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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Renin-associated, chronic psychosocial hypertension of 150-160 mmHg develops in groups of mice interacting socially in complex population cages. 2. The blood pressures of 16 males in a cage were measured and an intraperitoneal injection of the angiotensin coverting enzyme inhibitor captopril (SQ 14,225) was given. Three hours later blood pressures were measured again. 3. During the first 3 weeks of psychosocial hypertension SQ 14,225 was without effect. But at 1 month and subsequently up to 7 months, SQ 14,225 reduced blood pressure to the normal range of 120-130 mmHg. 4. Plasma renin activities were not related to the extent of blood pressure reduction by SQ 14,225. Hence other factors in addition to the renin-angiotensin mechanism play a part in maintaining chronic psychosocial hypertension.
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PMID:Effects of an angiotensin converting enzyme inhibitor on psychosocial hypertension in mice. 23 19

After four weeks of individual housing, male Wistar rats (selected for high or low spontaneous aggressiveness by multiple round-robin encounters) were housed three per cage and submitted to four weeks of chronic social stress consisting of changing membership in the social groups by daily rotation of the animals among cages every day according to a random permutation procedure. In addition, half the males in each condition were housed with three females. Each environmental condition triggered different neuroendocrine changes. Cohabitation with females increased the hypothalamo-pituitary-adrenocortical axis activity, including enlargement of adrenals and increased circulating corticosterone levels. On the other hand, daily rotation of the rats between different social groups activated part of the sympathetic nervous system, such as increased phenylethanolamine N-methyl transferase (PNMT) activity in the adrenals. The level of aggressiveness, however, had no direct influence but interacted with environmental factors on such neuroendocrine measures as circulating testosterone or plasma renin activity. These results indicate that during chronic stress, there is no single, unique response by the animal, but a highly complex set of neuroendocrine changes, dependent on the interaction between individual characteristics (the level of aggressiveness is an example) and situational factors.
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PMID:Multiple neuroendocrine responses to chronic social stress: interaction between individual characteristics and situational factors. 197 98

The purpose of this study was to assess the effects of chronic insulin infusion on blood pressure and urinary sodium excretion in Wistar rats. Fifteen Male Wistar rats weighing about 220 g were used. The rats were housed in metabolic cage and measured urine volume. Osmotic minipumps filled with insulin (0.57 U/day, Insulin group, n = 9) or saline (0.014 cc/day, Control group, n = 6) were implanted subcutaneously under ether anaesthesia, and blood pressure, urine volume, urinary sodium excretion (UNaV), plasma renin activity (PRA), plasma norepinephrine concentration (PNE) were measured for 4 weeks. In insulin group, there were no significant changes on plasma glucose levels, but systolic blood pressure rose significantly from 119 mmHg to 140 mmHg after 4 weeks. In this group, urine volume, UNaV, and PRA were significantly lower than those of control group and PNE was tended higher but not significant (P less than 0.1). Exogenous NE was given intravenously to assess the endogenous NE activity. Blood pressure elevation caused by exogenous NE in insulin group was suppressed significantly than that of control group. On the basis of these findings, we conclude that insulin can cause high blood pressure due to sodium retention and activation of endogenous NE.
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PMID:[Insulin and hypertension--the mechanisms of high blood pressure during chronic insulin infusion]. 268 19

Stress-induced renin and prolactin secretion was investigated using a conditioned emotional response paradigm. Three minutes after placement in a chamber the rats received an electric shock to their feet via the grid floor, then were immediately returned to their home cage. This procedure was repeated for 3 consecutive days. On the fourth day, instead of receiving an electric shock, they were removed after 3 min and sacrificed by decapitation. Control rats were treated identically with the exception that shock was not administered at any time. There was a significant increase in plasma renin activity and prolactin level in the stressed rats. The administration of the antianxiety drugs chlordiazepoxide (10 mg/kg i.p.) or midazolam (0.125-2 mg/kg i.p.) blocked the stress-induced increase in prolactin levels but not the stress-induced rise in plasma renin activity. Administration of the beta-blocker propranolol (1 mg/kg i.p.) inhibited, but did not completely block, stress-induced rise in plasma-renin activity and had no effect on stress-induced prolactin secretion. The opiate antagonist naloxone (0.1-10 mg/kg i.p.) and the acetylcholinesterase inhibitor diisopropyl fluorophosphate (0.5 mg/kg i.p.) did not block stress-induced renin or prolactin secretion. It is concluded that stress-induced prolactin secretion is regulated by a benzodiazepine-mediated mechanism and that stress-induced renin but not prolactin secretion is mediated in part via beta-receptors.
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PMID:Pharmacological studies on stress-induced renin and prolactin secretion: effects of benzodiazepines, naloxone, propranolol and diisopropyl fluorophosphate. 299 44

