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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-five stage I-II essential hypertension subjects aged 25-63 were examined after the 1st and 10th acupuncture to clarify the effect of a single procedure and a course of acupuncture treatment on blood ACTH, STH, TTH, beta-endorphine, neurotensin, thyroxine, aldosterone, hydrocortisone and plasma renin activity. The hormonal spectrum was determined by radioimmunoassay using special kits. The blood was obtained before acupuncture, 5 min after introduction of the needles, immediately and 30 min after their removal. It is shown that acupuncture-related decline of arterial pressure occurs in participation of pituitary and adrenal hormones as well as polypeptides beta-endorphine and neurotensin.
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PMID:[The effect of acupuncture on endocrine regulation in hypertensive patients]. 164 16

1. Spontaneously hypertensive rats (SHR) are useful for investigating the possible pathophysiological and neurochemical basis of human essential hypertension. 2. The accepted pathogenic mechanism of hypertension in SHR is an increased central sympathetic drive which results in an increased peripheral resistance. 3. The neurochemical basis of the increased sympathetic drive is unknown. The observation that there are reduced levels of neuropeptides (vasoactive intestinal peptide, neuropeptide Y, cholecystokinin octapeptide, neurotensin and calcitonin gene related peptide) in the spinal cord in SHR rats compared with age and gender matched Wistar-Kyoto normotensive rats could provide a basis for understanding the mechanism of hypertension in SHR.
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PMID:Altered levels of neuropeptides in the medulla and spinal cord of spontaneously hypertensive rats. 307 73

Plasma concentrations of beta-endorphin (beta-EP), leucine enkephalin (LEK), arginine vasopressin (AVP), neurotensin (NT), renin activity (PRA) and angiotensin II (AT-II) were determined before and after the treatment with clonidine in 117 patients with essential hypertension. Before the treatment, the patient group had lower levels of beta-EP and LEK (P < 0.001), higher levels of AVP, PRA and AT-II (P < 0.05-0.01), as compared with those in control group. After 14 days of the treatment, plasma levels of beta-EP, LEK increased significantly (P < 0.001), and correlated negatively with the decrease of the mean artery pressure (r = -0.369 and r = -0.441, respectively, P < 0.01). PRA and AT-II decreased significantly (P < 0.05, P < 0.01). Decrease of AVP level was also observed, but did not reach the statistical significance. NT did not change both before and after the treatment. These data suggest that beta-EP and LEK may be involved in pathogenesis of hypertension and in hypotensive action of clonidine.
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PMID:[Changes in plasma neuropeptides before and after clonidine in patients with essential hypertension]. 824 25

The changes of regulatory peptides in 100 patients with essential hypertension at different stages were studied. Four kinds of peptides in serum were measured by RIA method. The results showed that: (1) neurotensin, P-substances, beta-endorphin and leucine-enkephalin decreased significantly in the group (P < 0.01). (2) the levels of those parameters at different stages of hypertension were decreased in parallel with its severity and the difference between different stages is significant (P < 0.01). (3) norepinephrine showed negative correlation with four kinds of neuropeptides. (4) neurotensin, Beta-endorphin and leucine-enkephalin increased significantly after capton (P < 0.01). The possible mechanism and its clinical significance of the changes of those regulatory peptides in hypertension patients were discussed.
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PMID:[Changes in regulatory peptides at different stages of essential hypertension and their clinical significance]. 824 26

In order to investigate the changes of endogenous opiate systems in hypertension and their possible role in the pathogenesis in hypertension, we measured plasma concentrations of beta-endorphin, leucine-enkephalin, neurotension, arginine vasopressin, plasma renin activity and angiotensin II by radioimmunoassay in 60 normal persons and 120 patients with essential hypertension. The results showed that the patient group had lower levels of beta-endorphin and leucine enkephalin (P < 0.001), higher levels of arginine vasopressin, plasma renin activity and angiotensin II (P < 0.01, P < 0.05 and P < 0.05, respectively), and normal level of neurotensin, as compared with those in normal group. Plasma levels of leucine-enkephalin was correlated negatively to the mean artery pressure (r = -0.196, P < 0.05). Plasma level of arginine vasopressin was correlated to the duration of the hypertension (r = 0.216, P < 0.05). After 150 min and 14 days of treatment with clonidine, plasma levels of beta-endorphin, leucine-enkephalin increased significantly (< 0.01) and correlated negatively with the decrease of the mean artery pressure (r = -0.340 and r = -0.436 at 150 min, r = -0.369 and r = -0.441 on the 14th day, respectively, P < 0.01). Plasma renin activity and angiotensin II decreased significantly (P < 0.05 and P < 0.01). Arginine vasopressin and neurotensin did not change significantly. After intravenous administration of opiate antagonist-naloxone, the blood pressure and heart rate increased significantly (P < 0.01). The results suggested that the changes of endogenous opioids may be involved in the pathogenesis of hypertension and in the antihypertensive action of clonidine.
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PMID:Plasma levels of beta-endorphin, leucine enkephalin and arginine vasopressin in patients with essential hypertension and the effects of clonidine. 858 72

