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Biomedical subjects

R Garcia

Publications and source records attributed to R Garcia.

At least 361 records · Page 20Linked to original sources
PubMed1987

[ANF receptors at the glomerular level in reno-vascular hypertension in rats].

The effect that hypertension may have on plasma, atrial ANF levels and on isolate rat renal glomeruli ANF receptors was investigated. Different models of renal hypertension were studied: 1-K, 1-C (BP = 177 +/- 7 mmHg), 2-K, 1-C (BP = 158 +/- 3 mmHg) and their respective controls (BP = 100 +/- 2 mmHg). At this stage of hypertension (two weeks) plasma ANF was 56 +/- 9 and 25 +/- 2 pg/ml in 2-K, 1-C and controls respectively and 124 +/- 22 vs 35 +/- 4 pg/ml in 1-K, 1-C and controls. Atrial ANF content was lower in hypertensive animals. A marked up-regulation of the glomerular ANF receptor density was observed in 2-K, 1-C animals. In the right kidney we found 840 fmol/mg protein and 540 fmol/mg protein, and in the left 1,070 fmol/mg protein against 608 fmol/mg protein in 2-K, 1-C and control animals respectively. No change was observed in glomerular ANF receptor density in 1-K, 1-C animals. We have then demonstrated that glomerular ANF receptor density is higher in 2-K, 1-C hypertensive than in normotensive animals. It could be possible, however, that the receptor density may change during the evolution of high blood pressure in the models of experimental hypertension currently studied.

Animals↗
PubMed1987

Quantitative analysis of contrasuppressor T lymphocytes in leprosy; induction of Ia antigens with gamma interferon.

Lepromatous leprosy is characterized by immune anergy and abnormal suppressor T-cell function. Contrasuppressor cells are a subset of CD8+, vicia villosa-adherent T lymphocytes. T-contrasuppressor (Tcs) cells act on T-helper cells to cause them to become unresponsive to the action of T-suppressor cells. In 8 lepromatous (LL) and 7 tuberculoid (TT) patients, and 6 healthy contacts we studied the percent of the following lymphocyte subsets: CD3+, CD4+, CD8+, Ia+, vicia villosa+ (VV+), CD8, VV+, VV, Ia+, and Ia, Tac+. This was done in baseline status as well as post-stimulation with recombinant gamma interferon (rIFN-gamma). We found that peripheral blood mononuclear cells from LL and TT patients and controls exhibit a similar number of putative contrasuppressor lymphocytes (CD8, VV+ cells). However, in the contrasuppressor subset from LL patients we found a low percent of Ia+ (p less than 0.05 compared to controls or TT). In the three groups studied, the rIFN-gamma enhanced the percent of Ia+ lymphocytes in the CD8, VV+ cell subpopulation. However, the CD8, VV+ lymphocytes from LL patients, despite the effect of rIFN-gamma, continue to have a low percent of Ia+ cells (p less than 0.05 compared to controls or TT). These findings suggest that LL patients might have abnormalities in the contrasuppressor immune circuit. Future functional studies on the role of Tcs cells in the anergy seen in LL will be required in order to define the apparent dysfunction occurring in this disease.

Antigens, Surface↗
PubMed1987

An evaluation of the mosquitofish, Gambusia affinis, and the inland silverside, Menidia beryllina, as mosquito control agents in California wild rice fields.

The mosquitofish, Gambusia affinis, and the inland silverside, Menidia beryllina, were evaluated in experimental, one-tenth hectare wild rice plots in Lake County, California, for their impact on densities of Culex tarsalis, Anopheles freeborni and Anopheles franciscanus. Gambusia affinis were tested at 0.6 and 1.7 kg/ha and the silversides at ca. 0.9 kg/ha. The silversides did not survive well in the rice field system and none of the silverside guts examined contained mosquito larvae. The mosquitofish increased steadily throughout the season and mosquito larvae were found in 9% of the fish dissected. Analysis of variance did not reveal significant differences among the mosquito populations in the 3 fish treatments and controls on any sampling date. More than 40 species of aquatic insects were collected and population densities of selected aquatic insects were similar among the 4 treatments.

Animals↗
PubMed1987

Atrial natriuretic factor--its possible role in the pathogenesis and therapy of arterial hypertension.

