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Biomedical subjects

C Farsang

Publications and source records attributed to C Farsang.

At least 73 records · Page 4Linked to original sources
PubMed1983

Diurnal rhythm of beta endorphin in normotensive and hypertensive patients: the effect of clonidine.

Diurnal rhythm of plasma beta endorphin was established with the highest level in the morning and the lowest one at midnight in normotensive subjects and also in patients with essential hypertension. Clonidine (300 micrograms daily) significantly increased plasma beta endorphin concentrations only in the hypertensive patients. The significant linear correlation between the increase in plasma beta endorphin concentration and the decrease in blood pressure (both systolic and diastolic) in these patients may point to the role of this endogenous opioid in the antihypertensive action of clonidine.

Circadian Rhythm↗
PubMed1983

Possible role of an endogenous opioid in the antihypertensive action of propranolol in spontaneously hypertensive rats.

The effect on systolic blood pressure and heart rate of the acute and chronic intraperitoneal (i.p.) administration of d- and dl-propranolol was investigated on unanesthetised spontaneously hypertensive rats. The effect of naloxone on the propranolol induced hypotension was also studied to test the hypothesis that the antihypertensive effect of propranolol involves the release of an endogenous opiate. On i.p. administration, 3 mg/kg d-propranolol was inactive; 3 and 30 mg/kg dl-propranolol decreased blood pressure and heart rate in a dose-dependent manner. When the rats were pretreated with 2 mg/kg naloxone i.p., the effect of propranolol on the blood pressure was nearly completely abolished, while that on the heart rate was only partially blocked. Chronic administration of dl-propranolol (30 mg/kg b.i.d.) to spontaneously hypertensive rats from the age of 6 weeks (prehypertensive phase) for 29 days prevented the development of hypertension while the rats treated with physiological saline for 29 days (control group) developed hypertension. Naloxone (2 mg/kg i.p.) administered on the 29th day to chronically treated rats induced a reversal of the propranolol action on systolic blood pressure and heart rate, i.e., blood pressure and heart rate increased. Naloxone had no such effect in the control group. We suggest that the release of an endogenous opioid contributes to the acute and chronic antihypertensive action of i.p. propranolol in spontaneously hypertensive rats and that the secretion of endogenous opioids participating in the control of cardiovascular functions is influenced by adrenergic mechanisms.

Animals↗
PubMed1982

Possible involvement of an endogenous opioid in the antihypertensive effect of clonidine in patients with essential hypertension.

The effect of naloxone on the hypotensive and bradycardiac action of clonidine was studied in 27 hospitalized patients with uncomplicated mild-to-moderate essential hypertension. In a double-blind, crossover study, clonidine, 0.3 mg/day orally for 3 days, significantly reduced systolic and diastolic blood pressure and heart rate, whereas placebo was ineffective. Naloxone, 0.4 mg given intravenously on the third day of clonidine treatment, caused a rapid increase in blood pressure and heart rate in 14 patients (reacting group), but was ineffective in the remaining 13 patients (nonreacting group). Naloxone given during the placebo period was ineffective in all patients. Both the clonidine-induced hypotension and the rebound increase in blood pressure after cessation of clonidine were significantly greater in the reacting than in the nonreacting group. These observations suggest that release of an endogenous opioid contributes to the antihypertensive action of clonidine; this mechanism may be also involved in the discontinuation syndrome after cessation of clonidine.

Adult↗
PubMed1981

beta-Endorphin: possible involvement in the antihypertensive effect of central alpha-receptor activation.

Clonidine and L-alpha-methylnoradrenaline (but not D-alpha-methylnoradrenaline) increase the release of a substance with beta-endorphin immunoreactivity from slices of brainstem of spontaneously hypertensive rats, but not that of normotensive rats. It was reported earlier that opiate antagonists inhibit the hypotensive action of clonidine and alpha-methyldopa in spontaneously hypertensive but not in normotensive rats and that beta-endorphin has hypotensive effects of its own. Together, these findings indicate that release of beta-endorphin by central alpha-receptor agonists may contribute to the antihypertensive action of these drugs.

Adrenergic alpha-Agonists↗
PubMed1981

Effect of prazosin and oxprenolol on plasma renin activity and blood pressure in patients with essential hypertension.