Abnormalities in autonomic activity resulting in disturbances of the diurnal rhythm of many physiologic processes were recently revealed in hypertensive patients. These findings suggest deteriorations in the functioning of the suprachiasmatic nucleus (SCN), which is known to be the biological clock of mammals. To test this hypothesis, we carried out an immunocytochemical study of the SCN of primary hypertension patients who had died due to myocardial infarction or brain hemorrhage, and compared them with those of individuals with a normal blood pressure who had never had any autonomic disturbances and died from myocardial infarction after chest trauma or from hypothermia. We found that the staining for the three main neuronal populations of the SCN; i.e., vasopressin, vasoactive intestinal polypeptide, and neurotensin, reduced by more than 50% in the hypertensives compared with controls. The present data indicate a serious dysregulation of the biological clock in hypertensive patients. Such a disturbance may cause a harmful hemodynamic imbalance with a negative effect on circulation, especially in the morning, when the inactivity-activity balance changes. The difficulty in adjusting from inactivity to activity might be involved in the morning clustering of cardiovascular events.
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PMID:Neuropeptide changes in the suprachiasmatic nucleus in primary hypertension indicate functional impairment of the biological clock. 1117 8

The corticotrophin-releasing hormone (CRH)-expressing neurons were studied in the hypothalamus and brainstem of individuals who suffered from essential hypertension and had died due to acute myocardial infarction or brain hemorrhage. Healthy normotensive individuals who died in accidents made up the control group. In hypertensive patients we found extremely high expression of CRH in all parts of the hypothalamic paraventricular nucleus (Pa). In addition, CRH neuronal profiles were observed in the caudal hypothalamic area and dorsal parts of the extended amygdala. In the control group, CRH neurons were found only in the Pa and in much smaller numbers than in hypertensive patients. Also, in contrast to the controls, we found in hypertensives a very high number of CRH fibers running from the most rostral part of the Pa to the median eminence and innervating the caudal part of the suprachiasmatic nucleus (SCh). A quantitative evaluation showed that the area covered by CRH fibers in the SCh of hypertensives was about three times larger than that in the control SCh. Linear regression analysis demonstrated a negative correlation between the area of CRH fibers and the number of vasopressin (VP) or neurotensin (NT) neurons within the SCh. This relationship occurred particularly in hypertensive patients in whose SCh a larger CRH fiber area and a smaller number of VP or NT neurons were observed. We found a few CRH neuronal profiles and fibers in brainstem nuclei that are involved in cardiovascular regulation, but no apparent difference was observed between the control and hypertensive group.
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PMID:Corticotropin-releasing hormone neurons in hypertensive patients are activated in the hypothalamus but not in the brainstem. 1748 22

Spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) are frequently used as model rats not only in studies of essential hypertension and stroke, but also in studies of attention deficit hyperactivity disorder (ADHD). Normotensive Wistar-Kyoto rats (WKY) are normally used as controls in these studies. In this study, using these rats, we aimed to identify the genes causing hypertension and stroke, as well as the genes involved in ADHD. Since adrenal gland products can directly influence cardiovascular, endocrine and sympathetic nervous system functions, gene expression profiles in the adrenal glands of the 3 rat strains were examined using genome-wide microarray technology when the rats were 3 and 6 weeks of age, a period in which the rats are considered to be in a pre-hypertensive state. Gene expression profiles were compared between SHR and WKY and between SHRSP and SHR. A total of 353 genes showing more than a 4-fold increase or less than a 4-fold decrease in expression were isolated and candidate genes were selected as significantly enriched genes. SHR-specific genes isolated when the rats were 3 weeks of age contained 12 enriched genes related to transcriptional regulatory activity and those isolated when the rats were 6 weeks of age contained 6 enriched genes related to the regulation of blood pressure. SHRSP-specific genes isolated when the rats were 3 weeks of age contained 4 enriched genes related to the regulation of blood pressure and those isolated when the rats were 6 weeks of age contained 4 enriched genes related to the response to steroid hormone stimulus. Ingenuity pathway analysis of enriched SHR-specific genes revealed that 2 transcriptional regulators, cAMP responsive element modulator (Crem) and Fos-like antigen 1 (Fosl1), interact with blood pressure-regulating genes, such as neurotensin (Nts), apelin (Apln) and epoxide hydrolase 2, cytoplasmic (Ephx2). Similar analyses of SHRSP-specific genes revealed that angiotensinogen (Agt), one of the blood pressure-regulating genes, plays pivotal roles among SHRSP-specific genes. Moreover, genes associated with ADHD, such as low density lipoprotein receptor (Ldlr) and Crem, are discussed.
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PMID:Genetic analysis of genes causing hypertension and stroke in spontaneously hypertensive rats. 2352 2