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Biomedical subjects

C Farsang

Publications and source records attributed to C Farsang.

At least 55 records · Page 3Linked to original sources
PubMed1987

Prazosin improves atherogenic index and inhibits the deleterious effect of dihydrochlorothiazide in patients with essential hypertension.

Twenty-three patients with essential hypertension were treated consecutively with prazosin or dihydrochlorothiazide or the combination of the two, each treatment period lasting for three months. Blood pressure, heart rate (HR), serum levels of total cholesterol, triglycerides, HDL-c and LDL-c, uric acid, glucose, Na, and K were measured during the baseline and at the end of each treatment period. Both prazosin and dihydrochlorothiazide (THI) decreased blood pressure but the effect of the combination was more pronounced than that of the monotherapies. Prazosin had no effect on the plasma level of total cholesterol, triglycerides, uric acid, Na, K, and glucose but increased HDL-c, decreased LDL-c, and thereby significantly improved (decreased) atherogenic index (total cholesterol/HDL-c). THI increased total cholesterol, triglycerides, LDL + VLDL-c, glucose, and uric acid; decreased HDL-c and K levels; and significantly increased the atherogenic index. Prazosin neutralized the effects of THI on total cholesterol, triglycerides, HDL-c, and on LDL + VLDL-c but not on glucose, uric acid, or K. These results suggest that the effects of THI on plasma lipids may be mediated by alpha 1-adrenoceptor-related mechanisms but the effects on glucose, uric acid, and K, probably may not be mediated by these mechanisms.

Adult↗
PubMed1985

beta-Endorphin and essential hypertension: importance of the clonidine-naloxone interaction.

Analysis of the effect of naloxone (0.4 mg iv.) on clonidine hypotension in 80 patients with essential hypertension revealed that two groups could be separated. In the responding group (43 pts) naloxone increased blood pressure and heart rate in clonidine-treated patients while in the non-responding group (37 pts) it has no such effect. Patients in the responding group had higher cardiac output, stroke volume, plasma renin activity, plasma adrenaline and beta-endorphin levels and lower total peripheral resistance, shorter history of hypertension and lesser body weight than those in the non-responding group. The pressor effect of naloxone in four responding patients treated with clonidine for 29 months tended to be smaller compared to the response obtained after a 3-day clonidine therapy. Results favour the hypothesis of the existence of two (responding, non-responding) groups of patients with essential hypertension. Further work will clarify whether these groups represent different pathogenesis or they indicate only a different stage of hypertension.

Adult↗
PubMed1985

Surgical treatment of renovascular hypertension in children and adolescents.

Renovascular disorders are rather rare in children and adolescents but have severe consequences due to complicating hypertension. Six cases successfully treated by surgery are described. The importance of early diagnosis and vascular correction is stressed; normalization of blood pressure has been achieved in every case.

Adolescent↗
PubMed1984

Beta-endorphin contributes to the antihypertensive effect of clonidine in a subset of patients with essential hypertension.

Naloxone [0.4 mg iv.] increased blood pressure and heart rate of 13 clonidine-treated [0.3 mg per os for 3 days] patients with essential hypertension [reacting group] while it has no such effect in 11 clonidine-treated patients [non-reacting gr.] Clonidine increased plasma beta-endorphin concentration of the reacting patients by 17.53 +/- 1.68 pM/1 and in the non-reacting ones by 5.91 +/- 0.88 pM/1. Significant linear correlation was found between the clonidine-induced increase in plasma beta-endorphin level and the naloxone-induced change in mean blood pressure [r = 0.9572, n:24, p less than 0.001]. In another group of 8 patients clonidine [0.15 mg iv.] decreased mean blood pressure but naloxone, 30 min after the clonidine injection, did not reverse the clonidine hypotension. We suggest that beta-endorphin, released by chr. clonidine therapy, contributes to the anti-hypertensive effect only in the reacting group.

Adult↗
PubMed1984

Effects of clonidine and guanfacine in essential hypertension.

Daily doses of 0.3 mg clonidine and 3 mg guanfacine were equiactive in decreasing blood pressure and heart rate in 17 subjects with essential hypertension. Clonidine decreased cardiac output and guanfacine decreased total peripheral resistance, while clonidine had no effect on stroke volume but guanfacine increased it. Both clonidine and guanfacine decreased plasma renin activity. Naloxone, 0.4 mg iv, reversed the antihypertensive effect of clonidine but was ineffective even at higher doses (1.6 mg iv) when subjects were treated with placebo or guanfacine. It is suggested that the hemodynamic differences between the two centrally acting alpha 2-adrenoceptor agonist antihypertensive drugs may at least in part result from the involvement of opioid mechanisms only in the action of clonidine.

Adult↗
PubMed1984

Reversal by naloxone of the antihypertensive action of clonidine: involvement of the sympathetic nervous system.

The effects of clonidine, naloxone, and their combination on arterial blood pressure (BP), heart rate (HR), and hemodynamic and biochemical parameters were examined in 29 patients with essential hypertension. Treatment for 3 days with 0.3 mg/day clonidine reduced BP and HR, and these effects were quickly reversed by a single injection of 0.4 mg iv naloxone in 17 of the patients (responders), but not in the remaining 12 (nonresponders). Responders had higher control values for cardiac output, stroke index, plasma renin activity (PRA), and plasma epinephrine levels than did nonresponders. Basal BP was similar in the two groups, but clonidine decreased BP, PRA, and plasma epinephrine more in responders than in nonresponders. Naloxone given during placebo treatment had no significant effects. During clonidine treatment naloxone increased BP, HR, total peripheral resistance, PRA, and plasma epinephrine and norepinephrine, and decreased stroke volume in responders, whereas in nonresponders its only effect was a small increase in HR. It is concluded that in a subset of hyperadrenergic, hypertensive patients the antihypertensive effect of clonidine involves a naloxone-reversible inhibition of central sympathetic outflow, probably mediated by the release of an endogenous opioid.

Adult↗
PubMed1984

Thyrotropin releasing hormone and naloxone attenuate the antihypertensive action of central alpha 2-adrenoceptor stimulation through different mechanisms.

In various forms of shock, TRH is equivalent to naloxone in reversing the hypotension and improving the survival rate. The present findings indicate that in spontaneously hypertensive rats (SHR), TRH has another naloxone-like effect in antagonizing the antihypertensive response to clonidine and alpha-methyldopa. When given during the hypotensive response to alpha-methyldopa, both naloxone and TRH produce a pressor response. While this effect of naloxone is blocked by prazosin, the effect of TRH is not influenced by prazosin or hexamethonium but is inhibited by a vasopressin pressor antagonist. This suggests that the pressor response to naloxone is mediated by the sympathetic nervous system, whereas the similar action of TRH is independent of sympatho-adrenomedullary functions and it is mediated by vasopressin.

Animals↗