Can nonadrenergic inhibitory varicosities be Identified structurally

Daniel, E. E.; Taylor, Grahame S.; Daniel, Vino; Holman, Mollie E.

doi:10.1139/y77-035

Cited by 38 publications

(14 citation statements)

References 6 publications

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“…Since the excitatory effect of VIP and the 'off' depolarization both were abolished in Cl-free medium, it is possible that VIP acts by a similar or identical mechanism to that of the mediator of this response or is the mediator. As noted previously (Daniel et al 1977Daniel, 1979) the opossum lower oesophageal sphincter, like circular muscle ofthe oesophagus body, contains primarily nerve varicosities with mostly small agranular vesicles (s.a.v.) and some large granular vesicles (l.g.v.).…”

Section: Discussionmentioning

confidence: 55%

Neither a purine nor VIP is the mediator of inhibitory nerves of opossum oesophageal smooth muscle.

Daniel¹,

Helmy-Elkholy²,

Jager³

et al. 1983

The Journal of Physiology

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SUMMARY1. Effects of stimulation of intramural nerves in the circular smooth muscle layer of the body of the oesophagus of the opossum (Didelphis marsupialis) were studied, simultaneously measuring the membrane potential of muscle cells using the sucrosegap technique and contractions of the muscle.2. Electrical field stimulation of the preparation, superfused with Krebs solution at 27 0C, induced a transient hyperpolarization of the smooth muscle cell membrane (i.j.p.) followed by a transient depolarization on which muscle action potentials were often superimposed. The muscle did not develop active tension spontaneously; it therefore did not relax during the i

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Section: Discussionmentioning

confidence: 55%

Neither a purine nor VIP is the mediator of inhibitory nerves of opossum oesophageal smooth muscle.

Daniel¹,

Helmy-Elkholy²,

Jager³

et al. 1983

The Journal of Physiology

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“…Neuromuscular distance was measured from each micrograph. The nerve terminals or varicosities were defined as regions of axonal swelling containing at least six vesicles and few or no neurofilaments or neurotubules (Daniel et al, 1977). The diameters of the granular and agranular vesicles were 393 measured only from micrographs taken at 20,000x (final magnification 50,000x) with the aid of a micrometer fitted in the eye piece of a dissecting microscope.…”

Section: Electron Microscopymentioning

confidence: 99%

Altered cerebral vessel innervation in the spontaneously hypertensive rat.

Lee¹,

Saito²

1984

Circulation Research

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SUMMARY. Autonomic innervation in the cerebral arterial walls of adult male spontaneously hypertensive rats and of normotensive Wistar-Kyoto rats was studied. When examined by fluorescence microscopy, dense catecholamine fluorescence was observed in anterior cerebral and middle cerebral arteries of both Wistar-Kyoto and spontaneously hypertensive rats. However, vertebral and basilar arteries and small pial arteries of Wistar-Kyoto rats received extremely sparse or no catecholamine fluorescence, whereas, in the respective regions of spontaneously hypertensive rats, catecholamine fluorescence was found to be significantly elevated. The endogenous norepinephrine content was also higher in cerebral arteries of spontaneously hypertensive than of Wistar-Kyoto rats. When examined ultrastructurally (potassium permanganate fixation), the incidence of granular vesicle-containing nerves, indicative of sympathetic nerves, was found to be significantly elevated in all cerebral arteries of spontaneously hypertensive rats examined. In contrast, the agranular vesicle-containing nerve, indicative of nonsympathetic nerves, with close synaptic cleft distance (<2 /im) was found to decrease or remain unchanged in the cerebral arteries of spontaneously hypertensive rats. These results suggest that cerebral sympathetic vasoconstriction may become more prominent than nonsympathetic vasodilation in spontaneously hypertensive rats. This finding lends further credence to the previous in vivo findings that cerebral sympathetic vasoconstrictor nerves become more functional and exhibit a protective effect against brain lesions during hypertension. The potential roles of neurogenic components involved in cerebral blood flow autoregulation are also discussed. (Circ Res 55: 392-403, 1984)

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“…Neuromuscular distance was measured from each micrograph. The nerve terminals or varicosities were defined as regions of axonal swelling containing at least six vesicles and few or no neurofilaments or neurotubules (Daniel et al, 1977). The diameters of the granular and agranular vesicles were measured only from micrographs taken at 20,000 X (final magnification 50,000x) with the aid of a micrometer fitted in the eye piece of a dissecting microscope.…”

Section: Electron Microscopymentioning

confidence: 99%

Ultrastructural distribution of vasodilator and constrictor nerves in cat cerebral arteries.

Lee¹

1981

Circulation Research

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Morphological examination of the adventitia of cerebral blood vessels reveals nerves which exhibit two distinct profiles. When fixed with KMnO*, the terminal axons contain either small granular vesicles or agranular vesicles. The granular vesicle-containing nerves (GVN) are of sympathetic origin, whereas the agranular vesicle-containing nerves (AVN) apparently are not sympathetic, since they remain after sympathetic denervation of the blood vessels (Iwayama et al., 1970;Owman et al., 1974;Lee et al., 1980). Previous work has established that the GVN mediate vasoconstriction (Lee et al., 1976, and although it has been suggested that the AVN mediate vasodilation, this ideas has not been rigorously examined.Cerebral arteries of the cat are innervated by both GVN and AVN. Curiously, when studied in vitro these arteries dilate only when subjected to transmural nerve stimulation (TNS), a situation unlike that in rabbit cerebral arteries (Lee et aL, 1976(Lee et aL, , 1978. The cat blood vessels therefore were utilized in the present studies in order to evaluate the relationship between vasodilation and the AVN. The results indicate a strong correlation between the degree of TNS-induced vasodilation and AVN in the cerebral vessels. In addition, the relative distribution of the AVN and GVN in cerebral arteries of different sizes was compared in quest of possible regional variation of the vasoconstrictor and dilator innervation. MethodsAdult cats (2-3 kg) of either sex were anesthetized with pentobarbital (40 mg/kg, i.p.) and exsanguinated. The entire brain with blood vessels attached was rapidly removed and placed in ice-cold (4°C) normal saline. Basilar arteries (BA) (10 mm long, outer diamter 0.4-0.5 mm), middle cerebral arteries (MA) (5 mm long, outer diameter 0.4-0.6 mm), anterior cerebral arteries (AA) (5 mm long, outer diameter 0.2-0.4 mm) immediately adjacent to the circle of Willis, and small branches of middle cerebral arteries (SMA) (5 mm long, outer diameter 0.1-0.2 mm) from the surface area of sylvian sulcus were excised with the aid of a dissecting microscope. Electron MicroscopyFreshly dissected arterial segments were fixed in ice-cold 2% KMnO< in Millonig phosphate buffer (pH 7.4, 490 mOsmol). Preparation of the fixative, fixation, dehydration, and final embedding of the specimens were carried out as previously described . All blocks were oriented for transverse sectioning of the arteries. Ultrathin crosssections of the arteries were obtained with an LKB microtome fitted with a diamond knife. The sections were mounted on slot grids coated with Formvar and were stained with 0.4% uranylacetate and

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Can nonadrenergic inhibitory varicosities be Identified structurally

Cited by 38 publications

References 6 publications

Neither a purine nor VIP is the mediator of inhibitory nerves of opossum oesophageal smooth muscle.

Neither a purine nor VIP is the mediator of inhibitory nerves of opossum oesophageal smooth muscle.

Altered cerebral vessel innervation in the spontaneously hypertensive rat.

Ultrastructural distribution of vasodilator and constrictor nerves in cat cerebral arteries.

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