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Biomedical subjects

R Garcia

Publications and source records attributed to R Garcia.

At least 415 records · Page 23Linked to original sources

Effects of pancreatic polypeptide, caerulein, and bombesin on satiety in obese mice.

Congenitally obese mice are hyperphagic, suggesting that their obesity is secondary to defects in normal satiety mechanisms. The present study compares the effects of caerulein, bombesin, and pancreatic polypeptide (three equimolar doses each of 3, 9, and 27 nmol/kg) on food intake in 10 pairs of lean and obese mice. After the intraperitoneal injection of saline, obese mice eat 240% more of a liquid meal (Magnacal) than their lean littermates (P less than 0.01). All three doses of caerulein significantly inhibited food intake in both obese and lean mice. Although the highest dose of bombesin significantly decreased food intake in both obese and lean mice, the lowest dose was only effective in obese mice. In contrast, none of these doses of pancreatic polypeptide had a significant effect on food intake in either lean or obese mice. A dose of bovine pancreatic polypeptide of 200 nmol/kg was required to significantly reduce food intake in lean and obese mice. This study demonstrates that obese mice respond to satiety signals and may even be more sensitive than their lean littermates to some messengers. In addition, the previously described reversal of this obesity syndrome by pancreatic polypeptide in doses of approximately 2.5 and 25 nmol X kg-1 X day-1 is unlikely to be due to effects of this peptide on food intake.

Animals↗

T cell dependence of human IgE response: quantitative and functional studies.

In 108 allergic and nonallergic patients T3, T4 and T8 cells were quantified. No significant differences were found when comparing healthy and allergic individuals. Functionally, the role of T8 suppressor and cytotoxic population was studied by removing this subset, comparing the IgE produced in vitro by peripheral blood lymphocytes of unfractionated and T8-depleted cultures. Results indicate a statistically significant increase of the in vitro IgE production when cultures from healthy people and 'normoproducer' allergics (in vitro spontaneous IgE production no more than 900 pg/ml/10(7) cells) were depleted of T8 cells. The same experiments in 'hyperproducer' allergics (in vitro spontaneous IgE production more than 900 pg/ml/10(7) cells) show no significant difference in the IgE production when T8 cells were depleted.

Humans↗

Localization of immunoreactive synthetic atrial natriuretic factor (ANF) in the heart of various animal species.

The localization of two synthetic fragments of the C-terminal portion of atrial natriuretic factor: Arg 101-Tyr 126 which displays full biological activity and Leu 94-Arg 109 which is completely devoid of biological activity, has been investigated by immunohisto- and immunocytochemical methods in the heart of mammals (rat, mouse, guinea pig, hamster, rabbit, cat, dog, man) and nonmammalian vertebrates toad (Bufo marinus), frog (Rana catesbeiana), fish (Cyprinus carpio, Puntius schwanenfeldi, Cichlosoma biocellatum, Carrasius auratus), snake (Python reticulatus) and hen. Antibodies against the synthetic fragments of ANF were raised in rabbits and used either for immunofluorescence (Coons' technique), immunohistochemistry (unlabeled antibody technique) or immunocytochemistry (protein A-gold technique). Results obtained by immunofluorescence and by the unlabeled antibody technique were similar: antibodies against Arg 101-Tyr 126 ANF allowed visualization of granulated cardiocytes in the atria of all mammals. While the reaction was very strong in rat and mouse, it was less so in the rabbit and very weak in all other species studied including man. Antibodies against Leu 94-Arg 109 ANF produced a reaction only in the rat and mouse. In nonmammalian vertebrates, the reaction was always much stronger in atria than ventricles of all species with both antibodies.

Animals↗

Effect of atrial natriuretic factor [ANF (Arg 101--Tyr 126)] on kallikrein and cyclic GMP in the renovascular hypertensive rat.

The intravenous injection of an ED50 natriuretic dose (1 microgram) of synthetic ANF decreases blood pressure by 61 +/- 6 mmHg in 2-K, 1-C, and of 45 +/- 6 mmHg in 1-K, 1-C hypertensive rats, which was positively correlated with its initial level only in the 2-K, 1-C group. The hypotensive response lasted longer in the latter (greater than 40 min) than in normotensive sham-operated rats. No difference in duration was seen between 1-K, 1-C hypertensive and its uninephrectomized normotensive controls. The diuretic response to ANF was higher in 2-K, 1-C rats. No hematocrit changes were observed in any group. ANF induced a rise in urinary kallikrein in all groups but the 1-K, 1-C. Urinary kallikrein excretion was positively correlated with natriuresis in normotensive but not in hypertensive groups. ANF induced an increase in urinary cGMP excretion in all groups but the 1-K, 1-C, and an increase in plasma cGMP in the normotensive sham-operated animals. Our results suggest that the fall in blood pressure induced by synthetic ANF could be due to vasodilatation, a drop in cardiac output cannot, however, be eliminated. Whether the hypotensive effect of ANF is mediated by cGMP remains to be demonstrated.

Animals↗

Secretory patterns of atrial natriuretic factor (ANF) by cultured cardiocytes of right and left atrium from newborn and adult rats.

Atrial cardiocytes from newborn (2-5 day old) and adult rats were cultured and the secretory patterns of atrial natriuretic factor (ANF) from isolated right and left atrial cells were investigated by radioimmunoassay. Newborn atrial cardiocytes from the left atrium consistently secreted larger amounts of ANF than those from the right with a peak on the 6th day and a decrease up to the 12th day. In contrast, adult atrial cardiocytes secreted much less ANF and this decreased to very low levels from the 3rd day up to the 12th day in culture although ANF was present in measurable amounts in these cells.

