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Biomedical subjects

N Gulati

Publications and source records attributed to N Gulati.

At least 55 records · Page 3Linked to original sources
PubMed1983

Effects of leukotriene C4 and prostaglandin E2 on the rat mesentery in vitro and in vivo.

Leukotriene C4 (LTC4) and Prostaglandin E2 (PGE2) have been studied for their effects on the rat mesentery in vitro and in vivo. Their effects on the norepinephrine (NE) induced vasoconstrictions in the above vascular bed have also been investigated. LTC4 (10(-10)M) and PGE2 (2.8 X 10(-7)M) produced no direct effects on the perfusion pressure in the isolated perfused rat mesentery. However, LTC4 (10(-10)M) produced constriction of the arterioles in vivo. PGE2 (2.8 X 10(-7)M) did not produce any direct effect on the microcirculation. Indomethacin, when superfused for 10 min. in a concentration of 7 X 10(-5)M, produced significant arteriolar constriction; this effect was reversed when PGE2 was added to the superfusing media containing indomethacin. LTC4, perfused in a concentration of 10(-10)M, produced a time - dependent inhibitory effect on NE induced vasoconstrictions in vitro whereas PGE2 perfusions (2.8 X 10(-7)M) potentiated the NE responses. This potentiating effect of PGE2 was inhibited by indomethacin. In contrast, the topical application of PGE2 in vivo attenuated NE responses of the mesenteric arterioles.

Animals↗
PubMed1983

Modulatory effects of substance P on norepinephrine induced vasoconstrictor responses in the rat mesentery.

1. The role of substance P (SP) in adrenergic transmission has been studied in the isolated perfused rat mesentery. 2. Intra-arterial perfusion of SP (4 x 10(-9) to 4 x 10(-7)M) produced a dose dependent potentiation of norepinephrine (NE) induced vasoconstrictor responses and a shift of the log dose--response curve to the left. 3. Saralasin, a specific antagonist of angiotensin II (ang. II) when perfused at a concentration of 3 x 10(-9)M did not change the NE responses as such. However, the potentiating effect of SP could not be demonstrated in the presence of saralasin. 4. Indomethacin, a prostaglandin (PG) synthetase inhibitor, when perfused at a concentration of 2.8 x 10(-6)M, markedly attenuated the vascular responses to NE, which could not be normalized by the addition of SP. 5. It appears that SP's potentiating effect on NE responses in the perfused rat mesentery simulates ang. II and not prostaglandins. A direct non-specific post synaptic sensitizing effect of SP on vascular smooth muscle cell, for its potentiating property, cannot be ruled out.

Animals↗
PubMed1983

Pharmacological and hemodynamic studies on flunarizine.

Systemic administration of flunarizine (3 mg/kg i.v.) to rats decreased the vascular reactivity of their mesenteries to phenylephrine (PhE) and norepinephrine (NE). Intra-arterial perfusion of flunarizine (100 pg to 1 microgram/ml) produced dose dependent attenuation of the vasoconstrictor responses induced by PhE and Ne in the isolated perfused rat mesentery. Flunarizine (5 mg/kg i.p.) did not significantly affect general hemodynamics (i.e. mean blood pressure, heart rate, cardiac output and hematocrits) in anaesthetized rats. However, it produced significant decreases in the blood flows to the kidneys and the spleen associated with similar changes in the percentage distribution of the cardiac output to these organs. These studies indicate that in rats, flunarizine produced preferential effects in different vascular beds.

Animals↗
PubMed1983

The local edemogenic effects of leukotriene C4 and prostaglandin E2 in rats.

Leukotriene C4 (LTC4) and prostaglandin E2 (PGE2) have been studied for their effects on vascular permeability in rats. LTC4 and/or PGE2 were dissolved in 0.3% ethanol and were administered subcutaneously (0.1 m1) in the plantar surface of one of the hind paws of different series of rats. The changes in vascular permeability were measured by the radioactive marker (HSA.I125) method. LTC4 administered in dose of 2 X 10(-8) M produced marked increase (77 and 133%) in the vascular permeability (local edemogenic effect). PGE2 administered in a dose of 10(-6) M also produced significant increase (38 and 40%) in the vascular permeability. However, PGE2 in the same dose either administered along with LTC4 or administered at 30 minutes after the injection of LTC4 (2 X 10(-8) M) did not have any potentiating effect on the edemogenic response of LTC4.

Animals↗
PubMed1983

Pharmacodynamic studies with flunarizine, a calcium influx blocker.

