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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Opiates, like morphine, were long known to produce changes in blood pressure and cardiac functions. However, the nature of these changes are a subject of continuous controversy. The substantial differences in the opiate effects on the cardiovascular system is also apparent in more recent studies using enkephalins, beta-endorphin and dynorphins. The present review is aimed to indicate the source of the variations in the experimental data and analyze the relative contribution of different experimental factors to the observed effects of opiates and opioid peptides on the cardiovascular system. The major factors which contribute to the nature of the opioid effect on the cardiovascular system are: anesthesia, species, dose, site of action in the brain, respiratory changes and receptor specificity. However, the cardiovascular status per se is an important determinant of the opiates and opioid peptide effects on hemodynamic functions as indicated in states of hypertension and shock. A newly described factor is the plasticity of the opioid receptor system which changes its level and distribution pattern in different physiological and pathophysiological states. This review emphasizes the importance of utilization of highly specific ligands to opiate receptors administered to discrete brain areas in the conscious animal.
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PMID:The opioid system and central cardiovascular control: analysis of controversies. 300 75

The effects of exogenous corticotropin releasing factor and arginine vasopressin were evaluated in 6- and 11-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Basal adrenocorticotropic hormone (ACTH) and vasopressin levels did not differ between SHR and WKY, but basal corticosterone level was higher in 6-week-old SHR (p less than 0.01). To block endogenous corticotropin releasing factor secretion and nonspecific systemic responses, both groups were pretreated with chlorpromazine, morphine, and sodium pentobarbital anesthesia before measurement of ACTH responses to corticotropin releasing factor and vasopressin infusion. Basal ACTH level was lower in anesthetized 6-week-old SHR than in age-matched WKY (p less than 0.01), but no difference was seen between 11-week-old WKY and SHR. The ACTH response to corticotropin releasing factor in 6-week-old WKY was significantly greater than that in age-matched SHR (p less than 0.01), whereas in 11-week-old SHR and WKY the response was similar. Compared with responses in WKY, SHR showed an increased ACTH response to high doses of vasopressin (0.25 micrograms/100 g body weight) at both ages (p less than 0.05). These results indicate that the ACTH response to corticotropin releasing factor is blunted in the early stages of hypertension in SHR but later recovers. These abnormal responses to corticotropin releasing factor and vasopressin may be related to the development of spontaneous hypertension.
Hypertension 1986 May
PMID:Adrenocorticotropin responses to corticotropin releasing factor and vasopressin in spontaneously hypertensive rats. 300 24

Three problems were studied on the human and rabbit eye: to what extent the mineralocorticoids contribute to the control of Na+ and K+ transport in the lens epithelium, how do the glucocorticoids influence the concentration of glucose in the aqueous humour and what is the effect of the pituitary-adrenal axis on the hemato-ocular barrier. Specific receptor-like proteins binding aldosterone were found in the lens epithelium. Na+ and K+ concentrations in the aqueous were influenced by both aldosterone and spironolactone administration. The aldosterone concentration in human cataracts was found to be higher in cases of cataracts complicated by arterial hypertension. In spite of some indication of anticataractogenous action of mineralocorticoids, aldosterone did not prevent the formation of cortisol-induced cataract in chick embryos. Glucose concentration in the aqueous was increased by glucocorticoid administration as well as by stimulation of their secretion by ACTH. Further, the contribution of the pituitary-adrenal axis to the breakdown of the hemato-ocular barrier was investigated by measuring the changes of the total protein content in the aqueous. ACTH1-24 caused a partial breakdown of the barrier, as well as ACTH4-10 or alpha-MSH. As the latter two peptides lack the stimulative effect on the corticoid secretion and glucocorticoids themselves fail to increase the protein content in the aqueous, the breakdown of the hemato-ocular barrier seems to be essential for ACTH-linked peptide fragments and is not mediated by corticoids.
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PMID:The role of corticosteroids in the homeostasis of the eye. 300 76