Animals↗

Synthetic atrial natriuretic factor induces release (possibly receptor-mediated) of vasopressin from rat posterior pituitary.

The synthetic fragment (Arg 101-Tyr 126) of atrial natriuretic factor (ANF) induces release of arginine vasopressin from the isolated posterior lobe of the rat hypophysis in vitro. At a physiological concentration (3 X 10(-10)M) ANF was three times more effective than 61 mM KCL. In vitro binding studies with 125I-ANF revealed the presence of high affinity receptor sites displaying a pK = 9.9, a Kd = 0.14 nM, a Bmax = 20 fmol/posterior lobe and and IC50 = 200 pM. These results suggest that arginine vasopressin release by synthetic atrial natriuretic factor may be receptor mediated.

Animals↗

Effect of chronic infusion of synthetic atrial natriuretic factor (ANF 8-33) in conscious two-kidney, one-clip hypertensive rats.

Conscious two-kidney, one-clip hypertensive rats were chronically infused during 7 days with synthetic ANF (8-33) (1 microgram/hr/rat) by means of osmotic minipumps. The initial blood pressure of 183 +/- 4 mmHg gradually decreased to 116 +/- 5 mmHg the last 2 days of infusion. Pressure diuresis returned to normal and pressure natriuresis was attenuated. PRA was significantly lower (1.81 +/- 0.41 AI ng/ml/hr) than in not treated hypertensive rats (8.56 +/- 3.75 AI ng/ml/hr). A partial regression in cardiac hypertrophy was observed in the treated group. We suggest that the hypotensive response to ANF may be mainly due to vasodilatation, but the possibility that the decrease in PRA may play a partial role in lowering blood pressure, cannot be excluded.

Animals↗

Reduction of blood pressure and increased diuresis and natriuresis during chronic infusion of atrial natriuretic factor (ANF Arg 101-Tyr 126) in conscious one-kidney, one-clip hypertensive rats.

Conscious one-kidney, one-clip hypertensive rats and their normotensive controls were infused during 7 days with synthetic ANF (Arg 101-Tyr 126) at 100 ng/hr/rat (35 pmol/hr/rat) by means of osmotic minipumps. The basal blood pressure of 193 +/- 6 mmHg gradually declined to 145 +/- 6 mmHg at day 4 after the infusion was started. No changes in blood pressure were observed in ANF-infused normotensive rats. A significantly higher diuresis and natriuresis was observed in ANF-infused hypertensive rats when compared to the non-treated hypertensive group. No such changes were observed in ANF-treated normotensive animals. No differences in PRA were seen in any group. Atrial immunoreactive ANF was significantly lower in one-kidney, one-clip rats than in the normotensive animals, but whether this is the reflection of an increased release in the circulation remains to be elucidated. It is suggested that the hypotensive response of one-kidney, one-clip animals to ANF may be secondary to a dual mechanism, vasodilatation and volume depletion.

Animals↗

Chronic infusion of low doses of atrial natriuretic factor (ANF Arg 101-Tyr 126) reduces blood pressure in conscious SHR without apparent changes in sodium excretion.

Conscious SHR and WKY rats were infused during 7 days with synthetic ANF (Arg 101-Tyr 126), 100 ng/hr/rat (35 pmol/hr/rat) by means of miniosmotic pumps. The SHR initial blood pressure of 177 +/- 5 mmHg gradually dropped to 133 +/- 3 and 142 +/- 4 mmHg the last two days of infusion. No significant change in blood pressure was observed in the ANF-infused WKY group. No apparent difference in natriuresis or diuresis was observed in ANF-infused SHR and WKY when compared with non-infused control groups. A slight but significant lower immunoreactive ANF concentration was found in the atria of SHR than in their normotensive controls. No difference in cardiac weight was found between infused and non-infused rats. It is suggested that the hypotensive response observed in SHR and not in WKY is due to a decrease in vascular peripheral resistance. Whether ANF is involved in the development and maintenance of high blood pressure in SHR remains to be elucidated.

Animals↗

On the circulating form of atrial natriuretic factor.

Isolation and sequencing of IR-ANF from plasma reveal that the circulating form of ANF is a 28-amino acid peptide (Ser 99-Tyr 126) which inhibits basal aldosterone secretion from suspensions of rat zona glomerulosa cells to the same extent as synthetic Arg 101-Tyr 126. The same form (minus two N-terminal amino acids) (Arg 101-Tyr 126) has been isolated from culture media of atrial cardiocytes and sequenced. Structure activity studies of shorter, N- or C-terminally truncated versions of synthetic Arg 101-Tyr 126 show that the latter is the most potent one.

Amino Acid Sequence↗

Effects of ultrasound feedback on pregnancy anxiety, fetal activity, and neonatal outcome.

A group of pregnant women received video and verbal feedback during three ultrasound examinations. This group was compared with a no-feedback group on measures of pregnancy anxiety, fetal activity, and neonatal outcome. The feedback appeared to reduce pregnancy anxiety and fetal activity, particularly for the primiparous women. These women also experienced fewer obstetric complications and gave birth to neonates who were greater weight, more appropriate weight-for-length, less active and irritable, and showed better performance on the Brazelton neonatal behavior assessment.

Anxiety↗