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

Medetomidine and xylazine are alpha 2 adrenoceptor agonists which are used as sedatives and premedicants in small animals. However, bradycardia is a side effect and the use of atropine sulphate has been recommended to counteract it. This study investigated the effects of combining medetomidine (40 micrograms/kg) and atropine (30 micrograms/kg) on the cardiopulmonary function of six dogs. Medetomidine administered alone caused severe bradycardia, but hypertension was mild and transient. Medetomidine and atropine administered together caused an initial bradycardia, but within 15 minutes there was tachycardia accompanied by a mean arterial blood pressure of 210 mm Hg. When atropine was administered 30 minutes before medetomidine, tachycardia and hypertension were observed within five minutes of the medetomidine injection. Thus, although atropine will counteract medetomidine-induced bradycardia, its use results in prolonged and severe hypertension, in association with the tachycardia. Although atropine may be life-saving when bradycardia is profound, its indiscriminate use in combination with alpha 2 adrenoceptor agonists may be disadvantageous.
Vet Rec 1996 Jan 06
PMID:Cardiopulmonary effects of combinations of medetomidine hydrochloride and atropine sulphate in dogs. 882 26

More than 100 million women worldwide are thought to use steroid hormone contraceptive methods, with an estimated 93 million women using combined oral contraceptives (COCs). The composition and use of these contraceptive preparations, especially those of COCs, have changed dramatically over the years. The World Health Organization (WHO) convened a Scientific Group Meeting on Cardiovascular Disease and Steroid Hormone Contraception during November 3-7, 1997, to review current scientific data on the use of steroid hormone contraception as they relate to the risk of myocardial infarction, ischemic and hemorrhagic stroke, and venous thromboembolic disease. The group also reviewed the incidence of cardiovascular disease among women of reproductive age in general, how the effect of risk factors for cardiovascular disease may be changed using hormonal contraceptives, and whether different compositions of COCs have different cardiovascular risk profiles. The group was comprised of the authors of background papers prepared for the meeting and experts from around the world. The scientific group's conclusions are presented. The incidence and mortality rates of all cardiovascular diseases are very low among reproductive-age women. For women who do not smoke, who have their blood pressure checked, and who do not have hypertension or diabetes, the risk of myocardial infarction in COC users is not increased regardless of age. While current users of COCs have a low absolute risk of venous thromboembolism, their risk is still 3-6 times greater than that of nonusers, with the risk probably being highest during the first year of use.
Wkly Epidemiol Rec 1997 Nov 28
PMID:WHO scientific group meeting on cardiovascular disease and steroid hormone contraceptives. 940 87

Arterial hypertension produces changes along the vascular tree. However, there are few reports on its effect on human muscle capillaries. This study demonstrates the effects of essential hypertension on the capillaries of human quadriceps muscle. Muscle biopsy was taken from quadriceps femoris in eight men with recent diagnosis of essential hypertension, without treatment. Biopsies were also taken from eight normotensive men and were used as controls. Fiber types were classified by ATPase reaction, capillaries counted in alpha-amylase-PAS stained sections and ultrastructure studied by conventional methods of transmission electron microscopy. No changes were found in capillaries or muscle fiber types by histochemical methods. However, electron microscopy revealed abnormal capillaries with endothelial cells infoldings into the lumen, as well as occluded or degenerated capillaries. In some cases the endothelial cell area covered by pericytes was increased. Basement membrane of capillaries was frequently increased in width, sometimes irregularly, and in other instances it was reduplicated. In transversely sectioned capillaries lumen diameter was reduced and wall thickness was increased, although total diameter was unchanged. In hypertensive patients the finding of some degenerated capillaries adjacent to muscle fibers could be interpreted as the beginning of a process of rarefaction. Some capillaries showed morphological changes, and the ratio wall thickness/lumen was increased.
Anat Rec 1999 12 01
PMID:Capillary changes in skeletal muscle of patients with essential hypertension. 1058 28