The adrenocorticotropin (ACTH) response to hemorrhage (15 ml . kg-1 . 3 min-1) before and 30 min or 4 days after placement of bilateral electrolytic lesions of the nucleus tractus solitarius (NTS) were examined in anesthetized and in conscious rats. Two groups of rats were anesthetized with pentobarbital sodium (45 mg/kg). Femoral arterial and venous cannulas were placed acutely in the anesthetized group and chronically in the conscious group. Each rat received a hemorrhage 30 min before and 30 min after NTS lesions (in the anesthetized group) and 1 day before and 4 days after NTS lesions (in the conscious group). Plasma ACTH was determined before and 20 min after hemorrhage, and mean arterial blood pressure and heart rate were measured throughout. The baroreceptor reflex (bradycardia caused by a phenylephrine-induced rise in MABP) was determined 5 min before hemorrhage (in the anesthetized group) and 1 day before hemorrhage (in the conscious group) to assess the effectiveness of lesion. Hexamethonium was given to rats that developed hypertension postlesion and to sham-lesioned controls. Plasma ACTH did not increase after hemorrhage 30 min or 4 days after NTS lesions when compared with the other groups (sham, sham with hexamethonium, and missed lesion) and to prelesion controls. Also, lesions of the NTS had no effect on resting ACTH levels 4 days later. Mean arterial pressure and heart rate decreased during hemorrhage to similar extents before and after lesions in all groups. This study demonstrates that lesions of the NTS eliminate the ACTH response to hemorrhage immediately and 4 days after the lesions but have no effect on resting ACTH levels. The result suggests that the NTS is an essential part of the neural pathway for ACTH release after hemorrhage.
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PMID:Medullary lesions eliminate ACTH responses to hypotensive hemorrhage. 301 8

Dexamethasone-suppressible hyperaldosteronism is a rare familial syndrome in which hypokalemia, suppression of plasma renin concentration, and elevated aldosterone secretion are corrected by treatment with glucocorticoids. Regulation of adrenocortical function and body electrolytes was studied in two affected brothers. Both were hypertensive (210/128 and 160/106 mm Hg) with hypokalemia (3.3 and 3.5 mM) and low plasma renin concentrations. Aldosterone was elevated intermittently with levels as high as 45 ng/dl (normal range, 4-16 ng/dl). Cortisol concentrations were normal but were correlated with aldosterone levels (r = 0.9 and 0.7). Concentrations of 11-deoxycorticosterone (19 and 21 ng/dl; normal range, 4-16 ng/dl) and 18-hydroxycortisol (1000 and 950 ng/dl; normal range, 34-150 ng/dl) were elevated, and diurnal changes in both were the same as those seen with aldosterone. Infusion of adrenocorticotropic hormone (ACTH) caused exaggerated increases of aldosterone, 11-deoxycorticosterone, and 18-hydroxycortisol; cortisol response was normal. A 4-week trial of dexamethasone normalized blood pressure and caused a natriuresis, a fall in aldosterone, and a rise in plasma renin. Administration of ACTH after dexamethasone treatment again caused exaggerated increases of aldosterone. Aldosterone did not respond to angiotensin II before dexamethasone therapy (r = 0.01), but it showed a normal response after therapy (r = 0.8, p less than 0.01). Neither administration of dopamine (1 microgram/kg/min) nor long-term therapy with bromocriptine (2.5 mg t.i.d. for 4 weeks) affected aldosterone biosynthesis. Thus, loss of dopaminergic inhibition of mineralocorticoid biosynthesis does not account for hyperaldosteronism in this condition.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1986 Aug
PMID:Dexamethasone-suppressible hyperaldosteronism. Adrenal transition cell hyperplasia? 301 96

