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

Acute studies suggest that leptin has pressor and depressor actions, including stimulation of sympathetic activity as well as increased release of NO from the vascular endothelium. The goal of this study was to examine the role of NO in modulating the chronic blood pressure, heart rate, and renal responses to hyperleptinemia, comparable to that found in obesity-induced hypertension. Male Sprague-Dawley rats were implanted with arterial and venous catheters, and mean arterial pressure and heart rate were monitored continuously 24 h/d. After a 4-day control period, the rats were infused with isotonic saline vehicle (n=6) or N(G)-nitro-L-arginine methyl ester (L-NAME, 10 microgram/kg per minute; n=9) to inhibit NO synthesis for 7 days. After 7 days of vehicle or L-NAME administration, leptin was infused intravenously for 7 days at a rate of 0.5 microgram/kg per minute, followed by a leptin infusion at 1.0 microgram/kg per minute for 7 days, along with vehicle or L-NAME. A 21-day infusion of L-NAME alone (n=6) served as a control for the L-NAME+leptin rats. Although the low dose of leptin alone did not significantly elevate arterial pressure, it raised the heart rate by 18+/-3 bpm. The higher leptin infusion rate raised arterial pressure from 96+/-3 to 104+/-3 mm Hg but did not increase the heart rate further. L-NAME+leptin increased arterial pressure by 40+/-6 mm Hg and heart rate by 79+/-19 bpm compared with pretreatment levels. In control L-NAME rats, mean arterial pressure increased by 31+/-4 mm Hg, whereas the heart rate was not altered significantly compared with pretreatment levels. Neither chronic leptin infusion alone nor L-NAME alone altered the glomerular filtration rate or renal plasma flow significantly, but L-NAME+leptin reduced glomerular filtration rate by 27+/-11% and renal plasma flow by 47+/-9%. These results indicate that impaired NO synthesis mildly enhances the chronic renal hemodynamic and hypertensive effects of leptin but markedly amplifies the tachycardia caused by hyperleptinemia.
Hypertension 2001 Feb
PMID:Inhibition of NO synthesis enhances chronic cardiovascular and renal actions of leptin. 1123 Mar 54

A 21-year-old woman with a 6-year history of ulcerative colitis admitted to our hospital with chest pain, cough and fever of unknown origin in August 1998. On admission, laboratory data showed positive inflammatory signs. A chest radiograph and chest computed tomogram (CT) revealed nodular shadows in the right upper lung field. Fifty days after admission, hypertension developed and a bruit was audible in the neck and the upper abdomen. Digital subtraction angiography showed stenosis in carotid, renal and right upper pulmonary arteries. On the basis of these results, a diagnosis of aortitis syndrome was made. Moreover, these findings indicated pulmonary infarction in the right upper lobe due to aortitis syndrome. Aortitis syndrome preceded by pulmonary infarction involvement is very rare. Autoimmune disorders may have been involved in this case because of the association with ulcerative colitis.
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PMID:[Aortitis syndrome associated with ulcerative colitis, preceded by pulmonary infarction involvement]. 1148 30

Transgenic TGR(mREN2)27 rats (TGR), carrying an additional mouse renin gene, are characterized by severe hypertension, an inverse circadian blood pressure profile, a blunted response to photic entrainment signals, and an increased nocturnal production of the pineal hormone melatonin. In order to evaluate the contribution of the over-expressed renin-angiotensin system to the function of the pineal gland in TGR, we studied the adrenergic and angiotensin II (Ang II)-mediated regulation of melatonin synthesis using dispersed pinealocytes from TGR and from Sprague-Dawley control rats (SDR). Isoproterenol was more effective in stimulating melatonin release in pinealocytes from TGR than from SDR, whereas the maximum effect of norepinephrine (NE) stimulation did not differ between the strains. Prazosin reduced the NE-mediated melatonin release only in SDR but not in TGR pinealocytes. Competition experiments with (+/-)-, (+)-, (-)-propranolol and (+/-)-atenolol revealed one homogeneous population of beta1-adrenoceptors. Ang II had no significant effect on basal or isoproterenol-induced melatonin release in either strain. In conclusion, TGR pinealocytes were more sensitive to beta-adrenergic stimulation than SDR pinealocytes, but lacked the alpha1-adrenergic potentiation of beta-adrenergic induced melatonin release. The renin-angiotensin system was not directly involved in the regulation of melatonin synthesis by rat pinealocytes in vitro.
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PMID:Altered melatonin production in TGR(mREN2)27 rats: on the regulation by adrenergic agonists, antagonists and angiotensin II in cultured pinealocytes. 1158 61

