Wiley
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Opposite effects of centrally administered neuropeptide Y (NPY) on locomotor activity of spontaneously hypertensive (SH) and normal rats Centrally administered neuropeptide Y has been shown to produce sedation manifested by a suppression of locomotor activity and a synchronizing effect on the EEG pattern in normal rats. It has been suggested that this sedative effect of NPY is largely due to a facilitation of the α2 ‐adrenergic transmission line. In the spontaneously hypertensive (SH) rat, the NPY‐induced up‐regulation of α2 ‐adrenoceptors observed in normal rats is absent, and NPY produces a desynchronization of the EEG. In the present study, we have therefore examined the effects of NPY on locomotor activity of SH rats and of inbred controls of the Wistar‐Kyoto (WKy) strain, in both morning and evening sessions. In morning sessions, NPY (0.2–5.0 nmol intracerebroventricularly, i. c.v.) increased locomotor activity of SH rats in a dosc‐related manner. WKy rats were largelj inactive per se , and no effects of NPY could be detected. In evening sessions, when spontaneous activity is high, NPY (1.0 nmol i. c.v.) still increased the activity of the SH rats. In WKy rats, an activity suppression similar to that previously reported for normal Sprague‐Dawley rats was seen. The present results indicate that the sedative action of NPY in different rats strains correlates with the ability of the peptide to up‐regulate α2 ‐adrenergic receptors.,
Wiley - Tập 137 Số 2 - Trang 243-248 - 1989
The Absorption of Calcium as a Function of the Body Saturation with Calcium Summary. 1. The speed of absorption of calcium in rats is influenced by the levels of calcium in the diet; but only as long as the skeleton is kept unsaturated with calcium salts from an early age. 2. Calcium starvation in adult rats and in pregnancy does not increase the speed of absorption of calcium. 3. Thymus and the gonads do not appear to influence the absorption of Ca.
Wiley - Tập 5 Số 2-3 - Trang 200-211 - 1943
A Quantitative Determination of the Content of Contractive Substances in Human Sperm and their Significance for the Motility and Vitality of the Spermatozoa. Summary. 1. The total content of contractive substance in human sperm was determined from 155 specimens of sperm by titration on rabbit intestine in vitro, with prostaglandin as the standard. The content varied greatly in different specimens, but contractive substance was met with in all of them. 2. In certain specimens the factor which is active on rabbit intestine consists – apart from prostaglandin and choline – of at least one other substance, which leads to a very rapid increase in tonus and is indifferent to atropine. 3. There is no correlation between the total content of contractive substance and the motility and life of the spermatozoa.
Wiley - Tập 13 Số 1-2 - Trang 103-108 - 1947
In mice aggressive behaviour provokes vast increase in plasma renin concentration, causing only slight, if any, increase in blood pressure Abstract In mice aggressive behaviour causes a vast release of renin, which can result in about 600‐fold increase in plasma renin concentration, reaching 6 Goldblatt Units, corresponding to 15μg renin per ml. This increase is mainly due to release of submaxillary renin, but there is also a significantly increased renal renin release. The degree of renin release is influenced by the duration of the aggression and by previous contact with other mice. Contrasting with the vast increase in plasma renin the blood pressure is normal or only moderately increased. This disproportion is not due to the depletion of renin substrate, caused by the increased renin, as shown by the increased calculated renin activity, as well as by decrease in blood pressure elicited by blockade of the renin system. Nor is the disproportion due to change in the sensitivity of the vessels to angiotensin II, the cause of this lack of tachyphylaxis being unknown. By way of exclusion the lack of pronounced increase in blood pressure can be explained by homeostatic function of the cardiovascular reflexes, which may also account for the fact that the pressor response after injection of pure submaxillary renin is only short, contrasting with a prolonged marked increase in plasma renin concentration.