Using radioimmunoassay the authors investigated the plasma concentration of the immunoreactive atrial natriuretic factor (IR-ANF) and its content in the atria of 4-, 8-, 12-, 16-, and 20-weeks-old spontaneously hypertensive rats (SHR), and compared the results with data obtained in normotensive Wistar-Kyoto rats of the same age. With hypertension accelerating in SHR between the 8th and the 20th weeks of life, IR-ANF content in the atrium gradually decreased, and the plasma IR-ANF concentration increased. The decline in IR-ANF was due to its decrease primarily in the left atrium. Long-term (6-day) administration of synthetic ANF to SHR with fully developed hypertension led to normalization of BP. The results do not support the hypothesis that arterial hypertension in SHR is induced by a primary deficiency of ANF. The changes in IR-ANF in the atria and plasma occur rather as an adaptive and regulatory response to increasing BP. Prolonged administration of ANF to SHR had a hypotensive effect. Therapeutic application of ANF in man depends on the development of oral and long-acting analogues.

Animals↗
PubMed1987

Atrial natriuretic factor (ANF) in experimental and human hypertension.

The plasma levels of immunoreactive (IR)-ANF have been evaluated by radioimmunoassay in several models of experimental hypertension and in human hypertension. In all models of experimental hypertension so far studied, the plasma levels of IR-ANF are consistently increased. This is accompanied by a decrease, at certain time intervals, of the IR-ANF levels in the left atrium. In human essential hypertension, the plasma levels of IR-ANF are not increased except in the severe form (diastolic blood pressure above 110 mmHg). In renovascular hypertension, the peripheral levels of IR-ANF are not different from the normal levels but are increased above normal in aortic blood.

Animals↗
PubMed1986

Degradation of atrial natriuretic factor in the rat.

The biologically active circulating form of atrial natriuretic factor (ANF) in the rat is the 28-amino-acid peptide ANF-(Ser-99-Tyr-126). Degradation of this peptide in vivo as well as in vitro, in whole blood, in plasma and by the isolated mesenteric artery was investigated. Studies in vivo in the rat demonstrated that the elimination and degradation of ANF was extremely fast: within 3 min more than 95% of the injected immunoreactive material was eliminated from circulation. The production of a short C-terminal peptide was detected on injection of 125I-ANF-(Ser-99-Tyr-126) into the rat. This peptide increased proportionately with incubation time. Experiments in vitro in the presence of whole blood or plasma did not cause any major destruction of ANF even after incubation for 60 min. After this prolonged incubation in plasma, ANF-(Ser-99-Tyr-126) was partially converted into ANF-(Ser-103-Tyr-126), a less potent peptide. Isolated mesenteric-artery preparation appeared to degrade ANF in a manner very similar to the system in vivo. These results suggest that degradation of ANF may occur either after internalization in the vascular cells or by a membrane-bound enzyme in the vasculature.

Animals↗
PubMed1986

The morphine effect on plasma ANF.

The effect of acute morphine treatment on plasma immunoreactive atrial natriuretic factor (IR-ANF) was studied in conscious non-hydrated rats. Morphine treatment induced an 8-fold increase in plasma IR-ANF (P less than 0.001) from 68.1 +/- 9.3 (mean +/- S.E.) to 540.5 +/- 139.5 pg/ml and this increase was completely abolished by pretreatment with the opioid antagonist naloxone (P less than 0.001) to 37.9 +/- 2.8 pg/ml. Naloxone also significantly decreased the basal IR-ANF level (P less than 0.05) to 49.0 +/- 5.3 pg/ml. When naloxone-pretreated and control rats were infused with saline (8 ml) the IR-ANF response was the same in the two groups: 257.7 +/- 64 and 247 +/- 52 pg/ml respectively. Since ANF is a potent natriuretic and diuretic hormone, the morphine-induced increase of plasma IR-ANF may provide a rational basis for explaining the diuretic effect of morphine in conscious non-hydrated rats. Moreover, the decrease of basal plasma IR-ANF suggests the possible implication of endogenous opioids in the regulation of basal ANF secretion.

Animals↗
PubMed1986

Atrial natriuretic factor in human plasma.

A reproducible and sensitive radioimmunoassay (RIA) was developed to measure ANF in human plasma. Immunoreactive ANF was extracted from plasma with Sep-Pak cartridges, using 0.2% ammonium acetate (pH 4) with acetonitrile. The sensitivity of the assay was 3.9 pg/ml. The coefficient of variance for inter-assay and intra-assay was 16.8% and 6.8%, respectively. In normal healthy subjects (n = 67), ANF content was 11.9 +/- 1.3 pg/ml (mean +/- SEM). Significantly-higher ANF concentrations were found in proximal coronary sinus blood, being 6 to 37 times greater than in the peripheral circulation. Comparison of the prior extraction method with direct RIA revealed a good correlation (r = 91) in samples containing higher than 100 pg/ml ANF. No correlation was observed with lower values. The elution profiles of reverse-phase HPLC of peripheral and coronary sinus plasma extracts were similar but somewhat complex, with the main immunoreactive peak corresponding to a low-molecular-weight peptide.