A 21-year-old woman experienced severe headache and nausea one hour after taking pills containing 160 mg of phenylpropanolamine for common cold. She had no previous history of drug abuse or hypertension. Physical examination revealed slight left-sided hemiparesis. Her blood pressure was 100/52 mmHg. Subcortical hemorrhage was noted in the right frontal lobe with a cranial computed tomography. On the seventh hospital day, cerebral angiography demonstrated with segmental narrowing of a branch of the right anterior cerebral artery, indicating the presence of focal angitis. This finding disappeared on the 35th hospital day. In the majority of the reported cases of the intracerebal hemorrhage associated with the ingestion of phenylpropanolamine, focal angitis rather than induced hypertension is considered to be a causative factor for hemorrhage. Thus, we would like to emphasize that the administration of phenylpropanolamine should be avoided, even to the patients without hypertention or past history of intracerebral hemorrhage.
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PMID:[A case with cerebral subcortical hemorrhage following the administration of phenylpropanolamine]. 1180 51

In double transgenic rats (dTGR) harboring the human angiotensinogen (hAOGEN) and human renin (hREN) genes, we studied cardiac transcript levels of hypertrophy-related, Ca(2+) regulatory, and beta-adrenoceptor-associated proteins. The contractile properties and the cellular signaling of isolated hearts exposed to (-)isoproterenol and/or angiotensin (Ang) I were evaluated. dTGR developed hypertension of 174.1+/- 7.6 versus 109.6 +/- 2.0 mm Hg (P<0.05) in Sprague-Dawley rats and heart hypertrophy. In hearts of dTGR, the transcript levels of ANP, beta-MHC, and alpha-MHC were altered (percentage versus Sprague-Dawley rats, 100%) by 304%, 178%, and 78%, respectively. Transcript levels of L-type Ca(2+) channel, Ca(2+) release channel, SERCA2a, phospholamban, G(i)- and G(s)-proteins were unchanged. Isolated hearts of dTGR indicated higher baseline contractility versus Sprague-Dawley rats. (-)Isoproterenol-modified contractility occurred in both groups; however, the extent (predrug value, 100%) was less in hearts of dTGR versus Sprague-Dawley rats (+dP/dt, 310 +/- 42% versus 534 +/- 63%; P<0.05). Interestingly, (-)isoproterenol shortened the relaxation time by equivalent to 25% in both groups. This finding was reflected by a protein kinase A-related phospholamban phosphorylation. Ang I depressed the heart contractility but did not interact with the protein kinase A pathway. In conclusion, we have found that expression of the hAOGEN-hREN complex in dTGR elicited specific effects on transcripts of ANP and myofibrillar proteins. Although the beta-adrenergically mediated relaxation was not impaired in the hypertrophied hearts, the extent of beta-adrenergic inotropic responsiveness was reduced.
Hypertension 2002 Feb
PMID:Expression of human angiotensinogen-renin in rat: effects on transcription and heart function. 1184 87

There is a small increase in the functional beta2-adrenoceptor response on the spontaneously hypertensive rat (SHR) left atrium in the early stages of hypertension. In the present study, the functional beta1- and beta2-adrenoceptors of the left and right atrium in SHR pre-hypertension and age-matched (5-week-old) Wistar Kyoto (WKY) rats were characterized. Contractility methods with isoprenaline, T-0509 (a selective beta1-adrenoceptor agonist) and procaterol (a selective beta2-adrenoceptor agonist) were used. At 5 weeks, the SHRs were pre-hypertensive. Isoprenaline was more potent on the left atrium of 5-week-old SHRs than WKY rats. Bisoprolol, a selective beta1-adrenoceptor antagonist, was more potent against isoprenaline and T-0509 on the SHR than WKY rat left atrium. ICI 118,551, a selective beta(2)-adrenoceptor antagonist, was more potent against procaterol and T-0509 on the SHR than WKY rat left atrium. The results with bisoprolol and ICI 118,551 suggest that there are more functional beta(1)- and beta(2)-adrenoceptors on the left atrium of 5-week-old SHRs than WKY rats. Isoprenaline, T-0509 and procaterol were equipotent on the right atrium of 5-week-old WKY rats and SHRs. Bisoprolol was more potent against isoprenaline, T-0509 and procaterol on the SHR than WKY rat right atrium. ICI 118,551 was more potent against T-0509, but not isoprenaline and procaterol, on the SHR than WKY rat left atrium. This suggests there are more functional beta1-adrenoceptors, and probably more functional beta2-adrenoceptors, on the right atrium of 5-week-old SHRs than WKY rats. These functional differences in beta1- and beta2-adrenoceptor-mediated responses of the left and right atria of pre-hypertensive SHRs cannot be caused by hypertension, and may be associated with the onset of hypertension.
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PMID:Functional beta1- and beta2-adrenoceptors in the left and right atrium of pre-hypertensive rats. 1239 4