Wiley - Tập 105 Số 1 - Trang 64-72 - 1979
Intraglandular transport of <sup>125</sup>I‐glandular kallikrein in the rat submandibular salivary gland The transport of radiolabeled rat submandibular gland kallikrein was studied after local administration to the resting and activated rat submandibular gland. The iodinated kallikrein was electrophoretically, immunologically, and biologically indistinguishable from the intact enzyme. After intraductal and intraglandular application the radioactivity in venous effluent was quantitated and characterized. As judged by gel‐filtration 125 I‐kallikrein in venous effluent eluted at a position similar to that seen when the iodinated enzyme was mixed with plasma, but earlier than the elution of 125 I‐kallikrein in buffer. In plasma, therefore, glandular kallikrein is probably bound to macromolecules. The radioactive fractions in venous effluent did not contain free iodine. Maximum concentration of 125 I‐kallikrein in venous effluent of resting glands was repeatedly reached about 20 min after intraductal administration. Moreover, the ductal epithelium represented the main permeation barrier since after intraglandular application the maximum venous 125 I‐kallikrein concentration was reached almost immediately. In activated gland (parasympathetic and sympathetic nerve stimulation), the venous 125 I‐kallikrein concentration was inversely related to glandular blood flow. We conclude that kallikrein present in the duct lumen or in the interstitium is able to reach the circulation, thereby making possible the local generation of plasma‐kinins.
Wiley - Tập 109 Số 3 - Trang 315-323 - 1980
Differences in renal and submaxillary renin release after stimulation with isoprenaline and noradrenaline Abstract It is confirmed that while noradrenaline stimulates release of submaxillary as well as renal renin, isoprenaline only stimulates renal renin release. The effects of these two adrenergic agonists differ in several other ways. The kidneys respond to isoprenaline with a dose dependant renin release. As a contrast the submaxillary glands respond to noradrenaline by no or by non‐dose‐dependant release. After single doses of the agonists the isoprenaline induced renin release is of short duration, contrasting with a prolonged renin release after injection of noradrenaline. The kidneys are able to respond to repeated doses of both agonists, while the submaxillary glands most often only respond to the first dose. While the effect of noradrenaline is blocked by pretreatment with phenoxybenzamine, this blocker is without effect when given after noradrenaline. The two agonists do not provoke any increase in plasma renin in mice which have been both sialoadenectomized and nephrectomized.
Wiley - Tập 105 Số 1 - Trang 58-63 - 1979
Pituitary adenylate cyclase activating peptide (PACAP) in salivary glands of the rat: origin, and secretory and vascular effects Pituitary adenylate cyclase activating peptide (PACAP)‐38. injected Lv. to the anaesthetized rat. evoked secretion of saliva from the three major salivary glands. the submandibular glands responding with the greatest and the sublingual glands with the smallest volumes. The parotid saliva was rich in amylase and protein. In vitro. pieces of parotid and submandibular gland tissues released K+ and protein in response to PACAP‐38. with atropine and adrenoceptor antagonists present. The blood flow in the submandibular gland increased in response to PACAP‐38. despite a marked fall in mean aortic blood pressure. PACAP is a vasoactive intestinal peptide (VIP)‐like neuropeptide. A comparison between the two peptides showed PACAP‐38 to be more effective than VIP with respect to vascular responses and less or equi‐effective with VIP with respect to the secretory responses. thus suggesting the involvement of PACAP type I and type II receptors. respectively PACAP‐38 and ‐27 were present in the parotid gland as judged by radioimmunoassay. the concentration of the former being about twice that of the latter. Parasympathetic denervation. by cutting the auricula‐temporal nerve. reduced the total parotid gland contents of PACAP‐38 and ‐27 by 23 and 44%. respectively (compared with a previously demonstrated 95% reduction of VIP). Sympathetic de nervation. section of the facial nerve or treatment with the sensory neurotoxin capsaicin did not affect the content of PACAP. The difference in efficacy between PACAP and VIP in the vascular and secretory responses as well as the difference in localization suggest that the two peptides play different physiological roles in the salivary glands.