Adult↗
PubMed1986

Synthesis and activity profiles of atrial natriuretic peptide (ANP) analogs with reduced ring size.

Three deletion analogs of the atrial natriuretic peptide, [desGly-120]-ANP(103-126), [desLeu119, desGly120]ANP(103-126) and [desGly118,120,-desLeu119]-ANP(103-126), were synthesized by the solid-phase method. Successive elimination of the non-functional residues in positions 120-118 of the peptide sequence resulted in a progressive potency reduction in the rabbit aorta assay, in the bioassay monitoring suppression of aldosterone secretion from bovine zona glomerulosa cells and in a binding assay based on displacement of radioiodinated ANP(101-126) from bovine zona glomerulosa cell membranes. The fact that the deletion analogs showed quantitatively different relative potencies in each of the three in vitro assay systems was interpreted as further evidence in support of the existence of two or more classes of ANP receptors or binding sites.

Adrenal Glands↗
PubMed1986

Dehydration-induced changes in the secretion of atrial natriuretic factor in Brattleboro rats: effect of water-drinking.

The secretion of atrial natriuretic factor (ANF) was measured in Brattleboro rats (DI) subjected to 20-h dehydration and in normal Long-Evans rats (LE) subjected to 72-h dehydration and 7 times within the hour following voluntary rehydration by drinking water. In these rats, water deprivation caused a large, significant drop in plasma immunoreactive ANF (IR-ANF). Drinking water did not restore plasma IR-ANF values within one hour, even when indirect indices of intravascular volume such as serum osmolality, sodium and hematocrit returned to normal. The dehydration-induced decrease in plasma IR-ANF and its very low secretion after restoring drinking may be essential for the homeostasis of water conservation in both DI and LE rats.

Animals↗
PubMed1986

Mechanisms of release of atrial natriuretic factor. II. Effect of chronic administration of alpha- and beta-adrenergic and cholinergic agonists on plasma and atrial ANF in the rat.

The effect that chronic subcutaneous infusion of alpha- and beta-adrenergic and cholinergic agonists on plasma and atrial ANF was investigated. Isoproterenol, a beta-adrenergic agonist, and carbachol, a cholinergic agonist produced a 3-fold increase in plasma ANF levels which were constant until the end of the infusion period. An increased natriuresis was observed in the same groups which was positively correlated with plasma ANF. No differences were observed in atrial content of ANF between the experimental groups. A sharp post-surgery decline in plasma ANF was observed in control, phenylephrine and epinephrine-treated groups which was maintained during the observation period of five days. This suggests that the rise in plasma ANF induced by isoproterenol and carbachol may be secondary to hemodynamic changes and not to direct receptor stimulation, and may play a role in the observed natriuresis. It is also suggested that the depression of plasma ANF may contribute to the well known post-surgery sodium retention.

Adrenergic alpha-Agonists↗
PubMed1986

Comparative biological activities of ANF (Arg 101-Tyr 126) and the synthetic form of circulating ANF (Ser 99-Tyr 126).

The biological activities of ANF (Arg 101-Tyr 126) and of the circulating form, ANF (Ser 99-Tyr 126), were compared in the following assays: precontracted rabbit aortic strip and chick rectum, rat natriuresis, inhibition of aldosterone secretion and receptor affinity in bovine and rat adrenal zona glomerulosa cells, and receptor affinity in rabbit aorta and rat mesenteric artery cells. The results demonstrate that both peptides share the same biological activities. It is concluded that the addition of two amino acids to the N-terminal of ANF (Arg 101-Tyr 126) does not modify its biological characteristics, validating thus previous research employing this peptide.

Adrenal Glands↗
PubMed1986

Mechanisms of release of atrial natriuretic factor. I. Effect of several agonists and steroids on its release by atrial minces.

The effect that several substances may have on ANF release by atrial slices and on its tissular content was investigated. alpha- and beta-adrenergic and cholinergic agonists, vasopressin, met-enkephaline, dexamethasone and DOC, in concentration ranging from 10(-4) to 10(-8) M, were added into the incubation media and incubated 1 and 4 hours. No changes were observed in ANF concentration either in the media or in its tissular concentration as measured by a specific radioimmunoassay. When intact rats were previously treated with DEXA, DOC or DEXA + DOC and their atria incubated "in vitro", an increase in the release of ANF was observed in the Dexa-treated group only, but all treated groups had higher tissular ANF concentration. It is concluded that neither alpha- or beta-adrenergic, nor cholinergic agonists or vasopressin and met-enkephaline stimulate ANF release "in vitro". On the other hand steroids may regulate ANF release and synthesis in the intact rat. It seems likely that the ANF released into the media corresponds to a short peptide.

Animals↗