Flunarizine, a difluoro derivative of cinnarizine, has been used to study its antivasoconstrictor effects on isolated perfused rat mesentery. The vasoconstrictor responses induced by sequential intra-arterial injections of phenylephrine (PhE) and norepinephrine (NE), were measured as an increase in the perfusion pressure (mm Hg). Flunarizine was administered either by i.v. route in a dose of 3 mg/kg, 15-20 min before the isolation of the mesentery or it was added to the perfusing medium, in concentrations ranging from 100 pg to 1 microgram/ml (PhE experiments) and from 1 ng to 1 microgram/ml (NE experiments). Intravenous administration of flunarizine significantly decreased the vascular reactivity of rat mesentery to PhE and NE at all dose levels. Continuous perfusion of flunarizine attenuated the vasoconstrictor responses induced by PhE and NE. Flunarizine was further studied for its hemodynamic effects in anaesthetized rats using the radioactive microspheres technique. Flunarizine (5 mg/kg i.p.) was administered 60 min prior to the determination of hemodynamic parameters. It was found not to affect general hemodynamics (mean blood pressure, heart rate, cardiac output and hematocrit). However, it produced a significant decrease of renal and splenic blood flows. The changes in blood flows were associated with similar changes in the percentage distribution of cardiac output to these organs, thus indicating that local regulatory mechanisms were influenced by flunarizine. It appears that flunarizine has preferential effects on the different vasculatures in vivo, whereas it produces nonspecific inhibition of exogenous PhE and NE in the rat mesentery in vitro.

Animals↗
PubMed1982

Effects of captopril (SQ 14225) on norepinephrine-induced vasoconstriction in the isolated perfused mesentery and hindquarters of the rat.

Captopril (SQ 14225) is an orally active agent that inhibits the conversion of ang. I to ang. II and also potentiates the biological actions of kinins. This substance has been used to study the role of ang. II/kinins on the norepinephrine-induced vasoconstriction in the isolated perfused mesentery and hindquarters of the rat. The vasoconstrictor responses were measured as an increase in the perfusion pressure (mm Hg), induced by sequential injections of norepinephrine. Captopril/placebo (physiological saline solution) was administered in a dose of 1 mg/kg by oral route, 15-20 min before isolating the vascular beds from these rats. Oral administration of captopril, decreased the vascular reactivity to norepinephrine in both the vascular beds, when compared to the responses obtained in the placebo treated rats. In another series of experiments (normal rats) bradykinin (BK), at concentrations of 0.4 and 0.8 micrograms/ml in the perfusate, attenuated the norepinephrine-induced vasoconstriction dose dependently, only in the mesenteric bed. It may be concluded that captopril attenuated the vascular reactivity to norepinephrine either by decreasing ang. II formation and/or increasing the action of kinins in the vicinity of these two beds. The latter mechanisms, however, appears not to play any direct role in the hindquarter bed. The direct effects of captopril on the decreased vascular reactivity of these beds cannot, however, be ruled out.

Animals↗
PubMed1980

Effects of labetalol in chronic two-kidney Goldblatt hypertension (2-KGH) in rats.

Labetalol administered intra-gastrically in a dose of 30 mg/kg twice a day for 3 weeks significantly lowered systolic tail blood pressure (STBP) in chronic two-kidney Goldblatt hypertension in rats. Hypotensive response of labetalol in normotensive rats has also been demonstrated. Plasma renin activity (PRA) measured at the end of the treatment was similar in labetalol-treated and in dextrose-treated rats. The bradycardial response was evident in both hypertensive as well as in normotensive animals; however,, this change was statistically significant for the hypertensive rats only. Hypertension was associated with increase in the heart weight, which was not affected by labetalol treatment. Antihypertensive effect of labetalol is neither related to renin suppression nor to beta blockade.

Animals↗
PubMed1980

Organic growth factor requirements of some yeasts.

Some sporogenous yeasts (Brettanomyces bruxellensis, Debaryomyces hansenii, Hansenula ciferrii, Hansenula polymorpha, Pichia polymorpha, Saccharomycopsis guttulata, and Saccharomyces chevalieri), isolated from various fruits have been examined for their organic growth factor requisites. H. ciferrii was completely deficient in thiamine, biotin, inositol, riboflavin, niacin, and partially deficient in pantothenic acid. It required an external supply of 0.1-1.0 ppm thiamine, 0.01-0.1 ppm biotin, 10.0 ppm inositol, 0.10 ppm niacin and riboflavin for its optimum growth. H. polymorpha showed partial deficiency only in xanthine. P. polymorpha gave indications of partial deficiencies in thiamine and biotin. S. guttulata was completely deficient in biotin, and partially deficient in adenine sulphate. It required 0.01 ppm biotin for optimum growth. S chevalieri was completely deficient in pyridoxine and partially deficient in thiamine. It required 0.1 ppm pyridoxine for maximum growth. D. hansenii and B bruxellensis were auxoautotrophic for the various growth factors studied.

