Secretion of kallikrein and its role in vasodilatation in the submaxillary gland

Beilenson, Susanne; Schächter, M; Smaje, L. H.

doi:10.1113/jphysiol.1968.sp008655

Cited by 70 publications

(31 citation statements)

References 16 publications

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“…Both groups made use of the fact that parasympathetic nerve stimulation causes marked secretion but relatively little reduction in kallikrein content of the gland, whereas sympathetic nerve stimulation which causes less secretion can practically deplete the gland of its kallikrein (Beilenson, Schachter & Smaje, 1968). Both Barton et al (1975) and Garrett & Kidd (1975) came to the same conclusion, viz.…”

Section: Introductionmentioning

confidence: 53%

Direct evidence for the location of kallikrein in the striated ducts of the cat's submandibular gland by the use of specific antibody.

Hojima¹,

Maranda²,

Moriwaki³

et al. 1977

The Journal of Physiology

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SUMMARYKallikrein was located in the apical portion of the striated duct cells of the cat's submandibular gland by an immunohistochemical technique. This portion only of these cells showed an intense band of specific fluorescence. There was no evidence of specific fluorescence in the acinar and demilune cells nor in the interstitial tissue or blood vessels. In some sections the collecting ducts showed a very fine fluorescent luminal rim.

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Section: Introductionmentioning

confidence: 53%

Direct evidence for the location of kallikrein in the striated ducts of the cat's submandibular gland by the use of specific antibody.

Hojima¹,

Maranda²,

Moriwaki³

et al. 1977

The Journal of Physiology

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“…Are the substances released together or separately? The experiments of Beilenson et al (48) and Darke and Smaje (49) show that salivation and vasodilation are simultaneously activated by nerve stimulation. This observation has also been made in the nasal mucosa (4), thus indicating a concomitant release of VIP and AcCho.…”

Section: Discussionmentioning

confidence: 99%

Vasoactive intestinal polypeptide in cholinergic neurons of exocrine glands: Functional significance of coexisting transmitters for vasodilation and secretion

Lundberg

Änggård

Fahrenkrug

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

390

161

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The vasodilation induced by nerve stimulation in exocrine glands-e.g., submandibular salivary gland (1), tongue (2), sweat glands (3), and nasal mucosa (4)-is largely atropine resistant, whereas secretion easily can be blocked by muscarinic antagonists. The occurrence of a subpopulation of vasodilatory nerves was first suggested, but later a kinin mechanism was suggested to be responsible for this vasodilation (5-9). MATERIALS AND METHODSTen cats (body weight 2-4 kg) of both sexes were used for immunohistochemical studies. In two of these cats the superior cervical ganglion was excised unilaterally 14 days before they were killed. In four other cats vinblastine sulfate (Sigma) (1% in 0.9% NaCl) was locally applied to the submandibular and sphenopalatine ganglia and to pancreas 24 hr before perfusion with ice-cold 10% (vol/vol) formalin (21). These ganglia and parts of the submandibular gland, the nasal mucosa, tongue, lung, and pancreas were then processed for indirect immunohistochemical studies according to Coons (22) as described (see ref. 18) by use of a VIP antibody (5603-5; for detail about this antiserum, see refs. 23 and 24) and AcChoE staining (18,25,26). In some cases, immunohistochemical analysis for VIP and AcChoE staining were performed on the same section. Alternatively, adjacent sections were processed for the respective procedure. The latter approach was used because Triton X-100 (added to VIP antiserum to enhance penetration of antibodies) inactivated AcChoE (18,27). For details and validity of procedures and for controls, see ref. 18. Physiological experiments were done in 15 cats anesthetized with chloralose (50 mg/kg) plus urethane (100 mg/kg) intravenously. The trachea was cannulated. The blood pressure was recorded via a femoral artery. Rectal temperature was kept constant at 38°C. The submandibular gland, its duct, and nerve supply were exposed. The duct was cannulated with a polyethylene tube (PE 50) and salivation was measured with a drop recorder. The chorda-lingual nerve was cut, and the peripheral cut end was mounted to a bipolar platinum electrode. Preganglionic stimulation was performed with square wave pulses of either 2 or 15 Hz, 8 V, and a duration of 1 msec. To measure the venous outflow from the gland, we introduced a polyethylene catheter (PE 160) into the external jugular vein after all branches, except the one draining the submandibular gland, had been tied. Blood flow was measured by a drop recorder and blood was reinfused into the cephalic vein with a peristaltic pump. Heparin (1000 IU/kg) was given intravenously. The Abbreviations: VIP, vasoactive intestinal polypeptide; AcCho, acetylcholine; AcChoE, acetylcholinesterase. 1651The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact.

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“…Studies by Beilenson, Schachter & Smaje (1968) on submandibular glands of cats, using bioassay for determining kallikrein activity, showed it was secreted mainly by sympathetic stimulation; nevertheless, small amounts also entered parasympathetic saliva. These authors also showed that with both types of stimulation the kallikrein content of saliva tended to decrease with time.…”

Section: Introductionmentioning

confidence: 99%

Factors Affecting the Secretion of Submandibular Salivary Kallikrein in Cats

et al. 1987

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SUMMARYGlandular kallikrein has been assessed in submandibular saliva, homogenates and plasma by the fluorimetric substrate D-Val-Leu-Arg-7-amino-4-trifluoromethylcoumarin (AFC) and histochemically in tissue sections by the 4-methoxy-2-naphthylamide (MNA) analogue. Nerve stimulation was used to produce salivary secretion. Parasympathetic saliva contained low concentrations of kallikrein, independently of any circulating catecholamines from the adrenals. Sympathetic saliva contained very high concentrations of kallikrein; the amounts in individual drops rapidly reached a peak then declined gradually. Adrenergic blocking drugs during mixed parasympathetic and sympathetic stimulation showed that /J-adrenergic effects normally increase the secretion of kallikrein in response to the a-adrenergic influence from sympathetic nerve impulses. Small amounts of a glandular kallikrein-like activity are present in the plasma. Effluent blood from the submandibular gland before, during and after stimulation of either nerve gave no indication that submandibular kallikrein passes from the glandular compartment to the blood under conditions of unobstructed salivary flow. Excision of the chorda tympani indicated that parasympathetic nerve impulses are required for the normal resynthesis of submandibular kallikrein. The secretion of salivary kallikrein is essentially an exocrine function but its role in the saliva remains obscure. The results suggest that sudden mobilization of kallikrein may occur at times into the saliva and that a separate population of adrenergic axons, under separate central control, may pass to the striated ducts specially for this purpose.

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Secretion of kallikrein and its role in vasodilatation in the submaxillary gland

Cited by 70 publications

References 16 publications

Direct evidence for the location of kallikrein in the striated ducts of the cat's submandibular gland by the use of specific antibody.

Direct evidence for the location of kallikrein in the striated ducts of the cat's submandibular gland by the use of specific antibody.

Vasoactive intestinal polypeptide in cholinergic neurons of exocrine glands: Functional significance of coexisting transmitters for vasodilation and secretion

Factors Affecting the Secretion of Submandibular Salivary Kallikrein in Cats

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