Cardiac hypertrophy is often associated with an increased sympathetic drive, and both in vitro and in vivo studies have demonstrated the development of cardiomyocyte hypertrophy in response to either alpha- or beta-adrenergic stimulation. Because an association between the Na+/H+ exchanger and cellular growth has been proposed, this study aimed to analyze the possible role of the antiporter in isoproterenol-induced cardiac hypertrophy. Isoproterenol alone (5 mg/kg IP once daily) or combined with a selective inhibitor of the Na+/H+ exchanger activity (3 mg x kg(-1) x d(-1) BIIB723) was given to male Wistar rats for 30 days. Sex- and age-matched rats that received 0.9% saline IP daily served as controls. Echocardiographic follow-up showed a 33% increase in left ventricular mass in the isoproterenol-treated group, whereas it did not increase in the isoproterenol+BIIB723-treated group. Heart weight-to-body weight ratio at necropsy was 2.44+/-0.11 in controls and increased to 3.35+/-0.10 (P<0.05) with isoproterenol, an effect that was markedly attenuated by BIIB723 (2.82+/-0.07). Intense cardiomyocyte enlargement and severe subendocardial fibrosis were found in isoproterenol-treated rats, and both effects were attenuated by BIIB723. Myocardial Na+/H+ exchanger activity and protein expression significantly increased in isoproterenol-treated rats compared with the control group (1.45+/-0.11 vs 0.91+/-0.05 arbitrary units, P<0.05). This effect was significantly reduced by BIIB723 (1.17+/-0.02, P<0.05). In conclusion, our results show that Na+/H+ exchanger inhibition prevented the development of isoproterenol-induced hypertrophy and fibrosis, providing strong evidence in favor of a key role played by the antiporter in this model of cardiac hypertrophy.
Hypertension 2003 Jun
PMID:Regression of isoproterenol-induced cardiac hypertrophy by Na+/H+ exchanger inhibition. 1273 84

The hypothesis that cross-talk between membrane-active beta-adrenergic agonists and estrogens includes beta-adrenergic modulation of estrogen receptor (ER)-regulated gene expression was investigated. Vascular smooth muscle-derived A7r5 cells were transfected with an ERalpha expression plasmid (pCR3.1-hERalpha), the estrogen response element (ERE)-linked reporter pERE-E1b-luciferase (ERE-Luc), and pCMV-beta-galactosidase using a lysine-conjugated adenovirus transfection method. Hormone or agonist treatment and harvest followed 6 hours and 24 hours later, respectively. Treatment with 17beta-estradiol (E(2), 1 nmol/L) significantly stimulated ERE-Luc activity. Isoproterenol (10-9 to 10-6 mol/L) treatment alone did not stimulate ERE-Luc activity. Cotreatment with both E(2) and isoproterenol resulted in complete inhibition of E(2)-stimulated ERE-Luc activity. This isoproterenol effect was prevented by the beta-adrenergic antagonist propanolol (10-6 mol/L). Adrenomedullin treatment in these cells (1-50 nmol/L) did not inhibit ER/ERE-Luc activity, whether in the presence or absence of E(2). Moreover, isoproterenol did not affect vitamin D-stimulated VDRE-Luc expression, indicating that the inhibitory effect of isoproterenol on E(2)-directed ERE-Luc expression is specific among nuclear transcription factor receptors. Moreover, in MCF-7 breast cancer cells, there was no effect of isoproterenol on ER/ERE-directed transcription in the absence or presence of E(2), demonstrating tissue specificity of this isoproterenol effect. These studies demonstrate cross-talk between the beta-adrenergic agonist isoproterenol and ER-directed reporter gene expression in A7r5 cells. Furthermore, this cross-talk is specific with respect to agonist, nuclear receptor species, and cell type. These observations may have important implications both for the use of beta-adrenergic agents to treat hypertension and for possible gender-related differences in cardiovascular regulation.
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PMID:Cross-talk between beta-adrenergic stimulation and estrogen receptors: isoproterenol inhibits 17beta-estradiol-induced gene transcription in A7r5 cells. 1288 32

