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Biomedical subjects

J M Rojo-Ortega

Publications and source records attributed to J M Rojo-Ortega.

At least 19 recordsLinked to original sources
PubMed1993

Electrocardiographic patterns in V4R lead in experimental right ventricular infarction of rats.

Twenty-four male rats that became hypertensive after complete ligature of the abdominal aorta, just above the origin of the left renal artery, showed combined myocardial infarction. To study the electrocardiographic patterns of the experimental right ventricular infarction, the V4R right thoracic lead was recorded at different time intervals after aortic ligature. The patterns recorded were as follows: Q waves in 23 cases (95.8%), ST-T segment elevation in 11 cases (45.8%), ST-T segment depression in two cases (8.3%), and decrease in voltage of R wave in four cases (16.6%), with a predominance of the alterations of the ST-T segment in the acute phase and the appearance of Q waves during the subacute phase.

Animals↗
PubMed1987

[Reflex pressure response to the electric stimulation of different parts of the rat stomach].

The role of the autonomic nervous system in the pressor response to the electrical stimulation of different gastric zones has been studied in rats. The stimulus was applied before and after the following interventions: bilateral vagotomy, ganglionic blockade, alpha-adrenergic receptor blockade and beta-adrenergic receptor blockade. After the ganglionic blockade no pressor responses to the electrical stimulus were observed. After the alpha-adrenergic blockade a lower pressor response was observed. A hypertensive response can be induced by mechanical, chemical or electrical stimulation of gastric receptors. It is concluded that the pressor reflex following the application of an electrical stimulus on different zones of the digestive tract is mediated by the sympathetic nervous system and that the efferent pathways are mainly alpha-adrenergic ones.

Adrenergic alpha-Antagonists↗
PubMed1987

Reflex pressor response to gastric mechanical stimulation in rats.

Neural and humoral mechanisms involved in the reflex pressor response during mechanical stimulation of the stomach of rats were investigated. The arterial blood pressure response was prevented by inhibition of alpha-adrenergic vasoconstriction using either an alpha-adrenergic blocker or a ganglionic blocker. In addition, there was a small decrease in the response after nephrectomy. However, there were no alterations in the response after beta-adrenergic blockade, bilateral adrenalectomy, inhibition of converting enzyme activity with enalapril or bilateral cervical vagus nerve transection. The heart rate was not modified after either intervention. After vagotomy the time of recovery of the basal blood pressure was significantly prolonged. It can be concluded that the blood pressure response to mechanical stimulation of the stomach wall is of neural rather than of humoral origin and mainly involves activation of alpha-adrenergic receptors. Vagal efferent pathways could be also involved.

Adrenalectomy↗
PubMed1987

Predominant right ventricular infarction in malignant renovascular hypertension in rats.

Malignant hypertension was induced in Wistar rats of both sexes by complete aortic ligature just above the origin of the left renal artery. An acute and a late phase of hypertension, 4 days and 28 days after the aortic ligature respectively, were defined to study the relationship between the severity of hypertension and injury of the small arteries and myocardial necrosis. The most frequent finding in the heart was the presence of right ventricular infarction. In acute-phase hypertension most of the animals showed acute infarction of the right ventricle, but only focal left ventricular infarction was found. Lesions in the large coronary arteries were not observed. However, the small arteries and arterioles of the right ventricle presented fibrinoid necrosis lesions. In late-phase hypertension, the intramyocardial small vessels showed proliferative endarteritis and fibrinoid necrosis lesions, but this time they appeared in both ventricles. The severity of the myocardial infarcts and the percentage of small arteries and arterioles injured in the right ventricle were significantly higher than in the left ventricle despite the maintenance of blood pressure almost to the same level. No changes in the right ventricular pressure were observed in either phase. These observations suggest that in malignant renovascular hypertension the intramyocardial arteriolar lesions appear to be an important factor in the production and the severity of myocardial infarcts with predominance in the right ventricle.

Animals↗
PubMed1986

Reduced ethanol consumption during cyproheptadine administration in rats from a long-term alcohol-treated colony.