Biotin↗
PubMed1980

Effect of labetalol on adrenoceptors in the isolated perfused rat mesentery.

Isolated perfused rat mesentery has been used to define alpha- and beta-adrenoceptors. Norepinephrine was used as a reference substance to induce vasoconstrictor responses (increase in perfusion pressure). Log-dose response curves were obtained in the dose range between 0.3-10 mug. Labetalol, a known competitive inhibitor of both alpha- and beta-adrenoceptors, when administered as a single bolus injection (3 mug) initially induced predominant alpha-blockade lasting upto 75 min followed by potentiation of the vasoconstrictor responses to norepinephrine used at multiple dose levels. This potentiation was maximum between 150-195 min after injection of labetalol. This potentiating effect of labetalol observed in the later phase of the experiment might be related to its inhibitory mechanism of neuronal uptake.

Animals↗
PubMedDate not supplied

Increased plasma renin during renin inhibition. Studies with a novel immunoassay.

The response of renin release to the administration of renin inhibitors cannot be studied with conventional enzymatic methods used to measure plasma renin. In the present experiments, a novel multirange enzyme-linked immunosorbent assay for human and primate renin was used to investigate the changes in plasma immunoreactive renin after renin inhibition. A potent and long-acting statine-containing renin inhibitor, CGP 29 287, was injected in conscious marmosets after mild or severe sodium depletion. In mildly sodium-depleted marmosets, CGP 29 287 (0.1 mg/kg i.v.) reduced mean arterial blood pressure and completely inhibited plasma renin activity for up to 30 minutes. This response was associated with a transient increase in plasma immunoreactive renin concentration. After a dose of 1.0 mg/kg i.v., the reduction of mean arterial pressure and the complete inhibition of plasma renin activity persisted for up to 120 minutes. These effects were accompanied by a sustained increase in plasma immunoreactive renin concentration. In severely sodium-depleted marmosets, CGP 29 287 (1.0 mg/kg i.v.) induced a marked fall in systolic blood pressure and complete inhibition of plasma renin activity within 30 minutes of injection. Plasma immunoreactive renin levels increased to 257% of pretreatment values. The converting-enzyme inhibitor enalaprilat (2 mg/kg i.v.) induced a fall in systolic blood pressure of similar magnitude, which was accompanied by an increase in plasma renin activity. Levels of plasma immunoreactive renin increased to 210% of pretreatment values. Hydralazine (0.2 mg/kg i.v.) did not increase plasma renin activity or plasma immunoreactive renin levels despite a comparable hypotensive effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Effects of a specific and long-acting renin inhibitor in the marmoset.

Inhibition of renin was induced in conscious marmosets with CGP 29 287, Z-Arg-Arg-Pro-Phe-His-Sta-Ile-His-Lys (Boc)-OMe, a renin inhibitor with a prolonged duration of action. In vitro, CGP 29 287 is a potent inhibitor of primate plasma renin (inhibitory concentration, 50%: human = 1 X 10(-9) M; marmoset = 5 X 10(-9) M) and less potent against dog (2 X 10(-7) M) or rat (3 X 10(-5) M) plasma renin. CGP 29 287 is a weak inhibitor of other aspartic proteases such as porcine pepsin or bovine cathepsin D (inhibitory concentration, 50% = 4 X 10(-5) M). In furosemide-treated marmosets, CGP 29 287 lowered blood pressure and inhibited plasma renin activity during intravenous infusion and after intravenous bolus injection. The duration of action after intravenous injection was dose dependent and ranged from 1 hour after 0.1 mg/kg to more than 3 hours after 10 mg/kg. High doses of CGP 29 287 (100 mg/kg) were active after oral administration. In all experiments a close relation between inhibition of plasma renin activity and reduction of blood pressure was found. A maximum hypotensive response to CGP 29 287 was associated with complete inhibition of plasma renin activity, and the recovery of blood pressure was accompanied by recovery of plasma renin activity. The hypotensive effects of CGP 29 287 were smaller in untreated than in furosemide-treated marmosets. CGP 29 287 had no influence on blood pressure in marmosets after bilateral nephrectomy or after pretreatment with a converting enzyme inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