48 patients with normal-renin essential hypertension were treated with prazosin alone or in combination with oxprenolol. 1 h after a single dose of 2 mg prazosin tachycardia and a decrease in blood pressure developed. Renin activity in the peripheral plasma (PRA) increased from 1.04 +/- 0.15 to 2.64 +/- 0.20 ng AgT/ml/h. A 3-day treatment with 2 mg t.i.d. prazosin of 11 patients caused no further decrease in blood pressure, while PRA returned to the baseline level. Treatment for 3 days with 2 mg prazosin t.i.d. and 40 mg oxprenolol t.i.d. of 37 patients further decreased blood pressure as well as PRA. The increase in PRA after a single dose of prazosin could be related to the enhanced sympathetic activity. The decreased PRA after prazosin + oxprenolol therapy may be one of the factors responsible for the greater antihypertensive response to the combined therapy.

Adult↗
PubMed1980

Postocclusion hyperemia in the isolated fibrillating blood-perfused dog heart.

Reactive hyperemia following occlusions of 15, 30, 60 and 120 sec duration was studied in the left coronary vascular bed of the isolated fibrillating dog heart perfused with arterial blood at constant pressure or constant volume. Except for repayment, linear correlations were found between occlusion time and the characteristics of reactive hyperemia. At a basal perfusion pressure of 50 mm Hg the postocclusion reaction was absent. The maximum hyperemic response was observed at 100 mm Hg, while on a further increase of perfusion pressure reactive hyperemia decreased. The postocclusion reaction was more marked but of briefer duration under constant pressure perfusion. The results can be explained by the joint effects of metabolic, myogenic, and physical factors on coronary vascular tone.

Animals↗
PubMed1980

Possible role of an endogenous opiate in the cardiovascular effects of central alpha adrenoceptor stimulation in spontaneously hypertensive rats.

In unanesthetized sponatneously hypertensive rats (SHR), naloxone (0.5--2 mg/kg ip.) or naltrexone (2 mg/kg) inhibited the hypotension and bradycardia produced by clonidine (5--20 micrograms/kg iv.). Chronic treatment of SHR with clonidine (3 x 20 micrograms/kg/day orally for 12 days) reduced blood pressure and heart rate and these effects were acutely reversed by a single injection of naloxone. Naloxone also reversed the hypotension produced by a single injection of alpha-methyldopa (50--300 mg/kg ip.). In pentobarbital-anesthetized SHR, the hypotension and bradycardia produced by 5 micrograms/kg of clonidine were inhibited either by naloxone (2 mg/kg) or by yohimbine (1 mg/kg ip.). Morphine (0.33 mg/kg iv.) also reduced blood pressure and heart rate in these animals but these effects were only antagonized by naloxone and not by yohimbine. In conscious and anesthetized normotensive Wistar Kyoto rats, the reduction in blood pressure and heart rate by clonidine or alpha-methyldopa were smaller than in SHR, and these effects were not influenced by naloxone. These results confirm and extend earlier observations and suggest the existence of an "opioidergic" component in the antihypertensive action of central alpha adrenoceptor stimulants in SHR. They also show that a similar mechanism is either absent or inactive in the normotensive Wistar Kyoto rats.

Anesthesia↗
PubMed1980

Effect of phenoxybenzamine, propranolol, phenylephrine and isoproterenol on the circulation of rats bearing Guérin carcinoma.

Effects of phenoxybenzamine (1 mg per 100 g i.v.), propranolol (0.2 mg per 100 g i.v.), phenylephrine (0.1--0.3--1.0--3.0 micrograms per 100 g per min) and isoproterenol (0.01--0.03--0.1--0.3 micrograms per 100 g per min) were studied on cardiac output (Evans-blue dilution), organ and tumour blood flows (Sapirstein's isotope indicator dilution technique) in rats bearing Guérin carcinoma. In agreement with our earlier results data for haematocrit, blood pressure, TPR and organ vascular resistance were lower whereas cardiac index and organ blood flow were higher in control untreated tumour-bearing animals than in untreated normal rats. Phenoxybenzamine, depending on tumour size, decreased blood pressure, TPR and vascular resistance of organs, while it was found ineffective in rats with tumours of very large size (60--80 g). Propranolol treatment produced slight and similar effects in both normal and tumour-bearing rats. Phenylephrine enhanced peripheral resistance as a function of log dose in both normal and tumour bearing animals, nevertheless in the latter group it elicited more marked responses in the vascular bed of the kidneys, intestines and skin. The vasodilatory log dose dependent effect of isoproterenol was not present in tumour-bearing rats. In addition to the anaemia, the continuous decrease of alpha adrenergic activity in the systemic circulation parallel with tumour growth appears to be the most reasonable explanation for the "hyperkinesis" observed in tumour-bearing rats. Resistance of tumour vascular bed was increased by both phenoxybenzamine and propranolol. During the course of phenylephrine infusion (1.0 or 3.0 micrograms per min) the resistance of tumour vessels was more increased than that of other organs. Isoproterenol infusion resulted in a vasoconstriction of the tumour vessel. It appears that with maximally dilated vessels, vasoconstriction remains the only possible vascular response in Guérin carcinoma. In the vascular bed of the tumour a preponderance of beta adrenergic receptors also seems to be feasible.