The influence of cyproheptadine (CPH) on forced and voluntary ethanol intake was studied in long-term alcohol-treated rats. Wistar rats from a colony (WAC) that have been drinking alcohol as their only liquid fluid for the 25 previous generations and from a genetically related colony (WN) that had never been given alcohol were used. In the first experiment, daily IP doses of 15 mg/kg CPH were found to reduce forced ethanol consumption during CPH treatment in both WAC and WN rats which had been drinking ethanol for six months. In two additional groups of WAC and WN rats which were not given ethanol, water intake was not affected by CPH administration. In a second experiment, alcohol preference was reduced both during and after CPH, but total fluid intake (ethanol + water) was not affected. These findings suggest that the effect of CPH could be specific to ethanol. The decrease in ethanol consumption was associated with a significant body weight loss; this result may support the hypothesis of a link between the serotoninergic system, food intake, and alcohol drinking behavior that has been considered by earlier investigators.

Alcohol Drinking↗
PubMed1985

Blood pressure changes after gastric mechanical and electrical stimulation in rats.

The effect of different stimuli applied in several parts of the digestive tract on blood pressure was studied in unconscious Wistar rats. Gastric distension and electrical and pinching stimuli produced a significant increase in both systolic and diastolic arterial blood pressure. When different gastric zones were stimulated by either electrical or pinching stimuli, the highest pressor response was found in the antropyloric zone. The stimuli applied to the small intestine, outside the duodenum, did not modify the blood pressure. The pinching of the abdominal peritoneum caused a pronounced (P less than 0.001) blood pressure decrease. These data suggest that the pressor response to gastric distension could be mediated by gastric mechanoreceptors. The pressor response observed after stimulation of the gastric antropyloric zone suggests that this area has a greater number of mechanoreceptors.

Animals↗
PubMed1981

Evolution and characterization of renal immune complexes deposition in mice bearing a syngeneic tumor.

Immune complex deposition along the glomerular basement membrane (GBM) and in the mesangium in C57BL/6 mice bearing a transplantable syngeneic B16 melanoma is described. By immunofluorescence studies, IgG, IgM and C3 were found deposited along the GBM and the mesangium. Electron microscopy showed electron-dense deposits localized in GBM and mesangial matrix. The intensity of the immune complexes deposited in the glomeruli was correlated with progression of tumor size. In order to study the evolution of deposits, a monitoring protocol was designed. One group consisted of mice bearing B16 melanoma. They showed decreased immune complex deposition after tumor removal. Control mice inoculated with saline did not present immune complex deposition. Sham-operated mice bearing B16 melanoma showed progressive renal deposition of immune complexes. Immune complexes were made up of tumor antigen and antimelanoma antibodies and were partial characterized by elution, immunofluorescence and immunodiffusion procedures. Antimelanoma antibodies eluted from kidneys of tumor-bearing mice were of IgG class and reacted with a soluble product extracted from B16 melanoma cells.

Animals↗
PubMed1979

Effects of sodium chloride on early and chronic phases of malignant hypertension in rats.

Malignant hypertension was induced in Sprague-Dawley rats by a complete aortic ligation above the left renal artery. The effects of saline (0.9% NaCl) administration on the development and course of the malignant hypertensive vascular disease were studied and the treated rats were compared to non-saline-treated animals and to sham-operated controls in the early and chronic phases of the disease. In the early phase, blood pressure, hematocrit, body weight, and hypertensive vascular disease were characteristic of the malignant hypertensive process and were without significant difference in saline- and non-saline-treated animals. In contrast, the sham-operated rats remained normotensive and did not present abnormal histological findings. Plasma renin activity although decreased in the hypertensive saline-treated animals was not suppressed. In the chronic phase, NaCl administration caused an average increase of 40 g body weight during the 1-wk period this solution was given, but did not result in any improvement in blood pressure levels and vascular disease in treated rats compared to non-saline-treated animals.

Acute Disease↗
PubMed1977

The inhibition by substrate analogues of gamma-aminobutyrate aminotransferase from mitochondria of different subcellular fractions of rat brain.