Early toxicity occurring during or immediately after 3,4-methylenedioxymethamphetamine (MDMA, or "ecstasy") administration has not been investigated in detail, although in humans it is responsible for marked side effects, and even death. Acute toxicity induced by MDMA produces rhabdomyolysis involving the myocardium (myocytolysis). Cardiac symptoms, such as tachycardia, hypertension, and arrhythmia, are present to a variable extent in humans abusing ecstasy. In most cases, this substance is abused in the presence of loud noise, which may affect the myocardium. Despite the frequency of the concomitant exposure to ecstasy and loud noise, and the similarities between the early side effects of these two agents, to our knowledge no study has investigated the role of loud noise in modulating MDMA toxicity. Therefore, in the present study, we evaluated whether cardiac effects of MDMA administration following a typical "binging" pattern are enhanced by concomitant exposure to loud noise. We selected low doses of MDMA in order to avoid gross morphological alterations, or lesions detectable under light microscopy. The myocardial alterations observed were visible only at the ultrastructural level. We found a dramatic enhancement of alterations in the mouse heart upon MDMA administration during loud noise exposure. Remarkably, this enhancement was evident both as a decrease in the threshold dose of MDMA necessary to alter the myocardial ultrastructure, and as an increase in myocardial alterations produced by a higher dose of MDMA.
Anat Rec 2002 May 01
PMID:Morphological effects in the mouse myocardium after methylenedioxymethamphetamine administration combined with loud noise exposure. 1198 90

This study focuses on certain aspects of the renal structure of the giraffe, with some implications as to its function. About 4,000 collecting ducts open at the truncated end of a curved crest that juts into the renal pelvis as the inner medulla (IM). Extensions of the pelvis pass between the medullary (MP) and vascular (VP) processes almost to the corticomedullary border. The MPs contain an IM and an outer medulla (OM) containing clusters of capillaries (vascular bundles). The VPs contain the interlobar arteries and veins. All of the IM and almost all of the OM, with its vascular bundles, are bathed with pelvic urine. The cortex comprises 63% of the parenchyma. The OM has nine times the mass of the IM. The IM comprises 4% of the parenchyma. The ratio of mass of the adult cortex to the medulla is 1.7:1.0, and the number of glomeruli per kidney is 6.6 x 10(6). Glomerular mass is 6.2-6.7% of renal mass in the adult and 5.2% in the 6-month-old calf. The dimensions of the glomerular capsules are the same across the thickness of the cortex. Every terminal collecting duct drains an estimated 1,650 nephrons. In the adult giraffe the ratio of thickness of the muscularis of the main renal artery (RA) to its diameter is 0.117 (right RA) and 0.132 (left RA). These ratios are close to those in rhinoceros and ox but greater than in man. The visceral arteries (celiac, anterior mesenteric, and renal) have about the same muscularis : diameter ratio. Giraffes have arterial hypertension, but atherosclerosis is apparently absent and serum lipid fractions are low.
Anat Rec 2002 Jun 01
PMID:Kidney of giraffes. 1199 78

Ocular vasculopathy resulting from severe systemic hypertension affects retina, choroidea, and the optic nerve. While the pathologic changes of the arterial system, including luminal narrowing, are well documented, little is known about the ocular venous vessels in hypertension. Adult 18-week-old spontaneously hypertensive rats (SHRs) were untreated (control) or treated with lisinopril for 4 weeks; normotensive Wistar-Kyoto (WKY) rats were additional controls. The mean systemic blood pressure (MSP) was monitored chronically using telemetry. The ocular microvasculature was examined using scanning electron microscopy (SEM) of corrosion casts, histology of serial sections, and computer-based 3D reconstruction. The MSP in control SHRs (145 +/- 11.9 mmHg) was decreased to 68.1 +/- 4.9 mmHg (P < 0.001) following treatment, which was even below the baseline level of WKY (96.7 +/- 5.8) rats (P < 0.05). In addition to media thickening in arteries, the venous plexus of the choroidea in control SHRs revealed multiple tufts of smooth muscle cells (sphincters) that narrowed the lumen. Correlating to histology, SEM of casts and 3D reconstruction showed numerous constrictions and muscular tufts in veins of the choroidea, narrowing the vascular lumen up to 47%. Following antihypertensive treatment, the percentage of sphincter constriction was decreased to 6% (P < 0.001). The depth of venous sphincter contraction correlated significantly with MSP (r = 0.87). To our knowledge, these results indicate for the first time that venous sphincters occur in the choroidea of the SHRs, and that their muscularity correlates with MSP. Venous sphincters might be involved in the pathophysiology of hypertension-related ocular changes.
Anat Rec A Discov Mol Cell Evol Biol 2005 Jun
PMID:Venous sphincters in the choroidea of spontaneously hypertensive rats. 1580 78