Renin has been identified in the adrenal gland by several investigators. Nephrectomy is the most potent stimulator of adrenal renin, and in the present study we investigated the mechanism by which nephrectomy stimulates adrenal renin. The pituitary plays a permissive role since hypophysectomy abolished the response of adrenal renin to nephrectomy (from 117.3 +/- 14.55 to 10.37 +/- 1.63 ng angiotensin I/mg protein/hr) and adrenocorticotropic hormone (ACTH) treatment restored the response to nephrectomy in hypophysectomized rats to 120 +/- 20.62 ng angiotensin I/mg protein/hr. However, large doses of ACTH given to intact rats did not increase adrenal renin to the high level observed after nephrectomy. Potassium also plays an important role, since prevention of hyperkalemia after nephrectomy by treatment with a cation exchange resin, sodium polystyrene sulfonate (Kayexalate), significantly reduced the adrenal renin response to nephrectomy. A third factor involved is the lack of negative feedback by plasma angiotensin II. Infusion of angiotensin II intraperitoneally prevented the rise in adrenal renin after nephrectomy (from 65.25 +/- 7.60 to 9.27 +/- 0.99 ng angiotensin I/mg protein/hr) despite an increase in plasma potassium and corticosterone. In conclusion, three factors influence the response of adrenal renin to nephrectomy: 1) the pituitary through the release of ACTH, 2) a direct stimulation by high plasma potassium levels, 3) the lack of angiotensin II feedback inhibition. Whether the high adrenal renin contributes to the high aldosterone observed in rats after nephrectomy remains to be established.
Hypertension 1986 Nov
PMID:Mechanisms by which nephrectomy stimulates adrenal renin. 302 25

A possible influence of the central alpha 2-adrenergic system on beta-endorphin was examined in rat anterior pituitary, neurointermediate lobe, and plasma. The concentration of beta-endorphin in anterior pituitary, neurointermediate lobe, and plasma was determined by radioimmunoassay 15 minutes after subcutaneous injection of clonidine in 14-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Clonidine reduced the concentration of the plasma beta-endorphinlike immunoreactivity in SHR and to a lesser extent in WKY. No significant changes in the concentration of beta-endorphinlike immunoreactivity were observed in anterior pituitary. Clonidine increased the concentration of neurointermediate lobe beta-endorphinlike immunoreactivity in SHR in a dose-related manner but did not affect the concentration in WKY. Administration of yohimbine (1 mg/kg) completely blocked the clonidine-induced increase of neurointermediate lobe beta-endorphinlike immunoreactivity in SHR, while prazosin (1 mg/kg) had no effect. These data suggest that the central alpha 2-adrenergic activation increases the neurointermediate lobe concentration of beta-endorphinlike immunoreactivity in SHR by suppressing beta-endorphin release from the neurointermediate lobe into the circulation.
Hypertension 1987 Jun
PMID:Central alpha 2-adrenergic stimulation increases neurointermediate lobe immunoreactive beta-endorphin in spontaneously hypertensive rats. 303 77

In order to find out whether beta-endorphin (beta-E) is involved in the development of hypertension, we performed two series of experiments. Firstly, spontaneously hypertensive rats (SHR) and their normotensive Wistar Kyoto controls (WKY) were submitted to ether stress. Plasma concentrations of beta-endorphin-like immunoreactivity (beta-EI), adrenocorticotropin (ACTH) and alpha-melanotropin (alpha-MSH) were measured by radioimmunoassay. The basal concentration of beta-EI was similar in WKY and SHR, whereas WKY had higher levels of ACTH and lower levels of alpha-MSH than SHR. In both strains acute stress enhanced the plasma concentration of beta-EI to the same extent and with a similar time-course. The increase of plasma beta-EI coincided with a rise in ACTH but not alpha-MSH. Gel chromatography of beta-EI revealed that plasma extracts contain similar amounts of beta-lipotropin- (beta-LPH) and beta-E-sized immunoreactive components, and that acute stress elevated both forms of beta-EI. Secondly, isolated tail arteries of SHR and WKY were perfused and field stimulated with two pulses at 1 Hz. beta-E depressed stimulation-evoked vasoconstriction with the same potency in both strains. Thus, basal and stress-induced levels of beta-EI did not differ in SHR and WKY. Moreover, in the tail artery of both strains the sensitivity of presynaptic opioid receptors towards beta-E was almost identical. If the beta-E sensitivity of these receptors in other arteries of WKY and SHR is also similar a major role of the circulating peptide in the development of hypertension is rather unlikely.
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PMID:Plasma concentration and vascular effect of beta-endorphin in spontaneously hypertensive and Wistar Kyoto rats. 303 90

