolamine (10–6M) increased stimulation-induced overflow of tritium. Clonidine (10–6 to 10-5 M) and acetylcholine (10–6 M) diminished the stimulation-evoked overflow of tritium. After the overflow had been raised by either atropine (10–4M) or phentolamine (10–6 M), clonidine (10–6 M) decreased the overflow below control values. Clonidine (10–5M) prevented the enhancement of tritium overflow evoked by atropine (10–4M). A lower concentration of clonidine (10–6 M) only caused a partial prevention. Enhancement of the overflow by phentolamine (10–6 and 3 × 10–5M) was not altered by atropine (10–4M). Atropine (10–7M), in a concentration which was without any effect on the stimulation-induced tritium overflow, prevented the reduction evoked by acetylcholine (10–6 M). It is concluded that atropine in a low concentration blocks presynaptic inhibitory muscarinic receptors; at higher concentrations it blocks in additi

ISSN:1018-1172    

DOI:10.1159/000158203

出版商:S. Karger AG    

年代:1979

数据来源: Karger