Animals↗
PubMed1980

Cardiac output and total peripheral resistance in athletes and in non-athletes at rest.

Cardiac output (CO), blood pressure (BP) and heart rate (HR) were estimated in 13 non-athletes, in 10 highly trained athletes and in 8 lower-class athletes at rest. HR and BP were found to be lower in both trained groups than in the controls. CO was lower in the top athletes, while it proved to be higher in the lower-class athletes. Total peripheral resistance (TPR) was higher in the top athletes while it was found to be reduced in the lower-class athletes than in the controls. These results indicate that in the maintanance of resting blood pressure level in the physically trained subjects alpha adrenergic mechanisms predominate whereas the share of beta influences is lower, however, this shift is observed only in the highly trained, top-rank endurance athletes.

Cardiac Output↗
PubMed1979

Regional vascular reactivity in rats with Guérin carcinoma (GC).

Increased sensitivity to phenylephrin and a decreased one to isoproterenol has been found in regional vascular beds of GC implanted rats. Circulatory sympathetic reflex adaptation, alfa- and beta-adrenergic stimulation or blockade provoked a uniform response pattern: i.e. increase in vascular resistance of GC.

Animals↗
PubMed1979

Regulation of myocardial oxygen consumption by perfusion pressure in isolated fibrillating canine heart.

In order to evaluate whether perfusion pressure or coronary flow affect myocardial oxygen metabolism, oxygen consumption of the isolated fibrillating blood-perfused canine heart was investigated at perfusion pressures of 100, 150, and 200 mm Hg. To obtain different coronary flow rates at a given coronary perfusion pressure, alpha-adrenergic blockade by phenoxybenzamine (10 mg/kg b.w.) was applied, resulting in an increase in coronary flow and a decrease in myocardial oxygen extration. Myocardial oxygen consumption was increased by elevation of perfusion pressure in both the control and phenoxybenzamine-pretreated group. At the same level of perfusion pressure there was no significant difference between the oxygen consumption of control and phenoxybenzamine-pretreated preparations. It can be concluded that in the isolated fibrillating canine heart oxygen consumption is primarily regulated by perfusion pressure, and is independent from coronary blood flow.

Animals↗
PubMed1979

Naloxone reverses the antihypertensive effect of clonidine.

In unanesthetized, spontaneously hypertensive rats the decrease in blood pressure and heart rate produced by intravenous clonidine, 5 to 20 micrograms/kg, was inhibited or reversed by nalozone, 0.2 to 2 mg/kg. The hypotensive effect of 100 mg/kg alpha-methyldopa was also partially reversed by naloxone. Naloxone alone did not affect either blood pressure or heart rate. In brain membranes from spontaneously hypertensive rats clonidine, 10(-8) to 10(-5) M, did not influence stereoselective binding of [3H]-naloxone (8 nM), and naloxone, 10(-8) to 10(-4) M, did not influence clonidine-suppressible binding of [3H]-dihydroergocryptine (1 nM). These findings indicate that in spontaneously hypertensive rats the effects of central alpha-adrenoceptor stimulation involve activation of opiate receptors. As naloxone and clonidine do not appear to interact with the same receptor site, the observed functional antagonism suggests the release of an endogenous opiate by clonidine or alpha-methyldopa and the possible role of the opiate in the central control of sympathetic tone.

Animals↗
PubMed1979

Effect of haemorrhagic hypotension on the circulation of rats with Guérin carcinoma.

After transplanting Guérin carcinoma in rats the cardiac output (Evans-blue dilution), the distribution of cardiac output (Sapirstein's isotope indicator fractionation technique), the nutritive blood flow of the organs, and their circulatory resistance were investigated in haemorrhagic hypotension (40 or 70 mm Hg). The posthaemorrhagic redistribution of cardiac output in tumor-bearing rats was similar to that found in normal bled animals: the renal and skin fractions of cardiac output decreased and that of the brain, myocardium, and carcass increased. As a result of bleeding the decrease of the tumor fraction of cardiac output was the greatest compared to the other organs. Thus the tumor seems to be the main target organ of the posthaemorrhagic redistribution.

Animals↗