Wiley - Tập 160 Số 1 - Trang 15-22 - 1997
Exocrine and endocrine release of kallikrein after reflex‐induced salivary secretion Exocrine and endocrine release of rat submandibular gland kallikrein has been shown to be low after parasympathetic and β‐adrenergic stimulation but greatly increased after α‐adrenergic stimulation. In the present study, release of glandular kallikrein was investigated under conditions known to give a reflex‐induced salivary gland response. Heat stress induced a rich flow of saliva originating in the submandibular glands. Salivary kallikrein secretory rate was higher than after parasympathetic stimulation but lower than after sympathetic stimulation (P < 0.005). Only heat stress increased circulating glandular kallikrein (12.7 ± 0.8 ng ml‐1 before heat exposure and 53.3 ± 14.1 ng ml‐1 40 min afterwards, P < 0.005). There were no indications that the endocrine release of kallikrein was due to non‐specific leakage. Atropine abolished heatinduced salivation and endocrine kallikrein secretion, possibly through interference with central pathways (P < 0.05). However, phentolamine did not, which may indicate an as yet unidentified mediator of endogenous kallikrein release. The salivary gland response to acid and ether was comparable to that observed after parasympathetic nerve stimulation and was abolished by atropine (P < 0.005). Stimuli known to influence other salivary gland ductal cells, such as aggression and starvation followed by drinking, also did not increase the plasma concentration of glandular kallikrein. The fact that various conditions which induce salivation did not increase circulating glandular kallikrein, coupled with the fact that kallikrein concentration was the highest in animals that died from heat stress, may suggest that the increase in circulating glandular kallikrein seen after heat stress may be pathological and could contribute to the development of heat shock.
Wiley - Tập 139 Số 1-2 - Trang 29-37 - 1990
Exercise‐induced muscle damage and inflammation: fact or fiction? Physical exercise is necessary for maintaining normal function of skeletal muscle. The mechanisms governing normal muscle function and maintenance are vastly unknown but synergistic function of hormones, neurosignalling, growth factors, cytokines and other factors, is undoubtedly important. Because of the complex interaction among these systems the lack of complete understanding of muscle function is not surprising. The purpose of exercise‐induced changes in muscle cell function is to adapt the tissue to a demand of increased physical work capacity. Some of the approaches used to investigate changes in skeletal muscle cell function are exercise and electrical stimulation in animals and human models and isolated animal muscle. From these models, it has been concluded that during physical exercise, in an intensity and duration dependent manner, skeletal muscle is damaged and subsequently inflamed. The purpose of the inflammation would be to repair the exercise‐induced damage. Because of the design and methods used in a majority of these studies, concerns must be raised, and the question asked whether the paradigm of exercise‐induced muscle inflammation in fact is fiction. In a majority of conducted studies, a non‐exercising control group is lacking and because of the invasive nature of the sampling methods used to study inflammation it does not appear impossible that observed inflammatory events in human skeletal muscle after physical exercise are methodoligical artefacts.
Wiley - Tập 171 Số 3 - Trang 233-239 - 2001
Eccentric exercise‐induced injuries to contractile and cytoskeletal muscle fibre components Exercise involving lengthening of an activated muscle can cause injury. Recent reports documented the mechanics of exercise‐induced muscle injury as well as physiological and cellular events and manifestations of injury. Loss of the cytoskeletal protein desmin and loss of cellular integrity as evidenced by sarcolemmal damage occur early during heavy eccentric exercise. These studies indicate that the earliest events in muscle injury are mechanical in nature, while later events indicate that it may be more appropriate to conclude that intense exercise initiates a muscle remodeling process. We conclude that muscle injury after eccentric exercise is differently severe in muscles with different architecture, is fibre type‐specific, primarily because of fibre strain in the acute phase, and is exacerbated by inflammation after the initial injury.
Wiley - Tập 171 Số 3 - Trang 321-326 - 2001
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