Cytoplasmic-mitochondria-enriched and synaptosome-enriched subcellular fractions were prepared from rat brain to study certain kinetic properties of gamma-aminobutyrate: alpha-oxoglutarate aminotransferase (GABA-T) (EC 2.6.1.19) from each of the sources. From this study two differences emerged. Firstly, the cytoplasmic enzyme exhibited an eightfold greater affinity for gamma-aminobutyric acid (GABA) than did the synaptosomal GABA-T; the Km being 6.5 mM and 53 mM, respectively. Secondly, synaptosomal GABA-T is comparatively more susceptible to inhibition by the substrate analogues 2,4-diaminobutyric acid (DABA) and aminooxyacetic acid (AOAA) than is the enzyme from the cytoplasmic mitochondrial fraction. In each case the inhibition was of a competitive nature with respect to GABA. The Ki for the DABA was 13 mM for the cytoplasmic-derived enzyme and 8mM for the synaptosomal enzyme. With AOAA the Ki was 0.1 muM and 0.06 muM for the synaptosomal and cytoplasmic mitochondrial enzyme, respectively. These results provide further evidence that GABA-T from cytoplasmic mitochondria is different in several respects from the enzyme found in synaptosomes.

4-Aminobutyrate Transaminase↗
PubMed1977

Effects of reserpine on water, cation, and norepinephrine contents of cardiovascular tissues of normotensive dogs.

Six adult male mongrel dogs were treated orally with reserpine (0.03 mg/kg) for 6 weeks, after which time the arterial tissue content of water, cations (sodium, potassium, magnesium, and calcium), and norepinephrine was determined and compared with those of six untreated dogs. Reserpine administration resulted in sustained decreases in the mean arterial blood pressure and heart rate, and the arterial tissues of the treated dogs contained less potassium, calcium, and magnesium, the last-named being affected most, but the sodium remained the same. Arterial norepinephrine content was significantly decreased. There was a slight but significant increase in plasma magnesium, without any noticeable changes in other plasma cations. The reduction in the arterial magnesium by reserpine may help to regulate vascular tone and (or) vascular reactivity.

Animals↗
PubMed1977

Effects of angiotensin II on steroid metabolism and hepatic blood flow in man.

Metabolic clearance rates (MCR) of aldosterone, cortisol, 11-deoxycorticosterone (DOC), corticosterone, and progesterone were simultaneously measured by constant infusion in eight control subjects before and during angiotensin II infusion in subpressor (3 ng/min per kg) and pressor (22 ng/min per kg) doses. Plasma levels of aldosterone and cortisol, the heat-labile protein-bound fraction of aldosterone, and hepatic blood flow (HBF) (as estimated by the fractional clearance of indocyanine green) were determined concomitantly. Angiotensin II in a subpressor dose produced a significant decrease of the MCR of aldosterone (by 23%), cortisol (by 16%), DOC (by 26%), corticosterone (by 14%) and progesterone (by 33%). The pressor dose further decreased the respective MCR by 37%, 21%, 40%, 28%, and 42% of the baseline value. Plasma aldosterone levels rose by 317% with subpressor and by 434% with pressor doses. HBF decreased by 18% with subpressor and by 33% with pressor doses of angiotensin II. Furthermore, there were significant negative correlations between the MCR of each steroid and the respective values of the fractional clearance of indocyanine green. We conclude that angiotensin II, by its vasoconstrictive action on the splanchnic vascular bed, decreases the MCR of aldosterone, cortisol, DOC, corticosterone, and progesterone. This decrease has to be taken into account when considering the stimulatory effect of angiotensin II on various plasma steroid concentrations.

Adrenal Cortex Hormones↗
PubMed1977

The role of the adrenal cortex in human essential hypertension: keynote address.

The data presented establish that in early or mild essential hypertension there is a state of inappropriate hypermineralocorticoid activity represented by the sum of aldosterone and 18-hydroxy-11-deoxycorticosterone concentrations in the plasma. This disturbance, associated with a "normal" or excessive salt intake, would produce the arteriolar cationic changes in sodium, potassium, calcium, or magnesium leading to hypersensitivity or hyperresponsiveness of the arteriolar actomyosin to normal levels of circulating norepinephrine or angiotensin. The nature of the cationic changes in the arteriolar cells responsible for the increased tonicity of the arteriolar actomyosin, which is the fundamental cause of essential hypertension, remains to be elucidated.

18-Hydroxydesoxycorticosterone↗
PubMed1975

Arterial hypertension and neurofibromatosis: renal artery stenosis and coarctation of abdominal aorta.