The effects of chronic (4 days) arginine vasopressin (AVP) infusion were studied in two separate groups of animals: normal Na-restricted dogs with intact renal nerves (n = 8) and renal-denervated Na-restricted dogs (n = 5). Volume expansion during AVP infusion was prevented in these studies with a sensitive servo-controlled cage-scale system. With intravenous AVP infusion (0.36 ng X kg-1 X min-1), plasma AVP levels increased from nearly 3 to 15 pg/ml, whereas total body weight remained unchanged from the control level. In renal-innervated dogs, plasma renin activity (PRA) decreased significantly (P less than 0.05) from control levels of 5.50 +/- 0.61 to an average level of 3.45 +/- 0.76 ng angiotensin I (ANG I) X ml-1 X h-1 on days 1 and 2 of AVP infusion. Thereafter, PRA tended to remain decreased on days 3 and 4, averaging 3.82 +/- 1.02 ng ANG I X ml-1 X h-1, but this was not statistically significant. Urinary Na excretion and balance, however, were not significantly altered during the 4-day AVP infusion period. In renal-denervated dogs, the rise of PRA with Na restriction was 50% that seen in normal dogs. In this group, a transient suppression of PRA was observed on day 1 of AVP infusion from 2.84 +/- 0.75 to 1.46 +/- 0.47 ng ANG I X ml-1 X h-1. Urinary Na excretion increased transiently with a small net Na loss of 4.9 +/- 1.3 meq on day 2 of AVP infusion. No significant changes occurred in average 24-h mean arterial pressure (MAP) in response to AVP in either group of dogs. Thus, in contrast to our previous observations in Na-replete dogs, elevations of plasma AVP within the physiological range result in suppression of PRA, but for periods of no longer than 1-2 days in Na-restricted dogs. This decrease of PRA occurred in the absence of measurable changes in MAP, total body weight, or plasma catecholamines. In addition, this transient AVP-induced suppression of PRA was only partially blunted by prior renal denervation. Finally, in the Na-restricted dog, AVP appears to have minimal or no long-term effects on urinary Na excretion.
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PMID:Chronic effects of vasopressin on plasma renin activity in sodium-restricted dogs. 351 20

Stress-induced changes in renin and prolactin secretion were studied using a conditioned emotional response paradigm. Three minutes after being placed in a chamber, the stressed animals received a brief electric shock (1.0 mA for 10 s through the grid floor), then were returned to their home cage. This procedure was repeated for 3 consecutive days. On the fourth day, the rats were placed in the chamber for 3 min, but instead of receiving shock, they were removed and sacrificed. Control animals were treated in the same manner, except that they never received foot shock. The sham-operated stressed rats evidenced significant elevations in plasma renin activity (270%) and prolactin level (550%). Electrolytic lesions in the dorsal raphe nucleus blocked the stress-induced increase in plasma renin activity but did not affect the stress-induced increase in prolactin secretion. Electrolytic lesions in the median raphe nucleus did not affect prolactin levels in either control or stressed animals. However, median raphe lesions led to a significant increase in plasma renin activity in non-stressed rats and potentiated the stress-induced elevation in plasma renin activity. These results suggest that neurons within the dorsal and median raphe nuclei are involved in the regulation of renin but not prolactin secretion during stress. The results also suggest that median raphe neurons play a role in basal renin secretion.
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PMID:Role of midbrain raphe in stress-induced renin and prolactin secretion. 620 72

