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Biomedical subjects

K Varga

Publications and source records attributed to K Varga.

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↗
PubMed1979

Effect of long-term alcohol intake on the cardiovascular system of the rat.

A group of rats was fed on control liquid diet, while another group was fed on liquid diet containing alcohol up to 36% of the total calories. After 4, 8 and 12 weeks of treatment ECG, haematocrit, histological structure of the heart, blood pressure, cardiac output, distribution of the organ fraction of cardiac output (by Sapirstein's method and 85Sr labelled microsphere technique), nutritive blood flow and circulatory resistance of the organs were studied. A mild repolarization disturbance was shown by the ECG record of the alcohol exposed animals. Haematocrit values and the histological structure of the heart did not change in any of the groups. Relative heart weight increased, blood pressure, total peripheral resistance and nutritive blood flow of the myocardium decreased, while myocardial vascular resistance increased. There was no significant interaction between the effects of alcohol and the duration of exposure to alcohol for any of the parameters monitored. It is concluded that chronic alcohol intake should be taken into consideration in aetiology of ischaemic heart disease.

Animals↗
PubMedDate not supplied

Cardiovascular actions of cannabinoids and their generation during shock.

Marijuana is a widely abused recreational drug well known for its psychoactive properties. Cannabinoids, the active ingredients of marijuana, elicit their neurobehavioral effects by interacting with the CB1 cannabinoid receptor subtype, expressed primarily in the brain but also present in some peripheral tissues. A second receptor subtype, the CB2 receptor, is expressed on cells of the immune system and is thought to be responsible for the immunosuppressant effects of cannabinoids. Recently, endogenous lipidlike substances have been identified, including arachidonyl ethanolamide (anandamide) and 2-arachidonyl glyceride, that bind to cannabinoid receptors and mimic many of the neurobehavioral effects of plant-derived cannabinoids. Both plant-derived cannabinoids and the endogenous ligands have been shown to elicit hypotension and bradycardia via activation of peripherally located CB1 receptors. Possible underlying mechanisms include presynaptic CB1 receptor mediated inhibition of norepinephrine release from peripheral sympathetic nerve terminals, and/or direct vasodilation via activation of vascular cannabinoid receptors. The latter may also be the target of endocannabinoids of vascular endothelial origin. Recent studies indicate that a peripheral endogenous cannabinoid system in circulating macrophages and platelets is activated in hemorrhagic and septic shock and may contribute to the hypotension associated with these conditions via activation of vascular cannabinoid receptors. The potential role of this mechanism in human shock conditions is under investigation.

Animals↗
PubMedDate not supplied

The tachycardia associated with the defense reaction involves activation of both GABAA and GABAB receptors in the nucleus tractus solitarii.

In urethane-anesthetized rats, the tachycardia associated with the defense reaction can be elicited by unilateral microinjections of the GABAA-antagonist, bicuculline methyliodide (BMI, 20 pmol), into the dorsomedial nucleus (DMN) of the hypothalamus. This effect is thought to be mediated via a pathway that activates GABAergic interneurons in the medullary nucleus tractus solitarii (NTS) which, in turn, inhibit vagal outflow to the heart. Ipsilateral intra-NTS microinjection of BMI (10 pmol) or the GABAB-antagonist, 2-OH-saclofen (400 pmol), attenuated the tachycardia elicited from the DMN. The tachycardia was also inhibited by intra-NTS administration of the NMDA-receptor channel blocker, MK-801 (30 pmol), or the non-NMDA antagonist, CNQX (400 pmol). These findings are interpreted to indicate that a) GABAergic control of heart rate at the level of the NTS is mediated by both GABAA and GABAB receptors, and b) descending input from the DMN to the NTS releases GABA via glutamate acting on ionotropic glutamate receptors located on GABAergic interneurons.

6-Cyano-7-nitroquinoxaline-2,3-dione↗