A 10-year-old girl had arterial hypertension, generalized neurofibromatosis, coarctation of the abdominal aorta and multiple stenoses at the origin of each renal artery. After resection of the stenotic areas and reimplantation of the renal arteries in the aorta, her arterial pressure decreased substantially. However, hypertension recurred and radiologic follow-up 4 1/2 years later showed distinct progression of the coarctation and renewed stenosis of all renal arteries at their origin. The stenotic areas showed eccentric intimal proliferation, frequently bulging into the lumen, with small nodular aggregates of smooth muscle cells and proliferation of fibrous tissue containing spindle-shaped nuclei in a palisading pattern. Hypertension associated with neurofibromatotic vascular disease has been described in 47 other patients in the literature. These patients have been young (mean age, 14 years) and predominantly male. In contrast to fibromuscular dysplasia, in which 95% of all stenoses are found in the distal two thirds of the renal arteries, in vascular neurofibromatosis more than 50% of the stenoses are found at the origin.

Adolescent↗
PubMed1975

Aldosterone and renin in essential hypertension.

A review of some recent laboratory findings indicates definite disturbances in aldosterone metabolism and regulation in patients with mild essential hypertension: (a) a significant mean increase in plasma aldosterone concentration in patients with mild and stable essential hypertension, in contrast to the absence of any difference in patients with labile borderline essential hypertension when in a normotensive phase, compared with control subjects; and (b) a significant mean decrease in metabolic clearance rate of aldosterone, associated with a 12% decrease in hepatic blood flow and an increased binding of aldosterone to a transcortin-like plasma globulin. The secretion rate of 18-hydroxy-11-deoxycorticosterone is above the upper range of normal in 60% of patients with mild, uncomplicated essential hypertension. The incidence of low-renin hypertension, when age and race are taken into account, is much lower than previously assumed. Unless measurements are repeated over a long period, one or two low values of plasma renin cannot be considered a permanent marker indicating a special category of patients with essential hypertension. Tonin, a new enzyme discovered by Boucher, which forms angiotensin II directly from a plasma protein, from the tetradecapeptide substrate and from angiotensin I, is present in most tissues, but in highest concentration in the submaxillary gland. This enzyme is under the control of beta-adrenergic receptors.

18-Hydroxydesoxycorticosterone↗
PubMed1975

Cytochemical localization of adenyl cyclase in the rat colonic mucosa.

Adenyl cyclase has been demonstrated in the colonic mucosa with the aid of adenylyl-imidodiphosphate as a specific substrate. Coarse precipitates are located mainly in the basement membrane and in the junctional area between two epithelial cells and on the brush border of all epithelial cells of the descending colon. Hydrolysis of the substrate was found to be accelerated by 10 mM sodium fluoride in the incubation medium. However, in the ascending colon, the precipitate appeared only in the brush border.

Adenosine Diphosphate↗
PubMed1975

Water, cations, and norepinephrine content of cardiovascular tissues of unilaterally nephrectomized dogs treated with deoxycorticosterone and NaCl.

Deoxycorticosterone pivalate (2.5 mg/kg) given intramuscularly on four occasions 10-15 days apart over a period of 45 days to unilaterally nephrectomized adult male mongrel dogs, receiving as drinking solution 0.9% NaCl in 5% dextrose, resulted in an average sustained rise in the mean arterial blood pressure of 30 mm Hg (1 mm Hg - 133 N/m2) in 60% of the animals. Hypertensive dogs had in their arterial tissues generally more sodium, potassium, magnesium, and calcium than the similarly treated but non-hypertensive dogs, but compared to the tissues of operated untreated or unoperated normotensive dogs, only sodium and calcium were significantly higher. The dogs who were similarly treated but did not develop hypertension had in their arterial tissues less sodium, potassium, and magnesium than operated untreated or unoperated normotensive dogs. Norepinephrine content in the branches of mesenteric arteries of all deoxycorticosterone- and NaCl-treated animals, irrespective of their blood pressure, was significantly lower, and in the myocardium significantly higher, than either the unoperated normotensive or operated but not further treated dogs. It is concluded, therefore, that in deoxycorticosterone + NaCl treatment the dogs which developed hypertension had more arterial sodium, potassium, magnesium, and calcium than those who were similarly treated but remained within the limits of normal blood pressure, and that there was no difference between hypertensive and non-hypertensive dogs in regard to their cardiovascular norepinephrine content.

Animals↗