Studies were performed in normal mongrel dogs (n = 8) to assess whether changes observed with chronic administration of vasopressin (AVP) were a result of direct actions of AVP or the consequence of changes in body fluid volume. AVP was infused continuously for 2 wk (0.36 ng X kg-1 X min-1 iv), while total body weight and body water (TBW) were maintained constant (+/- 50 g) using a servo-controlled system. A metabolic cage was mounted on sensitive force transducers for continuous monitoring of TBW. The summed voltage output of these transducers was used to servo control an intravenous infusion pump that adjusted the rate of water intake required for maintenance of a constant TBW. AVP infused under these conditions chronically increased plasma AVP levels from 2 to 22 pg/ml but resulted in no change of average 24-h mean arterial pressure, plasma sodium, or osmolality. Urine excretion decreased from 800 to 200 ml/day, whereas urine osmolality increased from 430 to 1,200 mosmol/kg and remained at these levels throughout the 2-wk AVP infusion. A net loss of 20 meq sodium occurred during the 1st day of AVP infusion but thereafter was unchanged. Plasma sodium and osmolality were unchanged from control during AVP infusions. We conclude that AVP-induced changes of arterial pressure, plasma sodium concentration and osmolality, renal escape, suppression of renin activity, and most of the observed natriuresis are events normally dependent on volume expansion.
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PMID:Long-term blood pressure and metabolic effects of vasopressin with servo-controlled fluid volume. 638 81

A method is described for implanting arterial and venous cannulas in rats that requires only minor surgery. Catheters are introduced into the abdominal aorta through the ventral tail artery and into the vena cava through a lateral tail vein. The wounds are covered with an acrylic cuff and the catheters are brought out through a stainless steel spiral connected to the cuff and then attached to top of a metabolism cage used to house the rat. This method makes possible continuous access to the catheters in undisturbed, mobile animals. Using this model we compared mean arterial pressure, heart rate, plasma renin activity, and plasma catecholamine levels in freely moving Long-Evans rats and in Brattleboro homozygous rats.
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PMID:Chronic arterial and venous catheterization of conscious, unrestrained rats. 639 88

The effect of psychosocial stress produced by aggregation in a special cage designed by Henry was investigated in three separate experiments using Wistar-Kyoto (WKY), Sprague-Dawley (SD) and F1 hybrids of the Japanese spontaneously hypertensive and Wistar-Kyoto (SHR-WKY F1) rats. Each aggregated group displayed typical 'stressed' behavioural disturbances. Adrenal hypertrophy, elevation of plasma renin activity and gastric erosions were noted in male aggregated SD rats; while adrenal enlargement, elevation of plasma noradrenaline and gastric erosions were found in male aggregated SHR-WKY F1 rats. Sustained hypertension, however, did not develop in any strain nor in any subgroup within each strain. Gastric erosions were also noted in isolated SD and SHR-SKY F1 rats suggesting that long term isolation of rats also induces stress. Isolated rats also remained normotensive throughout. Reduced haematocrit was found in both aggregated and isolated male SHR-WKY F1 rats suggesting increased plasma volume. We conclude that neither stress due to psychosocial disturbances nor that due to isolation produces chronic hypertension in the three strains of rat studied.
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PMID:Failure of psychosocial stress to induce chronic hypertension in the rat. 654 22

Psychosocially stressed male mice competing in a Henry-Stephens complex population cage develop hypertension, cardiovascular damage, and chronic interstitial nephritis. Their plasma renin, noradrenaline, corticosterone, and adrenal-catecholamine synthetic enzymes are increased and they die prematurely. Adding 3.3 mg of caffeine a day per kilogram of mouse body weight (the equivalent of 20 micrograms/ml decaffeinated coffee) to their drinking water significantly intensifies most of these changes. A dose of 90 mg/kg of caffeine (the equivalent of 560 micrograms/ml, i.e., brewed tea or coffee) further increases the effects. The drug-induced enhancement of competitive social stimulation of the neuroendocrine system resulted in a further increase of plasma renin and corticosterone levels as well as blood pressure and adrenal weight. These effects together with accelerated mortality and increased pathology indicate that chronic consumption of caffeinated liquids adds to the risks of psychosocial stress.
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PMID:Caffeine as an intensifier of stress-induced hormonal and pathophysiologic changes in mice. 700


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