We report a case of benign intracranial hypertension (BIH) caused by all-trans retinoic acid (ATRA) in a patient with acute promyelocytic leukemia. A 21-year-old male was admitted to our hospital with pancytopenia. He was diagnosed as having acute promyelocytic leukemia due to increased promyelocytes, and PML-RAR alpha chimeric mRNA was detected. The administration of ATRA and idarubicin was started immediately. After 26 days of the chemotherapy, he complained of diplopia. Ophthalmologic examination revealed bilateral papilledema and hemorrhage. The cerebrospinal fluid showed an increase in pressure, but no other abnormalities. Computed tomography showed no intracranial abnormalities. The orbital MR imaging showed distension of the perioptic subarachnoid space and flattening of the posterior sclera. A diagnosis of BIH was made. After the discontinuation of ATRA, the symptoms improved and the MR abnormalities disappeared. As far as we know, there have been no reports illustrating MR abnormalities of BIH caused by ATRA, for the diagnosis and monitoring of which orbital MR imaging can provide important clues.
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PMID:[MR imaging provides important clues for the diagnosis of benign intracranial hypertension by all-trans retinoic acid in a patient with acute promyelocytic leukemia]. 1504 22

1. The aim of the present study was to investigate the activity of anterior hypothalamic beta-adrenoceptors and angiotensin (Ang) II receptors on blood pressure in normotensive rats and aortic-coarctated (ACo) animals at a chronic stage of hypertension. A possible interaction between beta-adrenoceptors and AngII pressor activity was also investigated. 2. Injection of isoproterenol (0.1-10 nmol) in the anterior hypothalamic area induced a dose-dependent decrease in mean arterial pressure (MAP) in sham-operated (SO), but not in ACo, animals. Isoproterenol (1 nmol) reduced blood pressure in SO rats (DeltaMAP -10.1+/-1.4 mmHg; n=10) but not in ACo animals (DeltaMAP -0.9+/-1.6 mmHg; n=10; P<0.05 vs SO rats). Whereas previous administration of atenolol (40 nmol) enhanced the cardiovascular effect of isoproterenol (1 nmol) in ACo rats but not in SO animals, propranolol (40 nmol) prevented the hypotensive action of isoproterenol in both experimental groups. Intrahypothalamic administration of clenbuterol decreased MAP in a dose-dependent manner; however, the depressor response to clenbuterol (10 nmol) was greater in ACo rats than in SO rats (DeltaMAP -26.8+/-3.2 vs -14.4+/-2.4 mmHg, respectively; n=5 for both; P<0.05). When AngII (50 ng) was injected into the anterior hypothalamic area, a greater pressor response was observed in ACo rats than in SO rats (DeltaMAP 19.6+/-1.1 vs 11.3+/-0.6 mmHg, respectively; n=5 for both; P<0.05). Atenolol (40 nmol) pretreatment partially and significantly prevented the pressor response to AngII in ACo rats, but not in SO rats. 3. In conclusion, these results provide pharmacological evidence for the existence of a beta1-adrenoceptor-mediated pressor mechanism in the anterior hypothalamic area of ACo rats that is absent in SO rats. The enhanced depressor beta2-adrenoceptor activity observed in chronic ACo rats could be a compensatory adjustment to pressor beta1-adrenoceptor activity. Conversely, pressor overactivity of AngII was observed in the anterior hypothalamic area of ACo rats at a chronic hypertensive stage; this enhancement could be explained, at least in part, by the pressor beta1-adrenoceptor activity.
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PMID:Anterior hypothalamic beta-adrenoceptors in chronic aortic-coarctated hypertensive rats: an interaction with central angiotensin II receptors. 1573 Apr 31


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