Several new problems in obesitology were pointed out in this book and commented with respect to experiments and experiences of our working group. The problem of the low triiodothyronine (T3) syndrome was treated in chapter 2. The decrease of serum T3 and increase of serum reverse T3 in obese subjects was induced by several factors, namely by fasting. A resistance to administered thyroxine and triiodothyronine was observed in these patients. This energy saving mechanism is at variance with slimming regimens. The prevention and treatment of this awkward complication was discussed. The next chapter (3) is concerned with the hormonal and metabolic effects of diet and motor activity in the course of slimming regimens. The different effects of diet and motor activity on epinephrine and norepinephrine in obese subjects were similar to those obtained by other investigators in nonobese humans. A great importance was attributed to an increased plasma level of cortisol in obese and nonobese subjects in the course of different forms of motor activity and related to a different intensity of exercise. Parallel to several of these experiments, beta-endorphin, thyroid hormones and glucagon were also estimated. It was suggested that motor activity for exercising subjects should not lead to an enhanced secretion of cortisol in view of the health deteriorating effects of increased cortisolemia and in view of an already stimulated secretion of this hormone in obese subjects on basal conditions. Vice versa, a decreased cortisolemia should be obtained in obese subjects treated with an appropriate motor activity and diet. It has been shown that diet without motor activity reduced the level of plasma androgens but in cooperation with motor activity, the level of androgens remained unaltered in the course of the reducing regimen. The conservation of a normal or even higher level of androgens is probably prerequisite for a positive nitrogen balance observed in the course of a combined slimming regimen, while diet without motor activity led in the studied conditions to a negative nitrogen balance. Chapter 4 was devoted to the role of motor activity in slimming regimens. In view of the metabolic effects of motor activity and the clinical late effects of obesity (osteoarthritis of the knees, hips and spine, arterial hypertension, overload of the cardiovascular system, diabetes mellitus etc.), a selection of motor activities was proposed. According to our long experience, we do not recommend jogging, running, jumping and all sports leading to collisions of players.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:New trends in obesitology. 307 25

Changes in brain neuropeptide content in spontaneously hypertensive rats may be primarily related to the development of hypertension or may be secondary consequences of it. We have measured brain concentrations of beta-endorphin, Leu-enkephalin, arginine vasopressin (AVP) and oxytocin (OXT) in stroke-prone spontaneously hypertensive rats (SHRSP) and in age-matched normotensive Wistar Kyoto (WKY) controls, as well as in SHRSP with normalized blood pressure by chronic treatment with clonidine. Opioid peptide contents were measured in 12-, 18- and 24-week-old rats. beta-Endorphin was measured in the neuro-intermediate and anterior lobes of the pituitary, the hypothalamus, mid-brain and brain stem; Leu-enkephalin in the neuro-intermediate lobe of the pituitary, hypothalamus, mid-brain, brain stem, as well as in the spinal cord and adrenal glands. AVP and OXT were measured in the neuro-intermediate lobe of the pituitary, hypothalamus, brain stem and spinal cord. beta-Endorphin in the neuro-intermediate lobe of the pituitary was significantly higher in 12- and 18-week-old SHRSP. Adrenal gland Leu-enkephalin was lower in SHRSP as compared with the WKY. OXT and AVP contents were markedly reduced in all brain regions of SHRSP except the neuro-intermediate lobe of the pituitary, where no significant changes were found. In no case did long-term antihypertensive treatment with clonidine reverse the altered peptide content in the SHRSP. We conclude that alterations in brain neuropeptide content in SHRSP are not secondary to hypertension. The blood pressure lowering activity of clonidine appears not to depend on major alterations of peptide concentrations. A genetic defect in the synthesis of adrenal enkephalins and hypothalamic OXT and AVP seems likely from these studies.
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PMID:Altered neuropeptide concentrations in spontaneously hypertensive rats: cause or consequence? 315 51


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