The 5500T allele variant of the C5500T single nucleotide polymorphism in the human G protein beta3 subunit (GNB3) has been reported to be associated with primary hypertension. In this study, the GNB3 gene of primary hypertensive and normotensive dogs was examined for an analogous nucleotide polymorphism associated with hypertension. The genomic GNB3 dna, with 10 exons and nine introns coding for 340 amino acids, is described. PCR product sequencing of the GNB3 exon 9 from 25 dogs (including five hypertensive animals) failed to detect any nucleotide polymorphism. In contrast to human beings, there was no polymorphism at either the analogous nucleotide or in the respective exon. Only the human hypertension-associated thymine was detected, regardless of whether the dogs were hypertensive or normotensive. Furthermore, examinations of 565 dogs of 85 distinct breeds for the presence of the human 5500C nucleotide at the analogous nucleotide side failed to detect a cytosine that is present with high allele frequency in normotensive man. Owing to the lack of allele variance, it is concluded that canine primary hypertension is not associated with a polymorphism at either the respective human hypertension-associated nucleotide site or in the entire exon.
Vet Rec 2007 May 12
PMID:Lack of GNB3 exon 9 polymorphism in primary hypertensive and normotensive dogs. 1749 72

A 15-year-old girl had exertion dyspnea, focal nodular hyperplasia of the liver, portal vein hypoplasia, portopulmonary hypertension, mental retardation, and minor facial abnormalities. Cytogenetic analysis demonstrated an abnormal chromosome 8 with 8p22-pter duplication and 8q24.3-qter deletion, with the duplicated 8p segment attached to band 8q24.3. Her mother had a pericentric inversion of chromosome 8, inv(8)(p22q24.3). Therefore, the girl's abnormal chromosome 8 was a recombinant of maternal inversion chromosome: 46,XX,rec(8)dup(8p)inv(8)(p22q24.3)mat. Further characterization of the recombinant chromosome, using array CGH and regional FISH analyses, defined 15 Mb distal 8p duplication and 0.5 Mb 8q deletion. Possible correlation of the recombinant chromosome and hepatic focal nodular hyperplasia in the patient is discussed.
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PMID:dup(8p)/del(8q) recombinant chromosome in a girl with hepatic focal nodular hyperplasia. 1750 94

Proteinuria and systemic hypertension are well recognised risk factors in chronic renal failure (CRF). They are consequences of renal disease but also lead to a further loss of functional kidney tissue. The objectives of this study were to investigate the associations between proteinuria, systemic hypertension and glomerular filtration rate (GFR) in dogs with naturally occurring renal and non-renal diseases, and to determine whether proteinuria and hypertension were associated with shorter survival times in dogs with CRF. Measurements of exogenous creatinine plasma clearance (ECPC), urine protein:creatinine ratio (UPC), and Doppler sonographic measurements of systolic blood pressure (SBP) were made in 60 dogs with various diseases. There was a weak but significant inverse correlation between UPC and ECPC, a significant inverse correlation between SBP and ECPC and a weak but significant positive correlation between UPC and SBP. Some of the dogs with CRF were proteinuric and almost all were hypertensive. Neoplasia was commonly associated with proteinuria in the dogs with a normal ECPC. CRF was the most common cause leading to hypertension. In the dogs with CRF, hypertension and marked proteinuria were associated with significantly shorter survival times.
Vet Rec 2008 Feb 02
PMID:Associations between proteinuria, systemic hypertension and glomerular filtration rate in dogs with renal and non-renal diseases. 1828 33

To test the hypothesis that acepromazine could potentiate the sedative actions and attenuate the pressor response induced by dexmedetomidine, the effects of acepromazine or atropine were compared in six healthy adult dogs treated with this alpha2-agonist. In a randomised block design, the dogs received intravenous doses of either physiological saline, 0.05 mg/kg acepromazine or 0.04 mg/kg atropine, 15 minutes before an intravenous dose of 5 microg/kg dexmedetomidine. The dogs' heart rate was reduced by 50 to 63 per cent from baseline and their mean arterial blood pressure was increased transiently from baseline for 20 minutes after the dexmedetomidine. Atropine prevented the alpha2-agonist-induced bradycardia and increased the severity and duration of the hypertension, but acepromazine did not substantially modify the cardiovascular effects of the alpha2-agonist, except for a slight reduction in the magnitude and duration of its pressor effects. The dexmedetomidine induced moderate to intense sedation in all the treatments, but the dogs' sedation scores did not differ among treatments. The combination of acepromazine with dexmedetomidine had no obvious advantages in comparison with dexmedetomidine alone, but the administration of atropine before dexmedetomidine is contraindicated because of a severe hypertensive response.
Vet Rec 2008 Jun 28
PMID:Sedative and cardiorespiratory effects of acepromazine or atropine given before dexmedetomidine in dogs. 1858 62


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